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Fcγ receptor‐ligating complexes improve the course of experimental autoimmune encephalomyelitis by enhancing basal Th2 responses
Author(s) -
La Flamme Anne C,
Harvie Marina,
McNeill Andrea,
Goldsack Lisa,
Tierney Joanna B,
Bäckström B Thomas
Publication year - 2006
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/j.1440-1711.2006.01464.x
Subject(s) - experimental autoimmune encephalomyelitis , immunology , receptor , multiple sclerosis , autoimmune disease , downregulation and upregulation , encephalomyelitis , cytokine , nitric oxide , biology , chemistry , medicine , endocrinology , antibody , biochemistry , gene
IL‐12p40 and macrophages are essential for the induction of disease in the mouse model of multiple sclerosis, experimental autoimmune encephalomyelitis. In this paper, we show that treatment of mice with opsonized erythrocytes, which have been shown to ligate Fcγ receptors on macrophages and alter their cytokine profile, significantly delayed the onset of experimental autoimmune encephalomyelitis. This protection correlated to the induction of Th2 responses by autoreactive T cells, enhanced basal systemic responses and a significant downregulation of IL‐12p40 and nitric oxide synthase‐2, but not IFN‐γ expression. IL‐4 was essential for the protection by opsonized erythrocytes as the effects of treatment were eliminated in IL‐4‐deficient mice. Together these studies suggest that the ligation of Fcγ receptors can modify the development of autoimmune disease by altering macrophage activation and enhancing Th2 responses.