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      Interleukin-6 Signaling Pathway and Its Role in Kidney Disease: An Update

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          Abstract

          Interleukin-6 (IL-6) is a pleiotropic cytokine that not only regulates the immune and inflammatory response but also affects hematopoiesis, metabolism, and organ development. IL-6 can simultaneously elicit distinct or even contradictory physiopathological processes, which is likely discriminated by the cascades of signaling pathway, termed classic and trans-signaling. Besides playing several important physiological roles, dysregulated IL-6 has been demonstrated to underlie a number of autoimmune and inflammatory diseases, metabolic abnormalities, and malignancies. This review provides an overview of basic concept of IL-6 signaling pathway as well as the interplay between IL-6 and renal-resident cells, including podocytes, mesangial cells, endothelial cells, and tubular epithelial cells. Additionally, we summarize the roles of IL-6 in several renal diseases, such as IgA nephropathy, lupus nephritis, diabetic nephropathy, acute kidney injury, and chronic kidney disease.

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          TGFbeta in the context of an inflammatory cytokine milieu supports de novo differentiation of IL-17-producing T cells.

          Marc Veldhoen, Richard J Hocking, Christopher Atkins … (2006)
          We describe de novo generation of IL-17-producing T cells from naive CD4 T cells, induced in cocultures of naive CD4 T cells and naturally occurring CD4+ CD25+ T cells (Treg) in the presence of TLR3, TLR4, or TLR9 stimuli. Treg can be substituted by TGFbeta1, which, together with the proinflammatory cytokine IL-6, supports the differentiation of IL-17-producing T cells, a process that is amplified by IL-1beta and TNFalpha. We could not detect a role for IL-23 in the differentiation of IL-17-producing T cells but confirmed its importance for their survival and expansion. Transcription factors GATA-3 and T-bet, as well as its target Hlx, are absent in IL-17-producing T cells, and they do not express the negative regulator for TGFbeta signaling, Smad7. Our data indicate that, in the presence of IL-6, TGFbeta1 subverts Th1 and Th2 differentiation for the generation of IL-17-producing T cells.
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            Complementary DNA for a novel human interleukin (BSF-2) that induces B lymphocytes to produce immunoglobulin.

            T Hirano, K Yasukawa, H Harada … (1986)
            When stimulated with antigen, B cells are influenced by T cells to proliferate and differentiate into antibody-forming cells. Since it was reported that soluble factors could replace certain functions of helper T cells in the antibody response, several different kinds of lymphokines and monokines have been reported in B-cell growth and differentiation. Among these, human B-cell differentiation factor (BCDF or BSF-2) has been shown to induce the final maturation of B cells into immunoglobulin-secreting cells. BSF-2 was purified to homogeneity and its partial NH2-terminal amino-acid sequence was determined. These studies indicated that BSF-2 is functionally and structurally unlike other known proteins. Here, we report the molecular cloning, structural analysis and functional expression of the cDNA encoding human BSF-2. The primary sequence of BSF-2 deduced from the cDNA reveals that BSF-2 is a novel interleukin consisting of 184 amino acids.
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              IL-6 switches the differentiation of monocytes from dendritic cells to macrophages.

              P Chomarat, J Banchereau, J. Davoust … (2000)
              Monocytes can give rise to either antigen presenting dendritic cells (DCs) or scavenging macrophages. This differentiation is initiated when monocytes cross the endothelium. But the regulation of DC and macrophage differentiation in tissues remains elusive. When stimulated with granulocyte-macrophage colony-stimulating factor (GM-CSF) and interleukin-4 (IL-4), monocytes yield DCs. However, we show here that the addition of fibroblasts switches differentiation to macrophages. On contact with monocytes, fibroblasts release IL-6, which up-regulates the expression of functional M-CSF receptors on monocytes. This allows the monocytes to consume their autocrine M-CSF. Thus, the interplay between IL-6 and M-CSF switches monocyte differentiation to macrophages rather than DCs, and IL-6 is an essential factor in the molecular control of antigen presenting cell development.
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                Author and article information

                Contributors
                Journal
                Journal ID (nlm-ta): Front Immunol
                Journal ID (iso-abbrev): Front Immunol
                Journal ID (publisher-id): Front. Immunol.
                Title: Frontiers in Immunology
                Publisher: Frontiers Media S.A.
                ISSN (Electronic): 1664-3224
                Publication date (Electronic): 21 April 2017
                Publication date Collection: 2017
                Volume: 8
                Electronic Location Identifier: 405
                Affiliations
                [1] 1Department of Nephrology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology , Wuhan, China
                Author notes

                Edited by: Massimo Gadina, National Institute of Arthritis and Musculoskeletal and Skin Diseases, USA

                Reviewed by: Behdad Afzali, King’s College London, UK; National Institutes of Health, USA; James R. Whiteford, Queen Mary University of London, UK

                *Correspondence: Chun Zhang, drzhangchun@ 123456hust.edu.cn

                Specialty section: This article was submitted to Inflammation, a section of the journal Frontiers in Immunology

                Article
                DOI: 10.3389/fimmu.2017.00405
                PMC ID: 5399081
                PubMed ID: 28484449
                SO-VID: 0a59ddbb-61ce-4443-9b07-2518b1f5ec29
                Copyright © Copyright © 2017 Su, Lei and Zhang.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

                History
                Date received : 21 January 2017
                Date accepted : 22 March 2017
                Page count
                Figures: 0, Tables: 1, Equations: 0, References: 155, Pages: 10, Words: 9529
                Funding
                Funded by: National Natural Science Foundation of China 10.13039/501100001809
                Award ID: 81522010, 81570671, 81470964, 31200872, 81570657, 81400720
                Categories
                Subject: Immunology
                Subject: Review

                ScienceOpen disciplines: Immunology
                Keywords: il-6 classic signaling,il-6 trans-signaling,podocyte,mesangial cells,endothelial cells,tubular epithelial cells,renal disease
                Data availability:
                ScienceOpen disciplines: Immunology
                Keywords: il-6 classic signaling, il-6 trans-signaling, podocyte, mesangial cells, endothelial cells, tubular epithelial cells, renal disease

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