PMID- 17767552 OWN - NLM STAT- MEDLINE DCOM- 20071127 LR - 20231213 IS - 0001-2815 (Print) IS - 0001-2815 (Linking) VI - 70 IP - 4 DP - 2007 Oct TI - Association of CD94/NKG2A, CD94/NKG2C, and its ligand HLA-E polymorphisms with Behcet's disease. PG - 307-13 AB - Inhibitory CD94/NKG2A and activating CD94/NKG2C receptors are expressed on natural killer, CD4, and CD8 T cells and recognize human leukocyte antigen (HLA)-E, resulting in the modulation of cytotoxic activity and cytokine production. An imbalance in cytotoxic activity and cytokine production has been implicated in Behcet's disease (BD). The results of this study showed that the NKG2A c.-4258*C, c.338-90*G, and CD94 c.-134*T alleles (P= 0.015, OR = 0.8; P < 0.0001, OR = 0.5; and P= 0.034, OR = 0.8, respectively) were associated with decreased risk and that NKG2A c.284-67_-62del, c.1077*C, and the activating receptor, NKG2C c.305*T were not associated with 345 patients with BD. But a significant difference in NKG2C c.305*T was detected among BD patients with ocular lesions and arthritis (P < 0.0001, OR = 2.1 and P= 0.0001, OR = 1.8, respectively). We already showed in our previous research that HLA-E*0101 also appears to contribute to a reduction in risk through the inhibitory CD94/NKG2A-mediated immune response. This result led us to the analyses of the combined risk of the HLA-E and the NKG2A for BD. Individuals harboring HLA-E*0101, NKG2A c.-4258*C, and c.338-90*G evidenced a reduced risk of BD compared with healthy controls (21.1% vs 40.1%, P < 0.0001, OR = 0.4). By way of contrast, individuals without the HLA-E*0101, NKG2A c.-4258*C, and c.338-90*G alleles evidenced a twofold increased risk of BD (P= 0.014, OR = 2.0). Individuals without HLA-E*0101, NKG2A c.-4258*G/*G, and c.338-90*G evidenced a 4.8-fold increase in BD risk (P= 0.0002, OR = 4.8). Although the effects of these single nucleotide polymorphisms (SNPs) remain unclear, our results indicate that the SNPs of the inhibitory receptor CD94/NKG2A and its haplotypes, as well as its ligand HLA-E, are associated with BD immune systems. FAU - Seo, J AU - Seo J AD - Department of Biology and Institute of Basic Science, Sungshin Women's University, 249-1 3-ga, Dongseon-dong, Sungbuk-ku, Seoul 136-742, Korea. FAU - Park, J S AU - Park JS FAU - Nam, J H AU - Nam JH FAU - Bang, D AU - Bang D FAU - Sohn, S AU - Sohn S FAU - Lee, E S AU - Lee ES FAU - Park, K S AU - Park KS LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Tissue Antigens JT - Tissue antigens JID - 0331072 RN - 0 (HLA Antigens) RN - 0 (Histocompatibility Antigens Class I) RN - 0 (Ligands) RN - 0 (NK Cell Lectin-Like Receptor Subfamily D) SB - IM MH - Alleles MH - Behcet Syndrome/*genetics/immunology/metabolism MH - CD8-Positive T-Lymphocytes/*immunology/metabolism MH - Case-Control Studies MH - Cohort Studies MH - Female MH - Genetic Predisposition to Disease MH - HLA Antigens/*genetics/immunology/metabolism MH - Histocompatibility Antigens Class I/*genetics/immunology/metabolism MH - Humans MH - Killer Cells, Natural/*immunology/metabolism MH - Ligands MH - Male MH - NK Cell Lectin-Like Receptor Subfamily D/*genetics/immunology/metabolism MH - *Polymorphism, Single Nucleotide MH - HLA-E Antigens EDAT- 2007/09/05 09:00 MHDA- 2007/12/06 09:00 CRDT- 2007/09/05 09:00 PHST- 2007/09/05 09:00 [pubmed] PHST- 2007/12/06 09:00 [medline] PHST- 2007/09/05 09:00 [entrez] AID - TAN907 [pii] AID - 10.1111/j.1399-0039.2007.00907.x [doi] PST - ppublish SO - Tissue Antigens. 2007 Oct;70(4):307-13. doi: 10.1111/j.1399-0039.2007.00907.x.