Involvement of Fcγ receptor IIIA genotypes in susceptibility to rheumatoid arthritis

Abstract

These results indicate that the FcgammaRIIIA-158 genotypes confer differential susceptibility to RA in our study population. Further studies to elucidate the role of this polymorphism in the pathogenesis of RA and other autoimmune diseases are warranted.

Genetic polymorphisms in Spanish rheumatoid arthritis patients: an association and linkage study

“…IL-6 promoter was studied by a PCR-RFLP technique 3 with primers 5 0 -GGAGTCACACACTCCACCT-3 0 and 5 0 -CTGATTGGAAACCT-TATTAAG-3 0 followed by digestion with FokI and Hsp92II. A similar approach was used for FcgRIIIA genotyping, 4 with primers 5 0 -ATAAGGTCACATATTTACAGAATGGCCAAG-3 0 and 5 0 -CAGTCTCTGAAGACACATTTTTACTCCGTA-3 0 , followed by digestion with Rsa I and Sty I. All the results were read by direct UV visualisation of amplicons in ethidium bromide stained agarose gels.…”

“…The allelic variants differ in their affinity: Val158 variants bind IgG1 and IgG3 more avidly than Phe158-containing alleles. A previous case-control positive association of homozygosity for FcgRIIIA Phe158 with RA has been reported, 4 but results are conflicting. 20,21 The present study has been performed with three different groups of RA patients.…”

“…[1][2][3][4] Here we attempt to extend further some of those results and to investigate possible associations with a new set of markers. We have focussed on polymorphisms with presumed functional relevance or previously reported to be associated with an autoimmune disease.…”

FcγR expression on NK cells influences disease severity in rheumatoid arthritis

“…19 In general, these polymorphisms have been shown to alter the ligand binding specificity of particular FcgR, such as FcgRIIa, 17 and FcgRIIIa. 14,16 These allelic polymorphisms have proved to be clinically significant in infectious 20,21 and autoimmune 12,13,[22][23][24] diseases.…”

Essential Role of Fcγ Receptors in Anti-Type II Collagen Antibody-Induced Arthritis

“…Fc␥RIIB is expressed on cells such as B cells, macrophages, dendritic cells, and mast cells. These FcRs have been shown to play central roles in disease models such as allergy, nephritis, and arthritis (13)(14)(15)(16)(17)(18)(19)(20). Thus, the involvement of FcRs in human diseases has been assumed (9,20).…”