The genetic contribution of CTLA‐4 dimorphisms in promoter and exon 1 regions in Japanese patients with rheumatoid arthritis

Overexpression and Secretion of the Soluble CTLA-4 Splice Variant in Various Autoimmune Diseases and in Cases with Overlapping Autoimmunity

“…Likewise, 5 out of 10 RA studies failed to show any significant association (Seidl et al, 1998;Gonzalez-Escribano et al, 1999;Barton et al, 2000;Yanagawa et al, 2000;Hadj-Kacem et al, 2001;Milicic et al, 2001;Lee et al, 2002Lee et al, , 2003Barton et al, 2004;Takeuchi et al, 2006) and this group comprised the Caucasians mostly.…”

Polymorphisms in the CTLA-4 Gene and Rheumatoid Arthritis Susceptibility: A Meta-analysis

“…Overall, there were 16 articles (including 19 case-control studies) for the +49A/G polymorphism [4-8, 12, 14, 16, 17, 19-21, 24, 27-29] and 8 articles (including 11 case-control studies) for the CT60 polymorphism [3,7,12,13,15,19,20,25]. Among 20 articles, 7 were from Asians [6,7,12,16,17,24,27], 11 were from Europeans [3, 5, 13-15, 19-21, 25, 28, 29], 1 from Americans [4], and 1 from Africans [8]. Different genotyping methods were used, including RFLP, TaqMan, PCR-DGGE, Sequenom, and MELDI-TOF.…”

“…Seven case-control studies were from Asians [6,7,12,16,17,24,27], 10 were from Europeans [5,14,19,20,25,28,29], 1 from Americans [4], and 1 from Africans [8]. As shown in Fig.…”

Association between the CTLA-4, CD226, FAS polymorphisms and rheumatoid arthritis susceptibility: A meta-analysis

“…Four articles were excluded because 2 were review articles, 1 contained duplicate data, and 1 had no data concerning the polymorphisms. Thus, 19 studies met our inclusion criteria [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31]. They consisted of 8 studies on the CTLA-4 polymorphism with 2093 patients and 2480 controls, 5 on the CD226 polymorphism with 2278 patients and 1940 controls, 6 on the FAS polymorphism with 546 patients and 618 controls, and 3 on the FASL polymorphism with 321 patients and 307 controls (Fig.…”

“…While some studies have found that CTLA-4 rs5742909, CD226 rs763361, FAS-670 rs1800682, and FASL rs763110 polymorphisms are associated with RA, other studies have reported no such association [13][14][15][16][17][18][19][20][21][22][23][24][25][26][27][28][29][30][31]. To overcome the limitations of individual studies, resolve inconsistencies, and reduce the likelihood that random errors are responsible for false positive or false negative associations [32][33][34], we performed a meta-analysis to determine whether these polymorphisms are associated with RA susceptibility.…”