CD4-positive effector memory T cells participate in disease expression in ANCA-associated vasculitis.
Although the cause of ANCA-associated vasculitis (AAV) remains undetermined, the presence of lymphocytic infiltrates in inflammatory lesions of patients suggests that vascular damage is immune mediated. Studies over the past decade have implicated a role for T cells in the pathogenesis of AAV as altered T cell phenotype has been observed in this disorder. The distribution of T cell subpopulations has been analyzed most intensely in Wegener's granulomatosis (WG), where an expanded population of circulating CD4(+) effector memory T cells (CD4(+)T(EM)) was demonstrated. CD4(+)T(EM) cells play a major role in the pathogenesis of several autoimmune diseases. Specific suppression of CD4(+)T(EM) cells inhibits delayed-type hypersensitivity (DTH) and has therapeutic potential in autoimmune disease. Thus, CD4(+)T(EM) cells may act as inducers of tissue injury and participate in the development of AAV. Therapies that target CD4(+)T(EM), without impairing the activity of other lymphocyte subsets, may hold therapeutic promise for AAV.
Abdulahad
Wayel H
WH
Department of Rheumatology and Clinical Immunology, University Medical Center Groningen, Hanzeplein 1, 9713 GZ, Groningen, the Netherlands. w.abdulahad@int.umcg.nl
Stegeman
Coen A
CA
Limburg
Pieter C
PC
Kallenberg
Cees G M
CG
D000818:Animals; D019268:Antibodies, Antineutrophil Cytoplasmic / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology*; D003922:Diabetes Mellitus, Type 1 / Q000276:immunology; D006801:Humans; D007156:Immunologic Memory / Q000276:immunology*; D010641:Phenotype; D014657:Vasculitis / Q000276:immunology* / Q000473:pathology* / Q000628:therapy