Cell Immunity in Inflammatory Vasculitis
Angelo Ferrante, Francesco Ciccia, Giuliana Guggino, Anna Rita Giardina and Giovanni TrioloAffiliation:
Dipartimento Biomedico di Medicina Interna e Specialistica, sezione di Reumatologia, Piazza delle Cliniche 2, 90123 Palermo, Italy.
AbstractThe vasculitis is a highly heterogeneous group of disorders characterized by blood vessel-wall inﬂammation. Giant cell arteritis (GCA) and Takayasu’s arteritis (TA) are the two primary large-vessel vasculitis. Two distinct cellular pathways have been identified in GCA: Th17 polarization and IL-17 secretion and generation of Th1 cells which secrete IFN-γ. These two pathways may play different roles in the pathogenesis of vasculitis. The antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAVs) are small vessels vasculitis associated with antibodies direct to myeloperoxidase (MPO-ANCA) such aseosinophilic granulomatosis with polyangiitis (EGPA) and microscopic polyangiitis (MPA) or with antibodies direct to proteinase 3 (PR3-ANCA) such as granulomatosis with polyangiitis (GPA).Both in vitro and in vivo experimental data have shown that MPO-ANCA can induce necrotizing small-vessel vasculitis; however the presence of granulomatous lesions suggests the involvement of cell-mediated immune responses. Behçet syndrome (BS) is a chronic relapsing vasculitis of arteries and veins with unclear etiology. Exogenous and endogenous antigens, innate immune cells such as dendritic, NK, neutrophils and monocyte andadaptive-immune cells are involved.
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