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especialmente de genes relacionados a doen&#231;as autoimunes e inflamat&#243;rias&#44; al&#233;m de fatores ambientais&#46;<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">3&#44;4</span></a> A literatura relata que v&#225;rios genes do sistema imunol&#243;gico contribuem para o desenvolvimento dessa doen&#231;a&#44; como o gene regulador autoimune &#40;AIRE&#41;&#44; ant&#237;geno leucocit&#225;rio humano &#40;HLA&#41;&#44; genes de interleucina &#40;IL&#41;&#44; ant&#237;geno 4 associado ao linf&#243;cito T citot&#243;xico &#40;CTLA4&#41;&#44; prote&#237;na tirosina fosfatase n&#227;o receptora 22 &#40;PTPN22&#41;&#44; fator de necrose tumoral da superfam&#237;lia 6 ou CD95 &#40;FAS&#41; e ligante FAS &#40;FASL&#41;&#44; entre outros&#46;<a class="elsevierStyleCrossRefs" href="#bib0125"><span class="elsevierStyleSup">5&#44;6</span></a></p><p id="par0010" class="elsevierStylePara elsevierViewall">O CTLA4 &#40;2q34&#41; &#233; membro da superfam&#237;lia imunoglobulinas que codificam uma prote&#237;na que &#233; potente reguladora negativa da resposta das c&#233;lulas T&#46; Por seu papel na manuten&#231;&#227;o da toler&#226;ncia imunol&#243;gica&#44; ele tem sido apontado como um gene de suscetibilidade em doen&#231;as autoimunes humanas&#44;e apresenta v&#225;rios polimorfismos associados ao seu desenvolvimento&#46;<a class="elsevierStyleCrossRef" href="#bib0135"><span class="elsevierStyleSup">7</span></a> Entre os polimorfismos&#44; duas variantes gen&#233;ticas podem contribuir para a suscetibilidade ao AA&#58;<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49AG &#40;rs231775&#41;&#44; uma varia&#231;&#227;o <span class="elsevierStyleItalic">missense</span> que leva a uma substitui&#231;&#227;o do amino&#225;cido treonina por alanina no c&#243;don 17 no pept&#237;deo l&#237;der &#40;T17A&#41; e CT60 &#40;rs3087243&#41;&#44; localizada em 236<span class="elsevierStyleHsp" style=""></span>bp <span class="elsevierStyleItalic">downstream</span> no gene CTLA4 &#40;3&#8217;&#8208;UTR&#41;&#46;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">8</span></a> No entanto&#44; estudos recentes feitos em diferentes popula&#231;&#245;es indicam que a rela&#231;&#227;o dessas variantes gen&#233;ticas no desenvolvimento de AA &#233; controversa&#46;<a class="elsevierStyleCrossRefs" href="#bib0115"><span class="elsevierStyleSup">3&#44;9</span></a></p><p id="par0015" class="elsevierStylePara elsevierViewall">O presente estudo teve como objetivo determinar se as variantes dos genes CTLA4<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49AG &#40;rs231775&#41; e CT60 &#40;rs3087243&#41; constituem um fator de predisposi&#231;&#227;o para AA em uma coorte de pacientes mexicanos&#46;</p></span><span id="sec0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0050">Material e m&#233;todos</span><span id="sec0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0055">Sele&#231;&#227;o de pacientes e controles</span><p id="par0020" class="elsevierStylePara elsevierViewall">O estudo incluiu 50 indiv&#237;duos mexicanos com diagn&#243;stico de AA n&#227;o relacionados entre si &#40;32 mulheres e 18 homens&#59; idade m&#233;dia&#58; 30<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>15 anos&#41; e 100 participantes saud&#225;veis &#40;59 mulheres e 41 homens&#59; idade m&#233;dia&#58; 25<span class="elsevierStyleHsp" style=""></span>&#177;<span class="elsevierStyleHsp" style=""></span>8 anos&#41;&#59; os controles apresentavam hist&#243;ria familiar m&#233;dica negativa para doen&#231;as autoimunes&#47;inflamat&#243;rias&#46; Os pacientes foram recrutados no Departamento de Dermatologia ap&#243;s a aceita&#231;&#227;o e assinatura do termo de consentimento livre e esclarecido&#46; Este estudo foi aprovado pelo Comit&#234; de &#201;tica em Pesquisa e registrado sob o c&#243;digo DE09&#8208;001&#46; Detalhes adicionais sobre as caracter&#237;sticas cl&#237;nicas e demogr&#225;ficas&#44; tipo de AA e distribui&#231;&#227;o de cada paciente foram obtidos durante a avalia&#231;&#227;o cl&#237;nica&#46;</p></span><span id="sec0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0060">Isolamento e genotipagem de DNA</span><p id="par0025" class="elsevierStylePara elsevierViewall">O DNA gen&#244;mico foi isolado do sangue venoso perif&#233;rico com o m&#233;todo <span class="elsevierStyleItalic">salting out</span> e suspenso em Tris&#8208;EDTA &#40;pH 7&#44;8&#41; a uma concentra&#231;&#227;o final de 0&#44;1 a 1&#44;0<span class="elsevierStyleHsp" style=""></span>&#956;g&#47;&#956;L antes do uso&#46; As frequ&#234;ncias genot&#237;picas e al&#233;licas das variantes do gene CTLA4<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49AG &#40;rs231775&#41; e CT60 &#40;rs3087243&#41; foram caracterizadas por PCR&#8208;RFLP com um termociclador MJ Mini PTC1148 &#40;Bio&#8208;Rad&#44; Hercules&#59; CA&#44; Estados Unidos&#41;&#44; <span class="elsevierStyleItalic">primers</span> oligonucleot&#237;dicos espec&#237;ficos &#40;IDT&#44; Coralville&#44; IA&#44; Estados Unidos&#41; e enzimas de restri&#231;&#227;o &#40;New England Biolabs&#44; Ipswich&#44; MA&#44; Estados Unidos&#41; de acordo com um protocolo publicado anteriormente&#46;<a class="elsevierStyleCrossRef" href="#bib0150"><span class="elsevierStyleSup">10</span></a> Os fragmentos obtidos foram analisados por eletroforese em gel de agarose a 2&#44;5&#37; com brometo de et&#237;dio&#44; observados no transiluminador UVP modelo 2UV de alto desempenho &#40;Upland&#44; CA&#44; E&#41; e documentados&#46;</p></span><span id="sec0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0065">An&#225;lise estat&#237;stica</span><p id="par0030" class="elsevierStylePara elsevierViewall">Para an&#225;lise gen&#233;tica&#44; o tamanho da amostra foi calculado com base na incid&#234;ncia mundial de AA de 2&#37;&#44;<a class="elsevierStyleCrossRef" href="#bib0155"><span class="elsevierStyleSup">11</span></a> assumiu&#8208;se um poder de 99&#44;0&#37; &#40;um valor&#8208;Z de 2&#44;33&#41;&#44; foi obtido o n&#250;mero m&#237;nimo de 43 indiv&#237;duos&#46;</p><p id="par0035" class="elsevierStylePara elsevierViewall">O <span class="elsevierStyleItalic">software</span> SPSS v21&#46;0 para Windows &#40;SPSS&#44; Inc&#46; Chicago&#44; IL&#44; Estados Unidos&#41; e o programa estat&#237;stico Epi&#8208;INFO<span class="elsevierStyleSup">TM</span> 7 &#40;Stone&#46; Mountain&#44; GA&#44; USD Inc&#41; foram usados para an&#225;lise dos dados&#46; O equil&#237;brio de Hardy&#8208;Weinberg para os alelos foi obtido por meio de um teste de qualidade de ajuste e a depend&#234;ncia genot&#237;pica entre pacientes e controles foi determinada com um teste de &#967;<span class="elsevierStyleSup">2</span>&#46; A raz&#227;o de probabilidades &#40;OR&#41; foi calculada a partir de tabelas de conting&#234;ncia 2<span class="elsevierStyleHsp" style=""></span>&#215;<span class="elsevierStyleHsp" style=""></span>2 &#40;p<span class="elsevierStyleHsp" style=""></span>&#60;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#46;</p></span></span><span id="sec0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0070">Resultados</span><span id="sec0035" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0075">Caracter&#237;sticas cl&#237;nicas dos participantes</span><p id="par0040" class="elsevierStylePara elsevierViewall">O presente estudo analisou a distribui&#231;&#227;o do gen&#243;tipo e a frequ&#234;ncia al&#233;lica das variantes do gene CTLA4<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49AG e CT60&#46; O universo do estudo &#40;n&#41; consistiu em 50 pacientes com AA e 100 controles&#46; A apresenta&#231;&#227;o cl&#237;nica da AA nos pacientes foi&#58; 41 pacientes com AA em placas &#40;unifocal n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>14&#44; oito mulheres e seis homens&#59; multifocal n<span class="elsevierStyleHsp" style=""></span>&#61;<span class="elsevierStyleHsp" style=""></span>27&#44; 19 mulheres e 8 homens&#41;&#44; quatro pacientes com AA ofi&#225;sica &#40;tr&#234;s mulheres e um homem&#41;&#44; uma mulher com AA total e quatro pacientes com AA universal &#40;tr&#234;s homens e um mulher&#41;&#46; Dez pacientes &#40;20&#37;&#41; tinham hist&#243;rico pessoal de doen&#231;as autoimunes &#40;vitiligo&#44; diabetes melito tipo 2&#44; entre outros&#41; e 36 indiv&#237;duos &#40;72&#37;&#41; tinham hist&#243;rico familiar de doen&#231;a imunol&#243;gica&#46;</p></span><span id="sec0040" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0080">An&#225;lise de alelos e gen&#243;tipos</span><p id="par0045" class="elsevierStylePara elsevierViewall">V&#225;rios testes foram feitos para ambas as variantes gen&#233;ticas&#44; a fim de avaliar o equil&#237;brio de Hardy&#8208;Weinberg &#40;EHW&#59; <a class="elsevierStyleCrossRef" href="#tbl0005">tabela 1</a>&#41;&#44; todos com p<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#44; indicaram que as variantes dos genes rs231775 e rs3087243 estavam em EHW nos pacientes com AA e controles&#46;</p><elsevierMultimedia ident="tbl0005"></elsevierMultimedia><p id="par0050" class="elsevierStylePara elsevierViewall">Os alelos e gen&#243;tipos do CTLA4 rs231775 e do rs3087243 do grupo controle foram comparados com os dos indiv&#237;duos com AA &#40;todos os tipos de AA&#41; e com os diferentes tipos de AA&#59; a <a class="elsevierStyleCrossRef" href="#tbl0005">tabela 1</a> apresenta os resultados dessa compara&#231;&#227;o&#46; Para CTLA4 rs231775&#44; 30&#37; dos pacientes com AA apresentaram gen&#243;tipo AA do tipo selvagem homozig&#243;tico&#44; 48&#37; apresentaram o gen&#243;tipo AG heterozig&#243;tico e os 22&#37; restantes&#44; gen&#243;tipo GG variante homozig&#243;tica&#46; Para CTLA4 rs3087243&#44; 44&#37; dos pacientes com AA apresentaram o gen&#243;tipo GG do tipo selvagem homozig&#243;tico&#44; 44&#37; apresentaram o gen&#243;tipo AG heterozig&#243;tico e os 12&#37; restantes&#44; AA variante homozig&#243;tica&#46;</p></span><span id="sec0045" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0085">Associa&#231;&#227;o dos gen&#243;tipos em pacientes com alopecia areata</span><p id="par0055" class="elsevierStylePara elsevierViewall">Quando os gen&#243;tipos e frequ&#234;ncias de alelos CTLA4 rs231775 e rs3087243 foram comparados entre toda a coorte &#40;todos os tipos de AA&#41; e controles&#44; observou&#8208;se que o gen&#243;tipo AG heterozig&#243;tico para CTLA4 rs231775 e rs3087243 era mais frequente nos controles do que em todos os grupos de pacientes com AA&#46; Al&#233;m disso&#44; n&#227;o se observou associa&#231;&#227;o entre variantes al&#233;licas e AA nos pacientes analisados &#40;p<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#59; <a class="elsevierStyleCrossRef" href="#tbl0010">tabela 2</a>&#41;&#46; Al&#233;m disso&#44; n&#227;o foi encontrada rela&#231;&#227;o entre o gen&#243;tipo e o tipo de AA com a hist&#243;ria pessoal&#47;familiar de doen&#231;as autoimunes ou o sexo dos pacientes analisados &#40;p<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#59; <a class="elsevierStyleCrossRef" href="#tbl0015">tabela 3</a>&#41;&#46;</p><elsevierMultimedia ident="tbl0010"></elsevierMultimedia><elsevierMultimedia ident="tbl0015"></elsevierMultimedia></span></span><span id="sec0050" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0090">Discuss&#227;o</span><p id="par0060" class="elsevierStylePara elsevierViewall">AA &#233; doen&#231;a autoimune com perda de cabelos que tem sido associada a m&#250;ltiplas variantes gen&#233;ticas&#44; v&#225;rias das quais participam de vias de resposta imune relacionadas ao HLA&#46;<a class="elsevierStyleCrossRef" href="#bib0160"><span class="elsevierStyleSup">12</span></a> O produto do gene CTLA4 &#233; um receptor expresso pelas c&#233;lulas T CD4<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>e CD8<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>&#46; Experimentos em camundongos <span class="elsevierStyleItalic">knockout</span> demonstraram o importante papel que o CTLA4 desempenha na prote&#231;&#227;o contra a autoimunidade&#46; O CTLA&#8208;4 &#233; um regulador negativo cr&#237;tico das respostas das c&#233;lulas T e sua a&#231;&#227;o nas c&#233;lulas Treg pode controlar a atividade de outras c&#233;lulas e a autoimunidade fatal&#46;<a class="elsevierStyleCrossRef" href="#bib0165"><span class="elsevierStyleSup">13</span></a></p><p id="par0065" class="elsevierStylePara elsevierViewall">Foi sugerida a associa&#231;&#227;o entre a presen&#231;a das variantes do gene CTLA4 e o desenvolvimento de diferentes doen&#231;as autoimunes&#46;<a class="elsevierStyleCrossRefs" href="#bib0170"><span class="elsevierStyleSup">14&#44;15</span></a> No entanto&#44; nas doen&#231;as imunol&#243;gicas dermatol&#243;gicas&#44; os resultados s&#227;o controversos&#59; no vitiligo&#44; a literatura relata tanto sua participa&#231;&#227;o como n&#227;o influ&#234;ncia&#46;<a class="elsevierStyleCrossRef" href="#bib0180"><span class="elsevierStyleSup">16</span></a> Uma situa&#231;&#227;o semelhante foi observada no desenvolvimento da psor&#237;ase&#46;<a class="elsevierStyleCrossRefs" href="#bib0185"><span class="elsevierStyleSup">17&#44;18</span></a></p><p id="par0070" class="elsevierStylePara elsevierViewall">Nesse sentido&#44; considerando a poss&#237;vel contribui&#231;&#227;o da fun&#231;&#227;o autoimune na alopecia&#44; estudos de variantes gen&#233;ticas do gene CTLA4 foram conduzidos em diversas popula&#231;&#245;es&#46; Uma an&#225;lise anterior dessa associa&#231;&#227;o sugeriu o poss&#237;vel envolvimento das variantes do gene CTLA4 como fator de risco no desenvolvimento de AA em uma popula&#231;&#227;o europeia&#44;<a class="elsevierStyleCrossRef" href="#bib0140"><span class="elsevierStyleSup">8</span></a> com efeito mais forte em pacientes com formas acentuadas da doen&#231;a&#46;</p><p id="par0075" class="elsevierStylePara elsevierViewall">Outro estudo feito em uma popula&#231;&#227;o italiana&#44; no qual foram analisadas as variantes dos genes rs231775 e rs3087243&#44; apontou esse &#250;ltimo como fator de risco no desenvolvimento de AA em placas&#46;<a class="elsevierStyleCrossRef" href="#bib0145"><span class="elsevierStyleSup">9</span></a> Por outro lado&#44; estudo feito no Ir&#227; n&#227;o conseguiu provar a associa&#231;&#227;o da variante do gene rs3087243 no desenvolvimento de AA&#46;<a class="elsevierStyleCrossRef" href="#bib0115"><span class="elsevierStyleSup">3</span></a></p><p id="par0080" class="elsevierStylePara elsevierViewall">Em estudo anterior&#44; os autores observaram a participa&#231;&#227;o de variantes gen&#233;ticas de TNF&#945; e PTPN22<a class="elsevierStyleCrossRef" href="#bib0195"><span class="elsevierStyleSup">19</span></a> como fator de risco para AA em pacientes mexicanos&#59; a fun&#231;&#227;o de ambos os genes est&#225; relacionada &#224; regula&#231;&#227;o dos mecanismos imunol&#243;gicos&#46; No entanto&#44; a participa&#231;&#227;o das variantes gen&#233;ticas do CTLA4 na AA n&#227;o foi analisada nessa popula&#231;&#227;o&#46;</p><p id="par0085" class="elsevierStylePara elsevierViewall">Alguns SNPs dentro do gene CTLA&#8208;4 j&#225; foram analisados quanto &#224; suscetibilidade &#224; artrite reumatoide &#40;AR&#41; na popula&#231;&#227;o mexicana&#59; entre eles&#44; rs5742909&#44; rs231775 e rs3087243&#59; sugere&#8208;se que o hapl&#243;tipo &#8208;319C&#47;<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49G&#47;CT60G do gene CTLA&#8208;4 &#233; fator de risco para AR&#44; enquanto que o SNP rs3087243 pode ser fator protetor contra esse tipo de doen&#231;a autoimune&#46;<a class="elsevierStyleCrossRef" href="#bib0200"><span class="elsevierStyleSup">20</span></a></p><p id="par0090" class="elsevierStylePara elsevierViewall">No entanto&#44; n&#227;o foram observadas diferen&#231;as significativas para rs231775 e rs3087243 no presente estudo &#40;<a class="elsevierStyleCrossRef" href="#tbl0010">tabela 2</a>&#41;&#44; sugeriu&#8208;se que essas variantes n&#227;o s&#227;o fator de risco no desenvolvimento de AA ou de AA em placas na popula&#231;&#227;o mexicana&#46;</p></span><span id="sec0055" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0095">Conclus&#227;o</span><p id="par0095" class="elsevierStylePara elsevierViewall">As variantes gen&#233;ticas rs231775 e rs3087243 do gene CTLA4 n&#227;o constituem fator de risco no desenvolvimento de AA na popula&#231;&#227;o mexicana de Monterrey&#44; M&#233;xico&#46; Al&#233;m disso&#44; essas variantes gen&#233;ticas n&#227;o apresentam associa&#231;&#227;o com antecedentes familiares&#47;pessoais de doen&#231;as autoimunes ou com o g&#234;nero dos sujeitos do estudo&#46;</p></span><span id="sec0060" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0100">Suporte financeiro</span><p id="par0100" class="elsevierStylePara elsevierViewall">Nenhum&#46;</p></span><span id="sec0065" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0105">Contribui&#231;&#227;o dos autores</span><p id="par0105" class="elsevierStylePara elsevierViewall">Mauricio Andr&#233;s Salinas Santander&#58; An&#225;lise estat&#237;stica&#59; aprova&#231;&#227;o da vers&#227;o final do manuscrito&#59; concep&#231;&#227;o e planejamento do estudo&#59; elabora&#231;&#227;o e reda&#231;&#227;o do manuscrito&#59; obten&#231;&#227;o&#44; an&#225;lise e interpreta&#231;&#227;o dos dados&#59; participa&#231;&#227;o efetiva na orienta&#231;&#227;o da pesquisa&#59; revis&#227;o cr&#237;tica da literatura&#59; revis&#227;o cr&#237;tica do manuscrito&#46;</p><p id="par0110" class="elsevierStylePara elsevierViewall">Cristina Susana Cantu&#8208;Salinas&#58; Aprova&#231;&#227;o da vers&#227;o final do manuscrito&#59; concep&#231;&#227;o e planejamento do estudo&#59; elabora&#231;&#227;o e reda&#231;&#227;o do manuscrito&#59; obten&#231;&#227;o&#44; an&#225;lise e interpreta&#231;&#227;o dos dados&#59; participa&#231;&#227;o efetiva na orienta&#231;&#227;o da pesquisa&#59; revis&#227;o cr&#237;tica da literatura&#59; revis&#227;o cr&#237;tica do manuscrito&#46;</p><p id="par0115" class="elsevierStylePara elsevierViewall">Jorge Ocampo&#8208;Candiani&#58; Aprova&#231;&#227;o da vers&#227;o final do manuscrito&#59; concep&#231;&#227;o e planejamento do estudo&#59; participa&#231;&#227;o efetiva na orienta&#231;&#227;o da pesquisa&#59; revis&#227;o cr&#237;tica da literatura&#59; revis&#227;o cr&#237;tica do manuscrito&#46;</p><p id="par0120" class="elsevierStylePara elsevierViewall">Victor de Jesus Suarez&#8208;Valencia&#58; Aprova&#231;&#227;o da vers&#227;o final do manuscrito&#59; elabora&#231;&#227;o e reda&#231;&#227;o do manuscrito&#59; obten&#231;&#227;o&#44; an&#225;lise e interpreta&#231;&#227;o dos dados&#59; revis&#227;o cr&#237;tica da literatura&#59; revis&#227;o cr&#237;tica do manuscrito&#46;</p><p id="par0125" class="elsevierStylePara elsevierViewall">Jennifer Guadalupe Ramirez&#8208;Guerrero&#58; Aprova&#231;&#227;o da vers&#227;o final do manuscrito&#59; elabora&#231;&#227;o e reda&#231;&#227;o do manuscrito&#59; obten&#231;&#227;o&#44; an&#225;lise e interpreta&#231;&#227;o dos dados&#59; revis&#227;o cr&#237;tica da literatura&#46;</p><p id="par0130" class="elsevierStylePara elsevierViewall">Celia Nohemi Sanchez&#8208;Dominguez&#58; Aprova&#231;&#227;o da vers&#227;o final do manuscrito&#59; elabora&#231;&#227;o e reda&#231;&#227;o do manuscrito&#59; revis&#227;o cr&#237;tica da literatura&#59; revis&#227;o cr&#237;tica do manuscrito&#46;</p></span><span id="sec0070" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0110">Conflitos de interesse</span><p id="par0135" class="elsevierStylePara elsevierViewall">Nenhum&#46;</p></span></span>"
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            0 => "Alopecia areata"
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        "resumen" => "<span id="abst0005" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0010">Fundamentos</span><p id="spar9030" class="elsevierStyleSimplePara elsevierViewall">Alopecia areata &#233; doen&#231;a autoimune que causa perda de cabelo sem cicatrizes na les&#227;o&#46; As variantes gen&#233;ticas do gene do ant&#237;geno 4 associado ao linf&#243;cito T citot&#243;xico &#40;CTLA4&#41;&#44; um regulador negativo da resposta das c&#233;lulas T&#44; foram associadas a predisposi&#231;&#227;o a doen&#231;as autoimunes em diferentes popula&#231;&#245;es&#59; no entanto&#44; o envolvimento dessas variantes gen&#233;ticas no desenvolvimento da alopecia areata &#233; controverso&#46;</p></span> <span id="abst0010" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0015">Objetivo</span><p id="spar0005" class="elsevierStyleSimplePara elsevierViewall">Avaliar a associa&#231;&#227;o potencial de duas variantes do gene CTLA4 e alopecia areata em uma popula&#231;&#227;o mexicana&#46;</p></span> <span id="abst0015" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0020">M&#233;todos</span><p id="spar0010" class="elsevierStyleSimplePara elsevierViewall">Foram genotipadas por PCR&#8208;RFLP as variantes<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49AG &#40;rs231775&#41; e CT60 &#40;rs3087243&#41; de 50 pacientes com alopecia areata e 100 controles saud&#225;veis&#46;</p></span> <span id="abst0020" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0025">Resultados</span><p id="spar0015" class="elsevierStyleSimplePara elsevierViewall">N&#227;o foi observada diferen&#231;a estat&#237;stica para alguma das variantes gen&#233;ticas quanto &#224;s frequ&#234;ncias al&#233;licas ou genot&#237;picas entre os pacientes com alopecia areata e controles quando considerados os par&#226;metros de hist&#243;ria familiar&#47;pessoal de doen&#231;as autoimunes ou sexo &#40;p<span class="elsevierStyleHsp" style=""></span>&#62;<span class="elsevierStyleHsp" style=""></span>0&#44;05&#41;&#46;</p></span> <span id="abst0025" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0030">Limita&#231;&#245;es do estudo</span><p id="spar0020" class="elsevierStyleSimplePara elsevierViewall">Amostra pequena de pacientes e coleta de dados em apenas uma popula&#231;&#227;o do nordeste do M&#233;xico&#46;</p></span> <span id="abst0030" class="elsevierStyleSection elsevierViewall"><span class="elsevierStyleSectionTitle" id="sect0035">Conclus&#227;o</span><p id="spar0025" class="elsevierStyleSimplePara elsevierViewall">As variantes gen&#233;ticas rs231775 e rs3087243 do gene CTLA4 n&#227;o s&#227;o um fator de risco para o desenvolvimento de alopecia areata na popula&#231;&#227;o mexicana analisada&#46;</p></span>"
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      0 => array:2 [
        "etiqueta" => "&#9734;"
        "nota" => "<p class="elsevierStyleNotepara" id="npar0005">Como citar este artigo&#58; Salinas&#8208;Santander MA&#44; Cantu&#8208;Salinas CS&#44; Ocampo&#8208;Candiani J&#44; Suarez&#8208;Valencia VJ&#44; Ramirez&#8208;Guerrero JG&#44; Sanchez&#8208;Dominguez CN&#46; CTLA4<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49AG &#40;rs231775&#41; and CT60 &#40;rs3087243&#41; gene variants are not associated with alopecia areata in a Mexican population from Monterrey Mexico&#46; An Bras Dermatol&#46; 2020&#59;95&#58;283&#8211;8&#46;</p>"
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        "nota" => "<p class="elsevierStyleNotepara" id="npar0010">Trabalho realizado no Departamento de Investiga&#231;&#227;o&#44; Faculdade de Medicina da Universidade de Saltillo&#44; Universidade Aut&#244;noma de Coahuila&#44; Saltillo&#44; Coahuila&#44; M&#233;xico e Servi&#231;o de Dermatologia&#44; Hospital Universit&#225;rio Dr&#46; Jos&#233; Eleuterio Gonz&#225;lez&#44; Faculdade de Medicina&#44; Universidade Aut&#244;noma de Nuevo Le&#243;n&#44; Nuevo Le&#243;n&#44; M&#233;xico&#46;</p>"
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                  """
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          "pt" => "<p id="spar0040" class="elsevierStyleSimplePara elsevierViewall">An&#225;lise das variantes gen&#233;ticas CTLA4<span class="elsevierStyleHsp" style=""></span>&#43;<span class="elsevierStyleHsp" style=""></span>49AG &#40;rs231775&#41; e CT60 &#40;rs3087243&#41; por sexo e hist&#243;ria pessoal&#47;familiar de doen&#231;as autoimunes</p>"
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Vol. 95. Núm. 3.
Páginas 283-288 (1 maio 2020)
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Vol. 95. Núm. 3.
Páginas 283-288 (1 maio 2020)
Investigação
Open Access
As variantes do gene CTLA4+49AG (rs231775) e CT60 (rs3087243) não estão associadas à alopecia areata em população mexicana de Monterrey, México
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Mauricio Andrés Salinas‐Santandera,
Autor para correspondência
msalinsa@yahoo.com

Autor para correspondência.
, Cristina Susana Cantu‐Salinasb, Jorge Ocampo‐Candianib, Victor de Jesus Suarez‐Valenciaa, Jennifer Guadalupe Ramirez‐Guerreroa, Celia Nohemi Sanchez‐Dominguezc
a Departamento de Investigação, Faculdade de Medicina da Universidade de Saltillo, Universidade Autônoma de Coahuila, Saltillo, México
b Serviço de Dermatologia, Hospital Universitário Dr. José Eleuterio González, Universidade Autônoma de Nuevo León, Monterrey, México
c Departamento de Bioquímica e Medicina Molecular, Faculdade de Medicina, Universidade Autônoma de Nuevo León, Nuevo León, México
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Tabelas (3)
Tabela 1. Testes para desvio do equilíbrio de Hardy‐Weinberg em pacientes com AA e controles saudáveis
Tabela 2. Frequência de alelos e genótipo das variantes genéticas CTLA4+49AG (rs231775) e CT60 (rs3087243) em pacientes com AA e controles saudáveis
Tabela 3. Análise das variantes genéticas CTLA4+49AG (rs231775) e CT60 (rs3087243) por sexo e história pessoal/familiar de doenças autoimunes
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Resumo
Fundamentos

Alopecia areata é doença autoimune que causa perda de cabelo sem cicatrizes na lesão. As variantes genéticas do gene do antígeno 4 associado ao linfócito T citotóxico (CTLA4), um regulador negativo da resposta das células T, foram associadas a predisposição a doenças autoimunes em diferentes populações; no entanto, o envolvimento dessas variantes genéticas no desenvolvimento da alopecia areata é controverso.

Objetivo

Avaliar a associação potencial de duas variantes do gene CTLA4 e alopecia areata em uma população mexicana.

Métodos

Foram genotipadas por PCR‐RFLP as variantes+49AG (rs231775) e CT60 (rs3087243) de 50 pacientes com alopecia areata e 100 controles saudáveis.

Resultados

Não foi observada diferença estatística para alguma das variantes genéticas quanto às frequências alélicas ou genotípicas entre os pacientes com alopecia areata e controles quando considerados os parâmetros de história familiar/pessoal de doenças autoimunes ou sexo (p>0,05).

Limitações do estudo

Amostra pequena de pacientes e coleta de dados em apenas uma população do nordeste do México.

Conclusão

As variantes genéticas rs231775 e rs3087243 do gene CTLA4 não são um fator de risco para o desenvolvimento de alopecia areata na população mexicana analisada.

Palavras‐chave:
Alopecia areata
Doenças autoimunes
Nucleotídeo único
Polimorfismo
Texto Completo
Introdução

A alopecia areata (AA) é doença autoimune que causa perda de cabelo sem cicatrizes na lesão e ocorre em qualquer idade.1 Ela normalmente se apresenta como áreas arredondadas de alopecia, únicas ou múltiplas, embora possa ocorrer calvície completa (AA total). AA universal é definida como a perda de pelos em todo o corpo. A AA também pode se apresentar na circunferência da cabeça, chamada AA ofiásica.2 A AA é considerada doença poligênica influenciada por herança geneticamente complexa, especialmente de genes relacionados a doenças autoimunes e inflamatórias, além de fatores ambientais.3,4 A literatura relata que vários genes do sistema imunológico contribuem para o desenvolvimento dessa doença, como o gene regulador autoimune (AIRE), antígeno leucocitário humano (HLA), genes de interleucina (IL), antígeno 4 associado ao linfócito T citotóxico (CTLA4), proteína tirosina fosfatase não receptora 22 (PTPN22), fator de necrose tumoral da superfamília 6 ou CD95 (FAS) e ligante FAS (FASL), entre outros.5,6

O CTLA4 (2q34) é membro da superfamília imunoglobulinas que codificam uma proteína que é potente reguladora negativa da resposta das células T. Por seu papel na manutenção da tolerância imunológica, ele tem sido apontado como um gene de suscetibilidade em doenças autoimunes humanas,e apresenta vários polimorfismos associados ao seu desenvolvimento.7 Entre os polimorfismos, duas variantes genéticas podem contribuir para a suscetibilidade ao AA:+49AG (rs231775), uma variação missense que leva a uma substituição do aminoácido treonina por alanina no códon 17 no peptídeo líder (T17A) e CT60 (rs3087243), localizada em 236bp downstream no gene CTLA4 (3’‐UTR).8 No entanto, estudos recentes feitos em diferentes populações indicam que a relação dessas variantes genéticas no desenvolvimento de AA é controversa.3,9

O presente estudo teve como objetivo determinar se as variantes dos genes CTLA4+49AG (rs231775) e CT60 (rs3087243) constituem um fator de predisposição para AA em uma coorte de pacientes mexicanos.

Material e métodosSeleção de pacientes e controles

O estudo incluiu 50 indivíduos mexicanos com diagnóstico de AA não relacionados entre si (32 mulheres e 18 homens; idade média: 30±15 anos) e 100 participantes saudáveis (59 mulheres e 41 homens; idade média: 25±8 anos); os controles apresentavam história familiar médica negativa para doenças autoimunes/inflamatórias. Os pacientes foram recrutados no Departamento de Dermatologia após a aceitação e assinatura do termo de consentimento livre e esclarecido. Este estudo foi aprovado pelo Comitê de Ética em Pesquisa e registrado sob o código DE09‐001. Detalhes adicionais sobre as características clínicas e demográficas, tipo de AA e distribuição de cada paciente foram obtidos durante a avaliação clínica.

Isolamento e genotipagem de DNA

O DNA genômico foi isolado do sangue venoso periférico com o método salting out e suspenso em Tris‐EDTA (pH 7,8) a uma concentração final de 0,1 a 1,0μg/μL antes do uso. As frequências genotípicas e alélicas das variantes do gene CTLA4+49AG (rs231775) e CT60 (rs3087243) foram caracterizadas por PCR‐RFLP com um termociclador MJ Mini PTC1148 (Bio‐Rad, Hercules; CA, Estados Unidos), primers oligonucleotídicos específicos (IDT, Coralville, IA, Estados Unidos) e enzimas de restrição (New England Biolabs, Ipswich, MA, Estados Unidos) de acordo com um protocolo publicado anteriormente.10 Os fragmentos obtidos foram analisados por eletroforese em gel de agarose a 2,5% com brometo de etídio, observados no transiluminador UVP modelo 2UV de alto desempenho (Upland, CA, E) e documentados.

Análise estatística

Para análise genética, o tamanho da amostra foi calculado com base na incidência mundial de AA de 2%,11 assumiu‐se um poder de 99,0% (um valor‐Z de 2,33), foi obtido o número mínimo de 43 indivíduos.

O software SPSS v21.0 para Windows (SPSS, Inc. Chicago, IL, Estados Unidos) e o programa estatístico Epi‐INFOTM 7 (Stone. Mountain, GA, USD Inc) foram usados para análise dos dados. O equilíbrio de Hardy‐Weinberg para os alelos foi obtido por meio de um teste de qualidade de ajuste e a dependência genotípica entre pacientes e controles foi determinada com um teste de χ2. A razão de probabilidades (OR) foi calculada a partir de tabelas de contingência 2×2 (p<0,05).

ResultadosCaracterísticas clínicas dos participantes

O presente estudo analisou a distribuição do genótipo e a frequência alélica das variantes do gene CTLA4+49AG e CT60. O universo do estudo (n) consistiu em 50 pacientes com AA e 100 controles. A apresentação clínica da AA nos pacientes foi: 41 pacientes com AA em placas (unifocal n=14, oito mulheres e seis homens; multifocal n=27, 19 mulheres e 8 homens), quatro pacientes com AA ofiásica (três mulheres e um homem), uma mulher com AA total e quatro pacientes com AA universal (três homens e um mulher). Dez pacientes (20%) tinham histórico pessoal de doenças autoimunes (vitiligo, diabetes melito tipo 2, entre outros) e 36 indivíduos (72%) tinham histórico familiar de doença imunológica.

Análise de alelos e genótipos

Vários testes foram feitos para ambas as variantes genéticas, a fim de avaliar o equilíbrio de Hardy‐Weinberg (EHW; tabela 1), todos com p>0,05, indicaram que as variantes dos genes rs231775 e rs3087243 estavam em EHW nos pacientes com AA e controles.

Tabela 1.

Testes para desvio do equilíbrio de Hardy‐Weinberg em pacientes com AA e controles saudáveis

Teste SNP/EHW  Casos de AA (valor‐p)  Controles (valor‐p) 
rs231775
Pearson  0,81  0,88 
Razão de verossimilhança  0,81  0,88 
Fisher exato  0,78  1,00 
rs3087243
Pearson  0,89  0,50 
Razão de verossimilhança  0,89  0,50 
Fisher exato  1,00  0,54 

Os alelos e genótipos do CTLA4 rs231775 e do rs3087243 do grupo controle foram comparados com os dos indivíduos com AA (todos os tipos de AA) e com os diferentes tipos de AA; a tabela 1 apresenta os resultados dessa comparação. Para CTLA4 rs231775, 30% dos pacientes com AA apresentaram genótipo AA do tipo selvagem homozigótico, 48% apresentaram o genótipo AG heterozigótico e os 22% restantes, genótipo GG variante homozigótica. Para CTLA4 rs3087243, 44% dos pacientes com AA apresentaram o genótipo GG do tipo selvagem homozigótico, 44% apresentaram o genótipo AG heterozigótico e os 12% restantes, AA variante homozigótica.

Associação dos genótipos em pacientes com alopecia areata

Quando os genótipos e frequências de alelos CTLA4 rs231775 e rs3087243 foram comparados entre toda a coorte (todos os tipos de AA) e controles, observou‐se que o genótipo AG heterozigótico para CTLA4 rs231775 e rs3087243 era mais frequente nos controles do que em todos os grupos de pacientes com AA. Além disso, não se observou associação entre variantes alélicas e AA nos pacientes analisados (p>0,05; tabela 2). Além disso, não foi encontrada relação entre o genótipo e o tipo de AA com a história pessoal/familiar de doenças autoimunes ou o sexo dos pacientes analisados (p>0,05; tabela 3).

Tabela 2.

Frequência de alelos e genótipo das variantes genéticas CTLA4+49AG (rs231775) e CT60 (rs3087243) em pacientes com AA e controles saudáveis

Genótipo  Pacientes com AA n (%)  Controles n (%)  χ2  OR  IC 95%  valor‐p 
Todos os tipos de AA  rs231775           
AA  15 (30)  28 (28,3)  0,086      0,958 
AG  24 (48)  50 (50,5)         
GG  11 (22)  21 (21,2)         
AG+GG  24 (48)+11 (22)  50 (50,5)+21 (21,2)  0,048  1,087  0,515‐2,292  0,827 
Alelos             
54 (54)  106 (53,5)  0,006  1,019  0,629‐1,650  0,939 
46 (46)  92 (46,5)  0,006  0,982  0,606‐1,590  0,939 
AA em placas             
AA  13 (31,7)  28 (28,3)  0,225      0,893 
AG  19 (46,3)  50 (50,5)         
GG  9 (22)  21 (21,2)         
AG+GG  19 (46,3)+9 (22)  50 (50,5)+21 (21,2)  0,164  1,177  0,534‐2,594  0,685 
Alelos             
45 (54,9)  106 (53,5)  0,042  1,056  0,630‐1,770  0,837 
37 (45,1)  92 (46,5)  0,042  0,947  0,565‐1,589  0,837 
AA multifocal             
AA  11 (40,7)  28 (28,3)  1,66      0,436 
AG  12 (44,5)  50 (50,5)         
GG  4 (14,8)  21 (21,2)         
AG+GG  12 (44,5)+4 (14,8)  50 (50,5)+21 (21,2)  1,541  1,743  0,721‐4,218  0,215 
Alelos             
34 (63)  106 (53,5)  1,527  1,476  0.795‐2,740  0,217 
20 (37)  92 (46,5)  1,527  0,678  0.365‐1,259  0,217 
Todos os tipos de AA  rs3087243           
AA  6 (12)  16 (16)  2,129      0,345 
AG  22 (44)  52 (52)         
GG  22 (44)  32 (32)         
AG+GG  22 (44)+22 (44)  52 (52)+32 (32)  0,426  0,716  0,262‐1,959  0,514 
Alelos             
34 (34)  84 (42)  1,788  0,711  0,432‐1,173  0,181 
66 (66)  116 (58)  1,788  1,406  0,853‐2,318  0,181 
AA em placas             
AA  6 (14,6)  16 (16)  1,168      0,558 
AG  18 (43,9)  52 (52)         
GG  17 (41,5)  32 (32)         
AG+GG  18 (43,9)+17 (41,5)  52 (52)+32 (32)  0,041  0,9  0,325‐2,49  0,839 
Alelos             
30 (36,6)  84 (42)  0,708  0,797  0,469‐1,353  0,4 
52 (63,4)  116 (58)  0,708  1,255  0,739‐2,132  0,4 
AA multifocal             
AA  4 (14,8)  16 (16)  0,031      0,985 
AG  14 (51,9)  52 (52)         
GG  9 (33,3)  32 (32)         
AG+GG  14 (51,9)+9 (33,3)  52 (52)+32 (32)  0,023  0,913  0,278‐2,998  0,881 
Alelos             
22 (40,7)  84 (42)  0,028  0,949  0,515‐1,749  0,868 
32 (59,3)  116 (58)  0,028  1,053  0,572‐1,941  0,868 
Tabela 3.

Análise das variantes genéticas CTLA4+49AG (rs231775) e CT60 (rs3087243) por sexo e história pessoal/familiar de doenças autoimunes

  AA  AG  GG  AA  AG  GG 
Sexo
Feminino (%)  8 (25%)  16 (50%)  8 (25%)  0,555  4 (12,5%)  14 (43,75%)  14 (43,75%)  0,990 
Masculino (%)  7 (38,9%)  8 (44,4%)  3 (16,7%)    2 (11,2%)  8 (44,4%)  8 (44,4%)   
História pessoal de doenças autoimunes
Sim (%)  3 (30%)  3 (30%)  4 (40%)  0,261  1(10%)  3 (30%)  6 (60%)  0,515 
Não (%)  12 (30%)  21 (52,5%)  7 (17,5%)    5 (12,5%)  19 (47,5%)  16 (40%)   
História familiar de doenças autoimunes
Sim (%)  10 (27,8%)  19 (52,8%)  7 (19,4%)  0,548  4 (11,1%)  17 (47,2%)  15 (41,7%)  0,761 
Não (%)  5 (38,4%)  4 (30,8%)  4 (30,8%)    2 (14,3%)  5 (35,7%)  7 (50%)   
Discussão

AA é doença autoimune com perda de cabelos que tem sido associada a múltiplas variantes genéticas, várias das quais participam de vias de resposta imune relacionadas ao HLA.12 O produto do gene CTLA4 é um receptor expresso pelas células T CD4+e CD8+. Experimentos em camundongos knockout demonstraram o importante papel que o CTLA4 desempenha na proteção contra a autoimunidade. O CTLA‐4 é um regulador negativo crítico das respostas das células T e sua ação nas células Treg pode controlar a atividade de outras células e a autoimunidade fatal.13

Foi sugerida a associação entre a presença das variantes do gene CTLA4 e o desenvolvimento de diferentes doenças autoimunes.14,15 No entanto, nas doenças imunológicas dermatológicas, os resultados são controversos; no vitiligo, a literatura relata tanto sua participação como não influência.16 Uma situação semelhante foi observada no desenvolvimento da psoríase.17,18

Nesse sentido, considerando a possível contribuição da função autoimune na alopecia, estudos de variantes genéticas do gene CTLA4 foram conduzidos em diversas populações. Uma análise anterior dessa associação sugeriu o possível envolvimento das variantes do gene CTLA4 como fator de risco no desenvolvimento de AA em uma população europeia,8 com efeito mais forte em pacientes com formas acentuadas da doença.

Outro estudo feito em uma população italiana, no qual foram analisadas as variantes dos genes rs231775 e rs3087243, apontou esse último como fator de risco no desenvolvimento de AA em placas.9 Por outro lado, estudo feito no Irã não conseguiu provar a associação da variante do gene rs3087243 no desenvolvimento de AA.3

Em estudo anterior, os autores observaram a participação de variantes genéticas de TNFα e PTPN2219 como fator de risco para AA em pacientes mexicanos; a função de ambos os genes está relacionada à regulação dos mecanismos imunológicos. No entanto, a participação das variantes genéticas do CTLA4 na AA não foi analisada nessa população.

Alguns SNPs dentro do gene CTLA‐4 já foram analisados quanto à suscetibilidade à artrite reumatoide (AR) na população mexicana; entre eles, rs5742909, rs231775 e rs3087243; sugere‐se que o haplótipo ‐319C/+49G/CT60G do gene CTLA‐4 é fator de risco para AR, enquanto que o SNP rs3087243 pode ser fator protetor contra esse tipo de doença autoimune.20

No entanto, não foram observadas diferenças significativas para rs231775 e rs3087243 no presente estudo (tabela 2), sugeriu‐se que essas variantes não são fator de risco no desenvolvimento de AA ou de AA em placas na população mexicana.

Conclusão

As variantes genéticas rs231775 e rs3087243 do gene CTLA4 não constituem fator de risco no desenvolvimento de AA na população mexicana de Monterrey, México. Além disso, essas variantes genéticas não apresentam associação com antecedentes familiares/pessoais de doenças autoimunes ou com o gênero dos sujeitos do estudo.

Suporte financeiro

Nenhum.

Contribuição dos autores

Mauricio Andrés Salinas Santander: Análise estatística; aprovação da versão final do manuscrito; concepção e planejamento do estudo; elaboração e redação do manuscrito; obtenção, análise e interpretação dos dados; participação efetiva na orientação da pesquisa; revisão crítica da literatura; revisão crítica do manuscrito.

Cristina Susana Cantu‐Salinas: Aprovação da versão final do manuscrito; concepção e planejamento do estudo; elaboração e redação do manuscrito; obtenção, análise e interpretação dos dados; participação efetiva na orientação da pesquisa; revisão crítica da literatura; revisão crítica do manuscrito.

Jorge Ocampo‐Candiani: Aprovação da versão final do manuscrito; concepção e planejamento do estudo; participação efetiva na orientação da pesquisa; revisão crítica da literatura; revisão crítica do manuscrito.

Victor de Jesus Suarez‐Valencia: Aprovação da versão final do manuscrito; elaboração e redação do manuscrito; obtenção, análise e interpretação dos dados; revisão crítica da literatura; revisão crítica do manuscrito.

Jennifer Guadalupe Ramirez‐Guerrero: Aprovação da versão final do manuscrito; elaboração e redação do manuscrito; obtenção, análise e interpretação dos dados; revisão crítica da literatura.

Celia Nohemi Sanchez‐Dominguez: Aprovação da versão final do manuscrito; elaboração e redação do manuscrito; revisão crítica da literatura; revisão crítica do manuscrito.

Conflitos de interesse

Nenhum.

Agradecimentos

A Daniel Díaz, Ph.D. por sua assistência na revisão deste manuscrito.

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Como citar este artigo: Salinas‐Santander MA, Cantu‐Salinas CS, Ocampo‐Candiani J, Suarez‐Valencia VJ, Ramirez‐Guerrero JG, Sanchez‐Dominguez CN. CTLA4+49AG (rs231775) and CT60 (rs3087243) gene variants are not associated with alopecia areata in a Mexican population from Monterrey Mexico. An Bras Dermatol. 2020;95:283–8.

Trabalho realizado no Departamento de Investigação, Faculdade de Medicina da Universidade de Saltillo, Universidade Autônoma de Coahuila, Saltillo, Coahuila, México e Serviço de Dermatologia, Hospital Universitário Dr. José Eleuterio González, Faculdade de Medicina, Universidade Autônoma de Nuevo León, Nuevo León, México.

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To improve our services and products, we use "cookies" (own or third parties authorized) to show advertising related to client preferences through the analyses of navigation customer behavior. Continuing navigation will be considered as acceptance of this use. You can change the settings or obtain more information by clicking here. Utilizamos cookies próprios e de terceiros para melhorar nossos serviços e mostrar publicidade relacionada às suas preferências, analisando seus hábitos de navegação. Se continuar a navegar, consideramos que aceita o seu uso. Você pode alterar a configuração ou obter mais informações aqui.