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T cells and IL-17 in lupus nephritis.

ABSTRACT: Systemic lupus erythematosus (SLE) is a complicated autoimmune disorder characterized by autoantibodies production, immune complex formation, and immune dysregulation, resulting in damage of multiple organs including the kidney. Lupus nephritis (LN) is the most common severe manifestation of SLE involving the majority of patients. Even though there are a number of reports indicating that interleukin-17 (IL-17) and Th17 cells play important roles in the pathogenesis of LN, the precise molecular mechanisms underline the development of LN have not been totally elucidated. In this review, we briefly summarize general characteristics of T and IL-17 cells in SLE. In addition, we discuss in detail T cell signaling pathways which control IL-17 production in patients with LN and in glomerulonephritis in lupus-prone mice. A better understanding of signaling and gene regulation defects in LN will lead to the identification of novel therapeutic targets and predictive biomarkers for diagnosis and prognosis of this disease.

SUBMITTER: Koga T

PROVIDER: S-EPMC5074925 | biostudies-other | 2017 Dec

REPOSITORIES: biostudies-other

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T cells and IL-17 in lupus nephritis.

Koga Tomohiro T Ichinose Kunihiro K Tsokos George C GC

Clinical immunology (Orlando, Fla.) 20160421

Systemic lupus erythematosus (SLE) is a complicated autoimmune disorder characterized by autoantibodies production, immune complex formation, and immune dysregulation, resulting in damage of multiple organs including the kidney. Lupus nephritis (LN) is the most common severe manifestation of SLE involving the majority of patients. Even though there are a number of reports indicating that interleukin-17 (IL-17) and Th17 cells play important roles in the pathogenesis of LN, the precise molecular m ...[more]

PMID: 27109641

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Project description:Systemic lupus erythematosus (SLE) is a disease characterized by dysregulation and hyperreactivity of the immune response at various levels, including hyperactivation of effector cell subtypes, autoantibodies production, immune complex formation, and deposition in tissues. The consequences of hyperreactivity to the self are systemic and local inflammation and tissue damage in multiple organs. Lupus nephritis (LN) is one of the most worrying manifestations of SLE, and most patients have this involvement at some point in the course of the disease. Among the effector cells involved, the Th17, a subtype of T helper cells (CD4+), has shown significant hyperactivation and participates in kidney damage and many other organs. Th17 cells have IL-17A and IL-17F as main cytokines with receptors expressed in most renal cells, being involved in the activation of many proinflammatory and profibrotic pathways. The Th17/IL-17 axis promotes and maintains repetitive tissue damage and maladaptive repair; leading to fibrosis, loss of organ architecture and function. In the podocytes, the Th17/IL-17 axis effects include changes of the cytoskeleton with increased motility, decreased expression of health proteins, increased oxidative stress, and activation of the inflammasome and caspases resulting in podocytes apoptosis. In renal tubular epithelial cells, the Th17/IL-17 axis promotes the activation of profibrotic pathways such as increased TGF-β expression and epithelial-mesenchymal transition (EMT) with consequent increase of extracellular matrix proteins. In addition, the IL-17 promotes a proinflammatory environment by stimulating the synthesis of inflammatory cytokines by intrinsic renal cells and immune cells, and the synthesis of growth factors and chemokines, which together result in granulopoiesis/myelopoiesis, and further recruitment of immune cells to the kidney. The purpose of this work is to present the prognostic and immunopathologic role of the Th17/IL-17 axis in Kidney diseases, with a special focus on LN, including its exploration as a potential immunotherapeutic target in this complication.

Dataset Information

T cells and IL-17 in lupus nephritis.

Publications

T cells and IL-17 in lupus nephritis.

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