期刊
CLINICAL KIDNEY JOURNAL
卷 12, 期 4, 页码 503-511出版社
OXFORD UNIV PRESS
DOI: 10.1093/ckj/sfz029
关键词
ANCA; crescentic glomerulonephritis; cytokine; glomerulonephritis; immunology; T-lymphocyte
资金
- Programa Comite de Recerca-HUB de Formacio Post-Residencia en Recerca, Convocatoria d'Ajuts per la Recerca Clinica 2016 (IDIBELL Biomedical Research Institute)
- European Regional Development Funds ISCIII, Red Tematica de Investigacion Cooperativa en Salud Red de Investigacion Renal [RD16/0009/0003]
Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is an autoimmune condition that commonly causes kidney impairment and can be fatal. The key participation of B-lymphocytes as ANCA producers and neutrophils as target of these antibodies is widely described as the mechanism of endothelial damage in this disease. There has been a rising interest in the role of T-lymphocytes in AAV in recent years. Evidence is strong from animal models, and T-lymphocytes can be found infiltrating kidney tissue and other tissue sites in AAV patients. Furthermore, the different subsets of T-lymphocytes are also key players in the aberrant immune response observed in AAV. Polarization towards a predominant Th1 and Th17 response in the acute phase of the disease has been described, along with a decline in the number of T-regulatory lymphocytes, which, in turn, show functional impairment. Interactions between different T-cell subsets, and between T-cells and neutrophils and B-cells, also enhance the inflammatory response, constituting a complex network. Novel therapies targeting T-cell immunity are emerging in this scenario and may constitute an interesting alternative to conventional therapy in selected patients. This review aims to summarize the available evidence regarding T-cell imbalances and functional impairment, especially focusing on renal involvement of AAV.
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