Background Macrophage-inducible C-type lectin （MINCLE） is an important member of C-type lectin superfamily, which has been shown evidence for susceptibility to arthritis in animal models. We aimed to investigate the possible association of MINCLE with rheumatoid arthritis （RA） susceptibility in Chinese Han population. Methods Haplotypes from HapMap database （Chinese Han Beijing, CHB） were used to select tag-single nucleotide polymorphism （SNP） （r2=0.8） residing in MINCLE gene. A total of 563 patients with RA and 404 healthy controls were TagMan genotyped for SNP rs10841845. Association analyses were performed on the whole data set and on RA subsets based on gender difference and the status of anti-cyclic citrullinated peptide （anti-CCP） antibody in RA patients. Association statistics were calculated by age and sex adjusted logistic regression. Results Overall, MINCLE SNP rs10841845 was not associated with susceptibility to RA. However, following anti-CCP stratification, rs10841845 GG genotypes conferred a significantly protective effects against anti-CCP-positive RA （OR 0.65, 95% CI 0.430-0.995, P=0.048）. Following gender stratification, SNP rs10841845 G allele appeared to insert its RA protective effect only in male patients, both at allele level （G vs. A OR 0.66, 95% CI 0.46-0.93, P=0.018） and at genotype level （GG vs. AA±AG, OR 0.429, 95% CI 0.20-0.95, P=0.036）. Notably, the male RA protective effect of rs10841845 G allele was only seen in anti-CCP-positive RA （G vs. A： OR 0.64, 95% CI 0.43-0.96, P=0.029; GG vs. AA＋AG： OR 0.375, 95% CI 0.14-0.94, P=0.038）. Furthermore, we observed a significant reduction of Disease Activity Score （DAS） 28 score （3.91±0.70 vs. 5.66±0.31, P=-0.022） and serum C-reactive protein levels （31.64±24.13 vs. 91.80±12.02, P=0.012） in male anti-CCP-positive RA patients carrying rs10841845 GG genotype, compared with patients carrying AA±AG genotypes. Conclusions Our study provides the evidence for a gender specific association
B cells are generally considered to be positive regulators of the immune response because of their capability to produce antibodies, including autoantibodies. The production of antibodies facilitates optimal CD4＋ T-cell activation because B cells serve as antigen-presenting cells and exert other modulatory functions in immune responses. However, certain B cells can also negatively regulate the immune response by producing regulatory cytokines and directly interacting with pathogenic T cells via cell-to-cell contact. These types of B Cells are defined as regulatory B （Breg） cells. The regulatory function of Breg cells has been demonstrated in mouse models of inflammation, cancer, transplantation, and particularly in autoimmunity. In this review, we focus on the recent advances that lead to the understanding of the development and function of Breg cells and the implications of B cells in human autoimmune diseases.
MicroRNA （miRNA）-mediated gene silencing at the translational level has led to novel discoveries for numerous biological processes. Recently, there has been increasing evidence to indicate that miRNAs are involved in normal immune functions and inflammation. In this review, we focus on recent advances that have elucidated the role of miRNAs in B-cell development, differentiation, apoptosis and function. While the regulatory mechanisms of miRNAs in controlling and maintaining B-cell fate remain largely uncharacterized, further studies on miRNAs and their targets will increase our understanding of B-cell development and function. Such studies may be able to provide new therapeutic strategies for treating autoimmune diseases.
