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The Journal of Immunology, 2002, 168: 2988-2996.
Copyright © 2002 by The American Association of Immunologists

Lamina Propria CD4+ T Lymphocytes Synergize with Murine Intestinal Epithelial Cells to Enhance Proinflammatory Response Against an Intracellular Pathogen1

Franck J. D. Mennechet*, Lloyd H. Kasper2,*, Nicolas Rachinel*, Wen Li*, Alain Vandewalle§ and Dominique Buzoni-Gatel*,{dagger},{ddagger}

* Departments of Microbiology, Immunology, and Medicine, Dartmouth Medical School, Lebanon, NH 03756; {dagger} Institut Pasteur, Unite Biologie Moleculaire du Gene, Paris, France; {ddagger} Departement de Pathologie Infectieuse et Immunologie, Institut National de la Recherche Agronomique, Nouzilly, France; and § Institut National de la Santé et de la Recherche Médicale, Faculté de Médecine Xavier Bichat, Paris, France

Acute and lethal ileitis can be elicited in certain strains of inbred mice after oral infection with the intracellular protozoan parasite Toxoplasma gondii. The development of this inflammatory process is dependent upon the induction of a robust Th1 response, including overproduction of IFN-{gamma}, TNF-{alpha}, and NO, as has been reported in other experimental models of human inflammatory bowel disease. In this study we have investigated the role of CD4+ T cells from the lamina propria (LP) in the early inflammatory events after T. gondii infection using isolated and primary cultured intestinal cells from infected mice and immortalized mouse mICcl2 intestinal epithelial cells. Primed LP CD4+ T cells isolated from parasite-infected mice produce substantial quantities of both IFN-{gamma} and TNF-{alpha}. IFN-{gamma}- and TNF-{alpha}-producing LP CD4+ T cells synergize with infected mICcl2 and enhance the production of several inflammatory chemokines including macrophage-inflammatory protein-2, monocyte chemoattractant protein-1, monocyte chemoattractant protein-3, macrophage-inflammatory protein-1{alpha}{beta}, and IFN-{gamma}-inducible protein-10. Furthermore, primed LP CD4+ T cells cocultured with infected mICcl2 inhibited replication of the parasite in the intestinal epithelial cells. Thus, LP CD4+ T cells can interact with parasite-infected intestinal epithelial cells and alter the expression of several proinflammatory products that have been associated with the development of intestinal inflammation. The interaction between these two components of the gut mucosal compartment (CD4+ T cells and enterocytes) may play a role in the immunopathogenesis of this pathogen-driven experimental inflammatory bowel disease model.




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