期刊
JOURNAL OF IMMUNOLOGY
卷 178, 期 7, 页码 4557-4566出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.7.4557
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资金
- Medical Research Council [MC_U105178805] Funding Source: researchfish
- MRC [MC_U105178805] Funding Source: UKRI
- Medical Research Council [MC_U105178805] Funding Source: Medline
- Wellcome Trust Funding Source: Medline
The propensity of a range of parasitic helminths to stimulate a Th2 or regulatory cell-biased response has been proposed to reduce the severity of experimental inflammatory bowel disease. We examined whether infection with Schistosoma mansoni, a trematode parasite, altered the susceptibility of mice to colitis induced by dextran sodium sulfate (DSS). Mice infected with schistosome worms were refractory to DSS-induced colitis. Egg-laying schistosome infections or injection of eggs did not render mice resistant to colitis induced by DSS. Schistosome worm infections prevent colitis by a novel mechanism dependent on macrophages, and not by simple modulation of Th2 responses, or via induction of regulatory CD4(+) or CD25(+) cells, IL-10, or TGF-beta. Infected mice had marked infiltration of macrophages (F4/80(+)CD11b(+)CD11c(-)) into the colon lamina propria and protection from DSS-induced colitis was shown to be macrophage dependent. Resistance from colitis was not due to alternatively activated macrophages. Transfer of colon lamina propria F4/80(+) macrophages isolated from worm-infected mice induced significant protection from colitis in recipient mice treated with DSS. Therefore, we propose a new mechanism whereby a parasitic worm suppresses DSS-induced colitis via a novel colon-infiltrating macrophage population.
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