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We are analyzing https://www.nature.com/articles/jhg2006114.

Title:
Role of B cell inhibitory receptor polymorphisms in systemic lupus erythematosus: a negative times a negative makes a positive | Journal of Human Genetics
Description:
B lymphocytes play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). Here, we will review our studies on the role of polymorphisms of two genes coding for B cell inhibitory receptors, FCGR2B and CD72. In FCGR2B, a single nucleotide polymorphism leading to a nonsynonymous substitution, Ile232Thr, within the transmembrane domain was identified, and a significant association of the 232Thr/Thr genotype with SLE was observed in Japanese, Thai and Chinese populations, while this allele was found to be rare in Caucasians. On the other hand, the association of FCGR2B promoter polymorphism with SLE in Caucasians has been reported by two independent groups, but this allele was not found to be present in Japanese. These observations demonstrate that the association of FCGR2B polymorphisms with SLE is common to multiple populations, but the alleles associated with SLE depend upon the genetic background of each population. Functional analyses using a human B cell line lacking endogenous FcγRIIb revealed that SLE-associated 232Thr allele product was partially excluded from membrane lipid rafts under resting conditions and after coligation with B cell receptor, and was significantly less potent at inhibiting B cell activation. Two haplotypes were identified in CD72, one of which was associated with increased production of an alternative splicing isoform that substantially alters the extracellular region of CD72. Interestingly, the presence of the haplotype significantly decreased the risk of SLE conferred by FCGR2B-232Thr in an epistatic manner. These observations emphasize the need to understand human immune system diversity if we are to improve our understanding of the pathogenesis of autoimmune diseases.
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pubmed, google, scholar, cas, fcgrb, human, receptor, association, sle, fcγriib, lupus, systemic, erythematosus, cells, genes, lipid, cell, polymorphisms, polymorphism, rafts, allele, susceptibility, populations, immunol, gene, fcγ, nature, tsuchiya, signaling, inhibitory, isoform, found, kyogoku, role, thr, splicing, bcr, ravetch, studies, reported, kono, tokunaga, genetic, immune, arthritis, honda, receptors, transmembrane, genotype, japanese,

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nature portfolio permissions reprints privacy policy advertising nature 439 nature 368 nature 387 nature social media strain-specific epistasis author information authors + anti-dna plasma cells author correspondence 13-amino-acid motif receptor-proximal events fcγ receptor-mediated phagocytosis c-terminal src kinase n-terminal palmitoylation site regulated pre-mrna splicing fcγ riiia-f158 allele full size image c-type lectin domain anti-dna antibody cd19-induced ca2+ mobilization detergent-insoluble membrane domains yin-yang1 transcription factors determined ligand-binding parameters fcγriib-deficient mice results fcγ receptor iib wild-type fcgr2b gene attenuates inhibitory effects systemic lupus erythematosus permissions lipid raft components lipid raft structure inhibitory receptor pd-1 akt tyrosine phosphorylation mrl/lpr lupus mice inhibitory coreceptors activated cell regulatory molecules function inhibitory receptor fcγ receptor iia amino acid substitution family-based association study correlated receptor expression spontaneously develop lupus spontaneously develop lupus fcγ receptor iiib case-control association study altered subcellular distribution

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Does the altered subcellular distribution of 232Thr, the partial exclusion from lipid rafts, provide a mechanistic basis for its phenotype?

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      headline:Role of B cell inhibitory receptor polymorphisms in systemic lupus erythematosus: a negative times a negative makes a positive
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