Association between T-lymphocyte regulatory gene CTLA4 single nucleotide polymorphism at position 49 in exon 1 and HLA-DRB1*08 in Japanese patients with psoriasis vulgaris

Lack of association between cytotoxic T-lymphocyte antigen-4+49A/G polymorphism and psoriasis and vitiligo: A meta-analysis of case–control studies

“…We found no significant association between CTLA-4 + 49A/G polymorphism and psoriasis in our overall analysis. In fact, only one case-control study (Hao et al, 2003) has reported increased risk of psoriasis in allele G carriers, whereas all other casecontrol studies showed no association between them (Kim et al, 2003;Tsunemi et al, 2003;Luszczek et al, 2008;Fernandez-Mestre et al, 2009;Muto et al, 2011), in line with our findings. There are some possible reasons for the lack of a significant effect of the CTLA-4 + 49A/G polymorphism on psoriasis.…”

“…The CTLA-4 + 49A/G polymorphism may interact with other genes and thereby have combined effects on psoriasis. In one case-control study (Muto et al, 2011), there was no significant difference in genotype and allele frequencies of CTLA-4 + 49 A/G between psoriasis patients and controls, whereas a Table 3 Association between the CTLA-4 + 49 A/G polymorphism and vitiligo. significant difference between the groups was observed (OR = 2.92, 95% CI = 1.30-6.53, P b 0.01) when the frequency of HLA-DRB1*08 allele was considered in combination with the (G/G + G/A) genotype at position 49 of CTLA-4, suggesting an additive requirement for CTLA-4 and the HLA-DRB1*08 alleles in psoriasis susceptibility.…”

“…Environmental triggers, particularly stress, infection, and trauma, have been correlated with both diseases (Barisic-Drusko and Rucevic, 2004). Association studies have implicated several genes in susceptibility to both diseases, such as those for the major histocompatibility complex (Mabuchi et al, 2007), TNF-α (Zhuang et al, 2013), protein tyrosine phosphatase non-receptor type 22 (PTPN22) (Song et al, 2013), and cytotoxic T-lymphocyte antigen-4 (CTLA-4) (Muto et al, 2011;Song et al, 2013), which are thought to play important roles in the development of autoimmunity. These genes may, at the least, represent a common affected event in the pathologic processes of psoriasis and vitiligo, although a recent retrospective study failed to find an increased prevalence of psoriasis in individuals with vitiligo, or vice versa (Sawchuk et al, 2012).…”

“…Furthermore, individuals with the G/G genotype at position +49 show higher proliferation and Studies further excluded (n = 5): Not case-control study (n = 1) Reported duplicated data (n = 2) Not provided relevant data (n = 1) Not focus on the polymorphism of rs231775 (n = 1) 1 contained data on two different groups activation of T cells than the A/A genotype (Kouki et al, 2000;Maurer et al, 2002). Some studies have looked for a possible association between CTLA-4 + 49A/G polymorphism and psoriasis (Hao et al, 2003;Kim et al, 2003;Tsunemi et al, 2003;Luszczek et al, 2008;Fernandez-Mestre et al, 2009;Muto et al, 2011) or vitiligo (Blomhoff et al, 2005;Gao et al, 2005;Tang, 2007;Birlea et al, 2009;Pehlivan et al, 2009;Deeba et al, 2010;Dwivedi et al, 2011), but the findings have been (Hao et al, 2003) which may be the major source of the heterogeneity. b Statistically significant result.…”

Myeloid-Derived Suppressor Cells in Psoriasis Are an Expanded Population Exhibiting Diverse T-Cell–Suppressor Mechanisms

“…Th17 and Th1 cells in psoriasis did not efficiently induce the co-inhibitor Tim-3 upon in vitro activation, compared to those from healthy donors (Kanai et al , 2012). Lastly, significant associations of polymorphisms in CTLA-4 gene with susceptibility to psoriasis were found in Japanese and Polish Caucasian patients (Luszczek et al , 2008; Muto et al , 2011). Consistent with our findings, these reports support the possibility that deficient co-inhibitory function contributes to the etiology of psoriasis.…”