For obvious reasons, we did not
have renal tissue of lupus patients without kidney problem to compare with. Further studies are needed to determine the pattern of intra-renal miRNA expression in relation to the histological class of lupus nephritis. This study was supported in part by the CUHK research account 6901031. All authors declare no conflict of interest. “
“The pathogenesis of systemic lupus erythematosus (SLE) entails a complex interaction between the different arms of the immune system. While autoantibodies production and immune complex deposition are cornered as hallmark features of SLE, there is growing evidence to propose the pathogenic selleck compound library role of cytokines in this disease. Examples of these cytokines include BLys, interleukin-6, interleukin-17, interleukin-18, type I interferons and tumour necrosis factor alpha. These cytokines all assume pivotal functions to orchestrate the differentiation, maturation and activation of various cell BIBW2992 types,
which would mediate local inflammatory process and tissue injury. The knowledge on these cytokines not only fosters our understanding of the disease, but also provides insights in devising biomarkers and targeted therapies. In this review, we focus on cytokines which have substantial pathogenic significance and also highlight the possible clinical applications of these cytokines. Systemic lupus erythematosus (SLE) is an autoimmune disorder which has multi-organ involvements. The pathogenesis of SLE, which involves the various facets of the immune system, is complex and perplexing. The orthodox understanding of this disease encompasses autoantibodies production and immune complex deposition, which will give rise to the subsequent Mirabegron autoimmune phenomenon. However, mounting evidence has emerged to suggest the crucial role of various cytokines in the pathogenesis of SLE. These cytokines are soluble factors which are vibrant mediators for the differentiation, maturation and activation of the various immune cells. The consequence of such would be an immune dysregulation followed by local inflammatory processes and tissue damage. The
understanding of these cytokines not only enhances our perception of SLE, but also instills novel ideas for the design of biomarkers and therapeutic agents. In this review, we highlight the cytokines which exert significant effects on the pathogenesis of SLE and their clinical applications. IL-6 is one of the first cytokines studied in the pathogenesis of SLE due to its close link with B lymphocytes. This cytokine is primarily secreted by the monocytes, fibroblasts and endothelial cells although the T- and B- lymphocytes also contribute to its production. It has an elaborated interaction with other cytokines as its levels is boosted by IL-1, IL-2 and tumour necrosis factor-α (TNF-α) but diminished by IL-4, IL-10 and IL-13.