vasculitis/proline

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Non-receptor type, proline-rich protein tyrosine kinase 2 (Pyk2) is a possible therapeutic target for Kawasaki disease.

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Ingia / Ingia

Kawasaki disease (KD) is a paediatric vasculitis whose pathogenesis remains unclear. Based on experimental studies using a mouse model for KD, we report here that proline-rich protein tyrosine kinase 2 (Pyk2) plays a critical role in the onset of KD-like murine vasculitis. The mouse model for KD was

MMP (Matrix Metalloprotease)-9-Producing Monocytes Enable T Cells to Invade the Vessel Wall and Cause Vasculitis.

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Ingia / Ingia

BACKGROUND Giant cell arteritis (GCA)-a primary vasculitis of medium and large arteries-is associated with vessel wall damage, elastic membrane fragmentation, and vascular remodeling. Proteinases are believed to contribute to pathogenesis by degrading extracellular matrix and causing tissue

Detachment of endothelial cells by polymorphonuclear leukocytes in vitro: potentiation by antibody coating and prevention by inflammatory exudate.

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Ingia / Ingia

A widely advocated hypothesis suggests that polymorphonuclear leukocytes release enzymes at sites of inflammation which in turn cause tissue damage, especially vasculitis. To test this we isolated and grew human endothelial cells and labelled them with chromium-51. Polymorphonuclear leukocytes were

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Herbal & Natural Medicine

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