Murine ileitis after intracellular parasite infection is controlled by TGF-β-producing intraepithelial lymphocytes

被引:73
作者
Buzoni-Gatel, D
Debbabi, H
Mennechet, FJD
Martin, V
Lepage, AC
Schwartzman, JD
Kasper, LH
机构
[1] Dartmouth Med Sch, Dept Med & Microbiol, Hanover, NH USA
[2] Dartmouth Med Sch, Dept Pathol, Hanover, NH USA
[3] Fac Pharm Tours, Inst Natl Rech Agron, Lab Associe Immunol Parasitaire, Tours, France
[4] Consejo Nacl Invest Cient & Tecn, Inst Nacl Microbiol Dr Carlos G Malbran, Dept Parasitol, RA-1033 Buenos Aires, DF, Argentina
关键词
D O I
10.1053/gast.2001.22432a
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Background & Aims:Acute inflammatory ileitis occurs in susceptible (C57BL/6) mice after oral infection with Toxoplasma gondii. Overproduction of interferon (IFN)-gamma and synthesis of nitric oxide mediate the inflammation. We evaluated the role of transforming growth factor (TGF)-beta produced by intraepithelial lymphocytes (IELs) in this process. Methods: We analyzed the histologic and immunologic consequences of adoptive transfer of antigen-primed IELs into susceptible mice treated with anti-TGF-beta before oral challenge with T. gondii cysts. An in vitro coculture of enterocytes and IELs assessed the production of chemokines and cytokines in the presence of anti-TGF-beta, Results: Antigen-primed IELs prevent acute ileitis in susceptible mice that is reversed with anti-TGF-beta. Resistant mice (CBA/J) develop ileitis after treatment with anti-TGF-beta. Antigen-primed IELs can induce systemic immunosuppression as measured by depressed IFN-gamma production. In vitro, primed IELs reduce the production of inflammatory chemokines by infected enterocytes and IFN-gamma by splenocytes, Conclusions: Regulation of the ileal inflammatory process resulting from T, gondii is dependent on TGF-beta -producing IELs, The IELs ape an essential component in gut homeostasis after oral infection with this parasite.
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页码:914 / 924
页数:11
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