CX3CR1+ cells facilitate the activation of CD4 T cells in the colonic lamina propria during antigen-driven colitis

Rossini, V.; Zhurina, D.; Radulovic, K.; Manta, C.; Walther, P.; Riedel, C. U.; Niess, J. H. (2014). CX3CR1+ cells facilitate the activation of CD4 T cells in the colonic lamina propria during antigen-driven colitis. Mucosal immunology, 7(3), pp. 533-548. Nature Publishing Group 10.1038/mi.2013.70

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Dendritic cells (DCs) and macrophages populate the intestinal lamina propria to initiate immune responses required for the maintenance of intestinal homeostasis. To investigate whether CX3CR1(+) phagocytes communicate with CD4 T cells during the development of transfer colitis, we established an antigen-driven colitis model induced by the adoptive transfer of DsRed OT-II cells in CX3CR1(GFP/+) × RAG(-/-) recipients challenged with Escherichia coli expressing ovalbumin (OVA) fused to a cyan fluorescent protein (CFP). After colonization of CX3CR1(GFP/+) × RAG(-/-) animals with red fluorescent E. coli pCherry-OVA, colonic CX3CR1(+) cells but not CD103(+) DCs phagocytosed E. coli pCherry-OVA. Degraded bacterial-derived antigens are transported by CD103(+) DCs to mesenteric lymph nodes (MLNs), where CD103(+) DCs prime naive T cells. In RAG(-/-) recipients reconstituted with OT II cells and gavaged with OVA-expressing E. coli, colonic CX3CR1(+) phagocytes are in close contact with CD4 T cells and presented bacterial-derived antigens to CD4 T cells to activate and expand effector T cells.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Gastro-intestinal, Liver and Lung Disorders (DMLL) > Clinic of Visceral Surgery and Medicine > Gastroenterology

UniBE Contributor:

Niess, Jan Hendrik

Subjects:

600 Technology > 610 Medicine & health

ISSN:

1933-0219

Publisher:

Nature Publishing Group

Language:

English

Submitter:

Lilian Karin Smith-Wirth

Date Deposited:

06 Oct 2014 16:31

Last Modified:

05 Dec 2022 14:34

Publisher DOI:

10.1038/mi.2013.70

BORIS DOI:

10.7892/boris.53048

URI:

https://boris.unibe.ch/id/eprint/53048

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