Abstract
Objective: Rheumatoid Arthritis (RA) is an autoimmune and chronic inflammatory disease of unknown etiology. Killer cell immunoglobulin-like receptors are expressed on the surface of natural killer cells and CD28nullT-cells, both present in synovial membrane of RA. Therefore we evaluated the associations ofKIRgenes with RA.Methods: 16KIRgenes were genotyped in 100 healthy subjects (HS) and 100 RA patients from Western Mexico using PCR-SSP. Differences inKIRgenotypes and gene frequencies were assessed using theX2test.Results: Gene frequency ofKIR2DL3was lower in RA than in HS (p= 0.0019), whereasKIR2DL2andKIR2DS2were higher in RA than HS (p= 0.0004 andp= 0.0487, respectively). In addition were identified 38 genotypes (from G1-G38) in both studied groups, and the genotype frequencies of G1, G6 and G14 showed significant differences (p= 0.0001,p= 0.0208 andp= 0.0300, respectively).Conclusions: The presence ofKIR2DL2,KIR2DS2and absence ofKIR2DL3are associated with RA. Moreover, two genotypes BX are associated with RA. These results suggest thatKIRscan be involved in RA susceptibility.
Highlights
Rheumatoid Arthritis (RA) is a chronic inflammatory autoimmune disease, affecting about 1% of the world population [1]
All patients were classified according to ACR-EULAR 2010 criteria, and were treated with disease modifying antirheumatic drugs (DMARDs) and/or non-steroidal anti-inflammatory drugs (NSAIDs)
The frequency of AA group was decreased in RA compared with healthy subjects (HS) (p = 0.0171, OR = 0.461), whereas BX group was significantly increased in RA patients (p = 0.0171, OR = 2.168)
Summary
Rheumatoid Arthritis (RA) is a chronic inflammatory autoimmune disease, affecting about 1% of the world population [1]. The etiologic fraction of HLA-DRB1 locus accounts for only 30% of genetic susceptibility This indicates that different genes to those of HLA-DR are involved in the susceptibility to disease [4,5]. The killer cell immunoglobulin-like receptors gene cluster has generated great interest due to its complex genetic variability which cause a high degree of KIR heterogeneity between individuals, besides that has been previously implicated in inflammatory and autoimmune conditions [6]. CD28null T-cells are expanded in RA, these cells produce large amounts of IFN-γ, and express granzyme B and perforin, giving them the capability to lyses target cells and cause damage to tissue [8,10] They tend to preferentially and even exclusively display KIR activating receptors as KIR2DS2 which could play role as co-stimulatory molecule. We examined whether KIR genes could be associated with RA in the western Mexico population
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