期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 7, 页码 4948-4955出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.7.4948
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资金
- NIAID NIH HHS [R01 AI052099, R01 AI 052099] Funding Source: Medline
- NIGMS NIH HHS [R01 GM 49758, R01 GM083204, R01 GM049758, R01 GM083204-01] Funding Source: Medline
IL 4 receptor a (IL-4R alpha) expression by non-bone marrow (BM)-derived cells is required to protect hosts against several parasitic helminth species. In contrast, we demonstrate that IL-4R alpha expression by BM-derived cells is both necessary and sufficient to prevent Schistosoma mansoni-infected mice from developing severe inflammation directed against parasite ova, whereas IL-4R alpha expression by non-BM-derived cells is neither necessary nor sufficient. Chimeras that express IL-4R alpha only on non-BM-derived cells still produce Th2 cytokines, but overproduce IL-12p40, TNF, and IFN-gamma, fail to generate alternatively activated macrophages, and develop endotoxemia and severe hepatic and intestinal pathology. In contrast, chimeras that express IL-4R alpha only on BM-derived cells have extended survival, even though the granulomas that they develop around parasite eggs are small and devoid of collagen. These observations identify distinct roles for IL-4/IL-13 responsive cell lineages during schistosomiasis: IL-4R alpha-mediated signaling in non-BM-derived cells regulates granuloma size and fibrosis, whereas signaling in BM-derived cells suppresses parasite egg-driven inflammation within the liver and intestine.
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