Martinez Valenzuela, LauraDraibe, JulianaFulladosa, XavierBestard Matamoros, OriolCruzado, Josep Ma.Torras Ambròs, Joan2020-10-272020-10-272019-04-192048-8505https://hdl.handle.net/2445/171564Anti-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.9 p.application/pdfengcc-by-nc (c) Martínez Valenzuela, Laura et al., 2019http://creativecommons.org/licenses/by-nc/3.0/esVasculitisCitoquinesVasculitisCytokinesinfo:eu-repo/semantics/article7000382020-10-27info:eu-repo/semantics/openAccess31384441