Abstract:
:Immune-mediated glomerular diseases (glomerulonephritis) encompass a heterogeneous collection of diseases that cause inflammation within the glomerulus and other renal compartments with significant morbidity and mortality. In general, CD4+ T cells orchestrate the immune response and play a unique role in autoimmune and chronic inflammatory diseases. In particular, the characterization of a distinct, IL-17 cytokines producing CD4+ T cell subset named TH17 cells has significantly advanced the current understanding of the pathogenic mechanisms of organ-specific immunity. Our group and others have shown that the recruitment of TH17 cells to the inflamed kidney drives renal tissue injury in experimental and possibly human crescentic glomerulonephritis (GN), but much remains to be understood about the biological functions, regulation, and signaling pathways of the TH17/IL-17 axis leading to organ damage. Here we review our current knowledge about the mechanisms and functions of IL-17 signaling in renal autoimmune diseases, with a special focus on experimental and human crescentic GN.
journal_name
Mol Immunoljournal_title
Molecular immunologyauthors
Schmidt T,Luebbe J,Paust HJ,Panzer Udoi
10.1016/j.molimm.2018.09.005subject
Has Abstractpub_date
2018-12-01 00:00:00pages
90-99eissn
0161-5890issn
1872-9142pii
S0161-5890(18)30764-8journal_volume
104pub_type
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journal_title:Molecular immunology
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pub_type: 杂志文章
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