Giant Cell Arteritis

Weyand, Cornelia M.; Goronzy, Jörg J.

doi:10.1002/9781118355244.ch24

Cited by 3 publications

(1 citation statement)

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“…Primary large vessel vasculitis can affect the aorta and any of its proximal branches. Giant cell arteritis (GCA), a large vessel vasculitis, is the most common form of primary systemic vasculitis, with an annual incidence of 25 per 100,000 in those over the age of 50 ( 2 ). Takayasu’s arteritis (TAK), another form of large vessel vasculitis, usually occurs before age 50.…”

Section: Introductionmentioning

confidence: 99%

Protective Role of Mast Cells in Primary Systemic Vasculitis: A Perspective

et al. 2017

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Mast cells are important cells of the immune system. Although traditionally considered as key players in allergic and hypersensitivity reactions, emerging evidence suggests that mast cells have many complex roles in vascular disease. These include regulation of vasodilation, angiogenesis, activation of matrix metalloproteinases, apoptosis of smooth muscle cells, and activation of the renin angiotensin system. Mast cells are also known to play an immunomodulatory role via modulation of regulatory T-cell (Treg), macrophage and endothelial cell functions. This dual role of the mast cells is evident in myeloperoxidase anti-neutrophil cytoplasmic antibodies-mouse model of glomerulonephritis in which mast cell deficiency worsens glomerulonephritis, whereas inhibition of mast cell degranulation is effective in abrogating the development of glomerulonephritis. Our previous work demonstrated that mast cell degranulation inhibits lipopolysaccharide-induced interleukin 6 (IL-6) production in mice. This effect was not seen in histamine-1-receptor knockout (H1R−/−) mice suggesting a role for histamine in IL-6 homeostasis. In addition, mast cell degranulation-mediated decrease in IL-6 production was associated with an upregulation of suppressor of cytokine signaling-1 protein in the aorta. We propose that mast cells regulate large artery inflammation through T-cells, shifting a primarily Th1 and Th17 toward a Th2 response and leading to enhanced IL-10 production, activation Treg cells, and the inhibition of macrophage functions.

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Section: Introductionmentioning

confidence: 99%