The role of cytokines in the pathogenesis of systemic lupus erythematosus – from bench to bedside

Abstract

ABSTRACT: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 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 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.

Hyperthyroidism is a Risk Factor for Developing Adhesive Capsulitis of the Shoulder: A Nationwide Longitudinal Population-Based Study

“…Regarding SLE patients, cytokines have been proposed to have a pathogenic role in autoantibody production and immune complex deposition. These cytokines are interleukin-6, interleukin-17, interleukin-18, type I interferons, and TNF-alpha20. Cytokines have also been found in the pathogenesis of rheumatoid arthritis.…”

Elevated Plasma cfDNA May be Associated with Active Lupus Nephritis and Partially Attributed to Abnormal Regulation of Neutrophil Extracellular Traps (NETs) in Patients with Systemic Lupus Erythematosus

“…Proinflammatory factors, including tumor necrosis factor (TNF)-α, interferon (IFN)-γ, interleukin (IL)-17 and IL-8, can also induce neutrophils to form NETs (7). SLE patients have an abnormal cytokine environment (8), which results in enhanced NET formation in vivo. Furthermore, new findings indicate that low-density granulocytes (LDGs) in the peripheral blood mononuclear cells (PBMCs) of SLE patients can form NETs spontaneously and more fiercely than normal autologous neutrophils (2,9).…”

Increased expression of TLR2 in CD4+ T cells from SLE patients enhances immune reactivity and promotes IL‐17 expression through histone modifications

“…2 D). There is evidence that IL-6, IL-10, IL-17A, IL-17F, TNF-α, and IFNs markedly contribute to the immune imbalance in SLE [21][22][23][24]. To further investigate the impact of TLR2 stimulation on the inflammatory response of CD4 + T cells from SLE patients, we collected the supernatant of cell culture in vitro and performed ELISA to detect the concentration of proinflammatory cytokines secreted by CD4 + T cells from SLE patients after TLR2 stimulation.…”