NDLI: Heligmosomoides polygyrus bakeri induces tolerogenic dendritic cells that block colitis and prevent antigen-specific gut T cell responses.

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Heligmosomoides polygyrus bakeri induces tolerogenic dendritic cells that block colitis and prevent antigen-specific gut T cell responses.

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Heligmosomoides polygyrus bakeri induces tolerogenic dendritic cells that block colitis and prevent antigen-specific gut T cell responses.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Leung, John Blum, Arthur M. Stoyanoff, Korynn M. Urban, Joseph P. Hang, Long Weinstock, Joel V. Setiawan, Tommy
Description	Country affiliation: United States Author Affiliation: Blum AM ( Division of Gastroenterology-Hepatology, Department of Internal Medicine, Tufts Medical Center, Boston, MA 02111, USA.)
Abstract	Immunological diseases such as inflammatory bowel disease (IBD) are infrequent in less developed countries, possibly because helminths provide protection by modulating host immunity. In IBD murine models, the helminth Heligmosomoides polygyrus bakeri prevents colitis. It was determined whether H. polygyrus bakeri mediated IBD protection by altering dendritic cell (DC) function. We used a Rag IBD model where animals were reconstituted with IL10â »/â » T cells, making them susceptible to IBD and with OVA Ag-responsive OT2 T cells, allowing study of a gut antigenic response. Intestinal DC from H. polygyrus bakeri-infected Rag mice added to lamina propria mononuclear cells (LPMC) isolated from colitic animals blocked OVA IFN-Î³/IL-17 responses in vitro through direct contact with the inflammatory LPMC. DC from uninfected Rag mice displayed no regulatory activity. Transfer of DC from H. polygyrus bakeri-infected mice into Rag mice reconstituted with IL10â »/â » T cells protected animals from IBD, and LPMC from these mice lost OVA responsiveness. After DC transfer, OT2 T cells populated the intestines normally. However, the OT2 T cells were rendered Ag nonresponsive through regulatory action of LPMC non-T cells. The process of regulation appeared to be regulatory T cell independent. Thus, H. polygyrus bakeri modulates intestinal DC function, rendering them tolerogenic. This appears to be an important mechanism through which H. polygyrus bakeri suppresses colitis. IFN-Î³ and IL-17 are colitogenic. The capacity of these DC to block a gut Ag-specific IFN-Î³/IL-17 T cell response also is significant.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1102892
Journal	The Journal of Immunology
Issue Number	5
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-09-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Colitis Immunology Dendritic Cells Immune Tolerance Inflammatory Bowel Diseases Strongylida Infections T-lymphocyte Subsets Adoptive Transfer Animals Cells, Cultured Parasitology Prevention & Control Pathology Disease Models, Animal Enterocolitis Epitopes, T-lymphocyte Interleukin-10 Administration & Dosage Deficiency Genetics Intestinal Mucosa Mice Mice, Inbred C57bl Mice, Knockout Mice, Transgenic Nematospiroides Dubius Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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