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Title: | Regulatory T cells in renal disease. | Authors: | Kitching A.R. ;Ooi J.D.;Alikhan M.A.;Huynh M. | Institution: | (Alikhan, Huynh, Kitching, Ooi) Centre for Inflammatory Diseases, Department of Medicine, Monash University, Monash Medical Centre, 246 Clayton Road, Clayton, VIC 3168, Australia (Kitching) Department of Nephrology, Monash Health, Clayton, VIC, Australia (Kitching) Department of Paediatric Nephrology, Monash Health, Clayton, VIC, Australia | Issue Date: | 7-Feb-2018 | Copyright year: | 2018 | Publisher: | Wiley-Blackwell (E-mail: cs-journals@wiley.com) | Place of publication: | United Kingdom | Publication information: | Clinical and Translational Immunology. 7 (1) (no pagination), 2018. Article Number: e1004. Date of Publication: 2018. | Abstract: | The kidney is vulnerable to injury, both acute and chronic from a variety of immune and metabolic insults, all of which at least to some degree involve inflammation. Regulatory T cells modulate systemic autoimmune and allogenic responses in glomerulonephritis and transplantation. Intrarenal regulatory T cells (Tregs), including those recruited to the kidney, have suppressive effects on both adaptive and innate immune cells, and probably also intrinsic kidney cells. Evidence from autoimmune glomerulonephritis implicates antigen-specific Tregs in HLA-mediated dominant protection, while in several human renal diseases Tregs are abnormal in number or phenotype. Experimentally, Tregs can protect the kidney from injury in a variety of renal diseases. Mechanisms of Treg recruitment to the kidney include via the chemokine receptors CCR6 and CXCR3 and potentially, at least in innate injury TLR9. The effects of Tregs may be context dependent, with evidence for roles for immunoregulatory roles both for endogenous Tbet-expressing Tregs and STAT-3-expressing Tregs in experimental glomerulonephritis. Most experimental work and some of the ongoing human trials in renal transplantation have focussed on unfractionated thymically derived Tregs (tTregs). However, induced Tregs (iTregs), type 1 regulatory T (Tr1) cells and in particular antigen-specific Tregs also have therapeutic potential not only in renal transplantation, but also in other kidney diseases. The kidney is vulnerable to immune mediated injury. Regulated T cells can modulate the systemic autoimmune and allogenic responses in glomerulonephritis and transplantation. Furthermore, intrarenal regulatory T cells can effect suppression on immune and intrinsic kidney cells.Copyright © 2018 The Authors. Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australasian Society for Immunology Inc. | DOI: | http://monash.idm.oclc.org/login?url=http://dx.doi.org/10.1002/cti2.1004 | ORCID: | Alikhan, Maliha A; ORCID: http://orcid.org/0000-0002-2578-3457 Kitching, A Richard; ORCID: http://orcid.org/0000-0002-2713-2391 | Link to associated publication: | Click here for full text options | ISSN: | 2050-0068 (electronic) | URI: | https://repository.monashhealth.org/monashhealthjspui/handle/1/36859 | Type: | Review | Subjects: | innate immunity acute kidney failure/et [Etiology] adaptive immunity adriamycin-induced nephropathy ANCA associated vasculitis/et [Etiology] antigen specificity autoimmunity chronic kidney failure/et [Etiology] diabetic nephropathy/et [Etiology] glomerulonephritis/et [Etiology] Goodpasture syndrome/et [Etiology] human immunocompetent cell immunoglobulin A nephropathy/et [Etiology] immunomodulation immunoregulation kidney cell *kidney disease/et [Etiology] kidney ischemia/et [Etiology] kidney transplantation lupus erythematosus nephritis/et [Etiology] nephrotoxicity phenotype priority journal protein expression *regulatory T lymphocyte review sepsis chemokine receptor CCR6/ec [Endogenous Compound] chemokine receptor CXCR3/ec [Endogenous Compound] transcription factor T bet/ec [Endogenous Compound] toll like receptor 9/ec [Endogenous Compound] STAT3 protein/ec [Endogenous Compound] HLA antigen/ec [Endogenous Compound] doxorubicin/to [Drug Toxicity] cisplatin/to [Drug Toxicity] immunoglobulin A nephropathy / etiology immunomodulation immunoregulation innate immunity kidney cell *kidney disease / *etiology kidney ischemia / etiology kidney transplantation lupus erythematosus nephritis / etiology nephrotoxicity phenotype priority journal protein expression *regulatory T lymphocyte Review sepsis adriamycin-induced nephropathy antigen specificity autoimmunity chronic kidney failure / etiology diabetic nephropathy / etiology glomerulonephritis / etiology Goodpasture syndrome / etiology human immunocompetent cell acute kidney failure / etiology adaptive immunity ANCA associated vasculitis / etiology |
Type of Clinical Study or Trial: | Review article (e.g. literature review, narrative review) |
Appears in Collections: | Articles |
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