Cell-autonomous regulation of complement C3 by factor H limits macrophage efferocytosis and exacerbates atherosclerosis
Misregulation of complement cascade is associated with chronic inflammatory disease. Kiss et al. report the impact of local complement regulation on atherosclerotic lesions, finding that monocyte-derived complement factor H limits cell-autonomous alternative complement activation. This regulation restricts monocyte-derived macrophages’ pro-resolving functions and promotes plaque necrosi s in a murine model of atherosclerosis.
Source: Immunity - Category: Allergy & Immunology Authors: M áté G. Kiss, Nikolina Papac-Miličević, Florentina Porsch, Dimitrios Tsiantoulas, Tim Hendrikx, Minoru Takaoka, Huy Q. Dinh, Marie-Sophie Narzt, Laura Göderle, Mária Ozsvár-Kozma, Michael Schuster, Nikolaus Fortelny, Anastasiya Hladik, Sylvia Knap Tags: Article Source Type: research
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