Cell Immunity in Inflammatory Vasculitis

ISSN: 1875-631X (Online)
ISSN: 1573-3955 (Print)

Volume 11, 2 Issues, 2015

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Current Immunology Reviews

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Cecil Czerkinsky
Institut de Pharmacologie Moleculaire et Cellulaire
660 Route des Lucioles
Valbonne, 06560

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Cell Immunity in Inflammatory Vasculitis

Author(s): Angelo Ferrante, Francesco Ciccia, Giuliana Guggino, Anna Rita Giardina and Giovanni Triolo

Affiliation: Dipartimento Biomedico di Medicina Interna e Specialistica, sezione di Reumatologia, Piazza delle Cliniche 2, 90123 Palermo, Italy.


The 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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Article Details

Volume: 10
First Page: 1
Page Count: 1
DOI: 10.2174/1573395510666140626210842

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