The weight of interleukin-6 in B cell-related autoimmune disorders

Epidermal loss of JunB leads to a SLE phenotype due to hyper IL-6 signaling

“…The major sources of IL-6 are reported to be monocytes, fibroblasts, and endothelial cells (3). IL-6 is bound as a dimer within an IL-6R␣ hexameric ligand-receptor complex (4) and can induce Ig production, T-cell maturation, as well as glomerulonephritis and plasmocytosis (5)(6)(7). SCID-IL-6 transgenic mice do not show such abnormalities (8).…”

Sweet Syndrome in a Patient With Systemic Lupus Erythematosus Flare.

“…The hypersensitivity reactions may be immune mediated through 1395 stimulating the production of cytokines that promote neutrophil activation and infiltration [9], triggered by a variety of antigens including bacteria, viruses, medications, and malignancies. Several cytokines have been implicated in the pathogenesis of SS, of them, certain cytokines like IL-6 may also play a role in SLE through a variety of mechanisms including B cell stimulation and induction of acute phase reactants [10]. Genetically, HLA-B54 has been linked to Sweet syndrome in Japanese patients [11].…”

Interplay of Cytokines and Chemokines in the Pathogenesis of Systemic Lupus Erythematosus

“…Shiroiwa group has suggested that the role of IL-4 in the pathogenesis may differ between certain subsets of SLE, even if they show similar disease phenotypes. Several lines of evidence suggest that IL-6 plays a central role in the pathogenesis of SLE; including regulation of growth and differentiation of B cells and auto-antibody production and that it may have a direct role in mediating tissue damage (Youinou and Jamin, 2009). In our study, serum IL-6 was found to be higher in lupus nephritis patients (n = 6) and it also positively correlated with ESR and SLEDAI score.…”