Schey, R; Dornhoff, H; Baier, J L C; Purtak, M; Opoka, R; Koller, A K; Atreya, R; Rau, Tilman; Daniel, C; Amann, K; Bogdan, C; Mattner, J (2016). CD101 inhibits the expansion of colitogenic T cells. Mucosal immunology, 9(5), pp. 1205-1217. Nature Publishing Group 10.1038/mi.2015.139
Full text not available from this repository.CD101 exerts negative-costimulatory effects in vitro, but its function in vivo remains poorly defined. CD101 is abundantly expressed on lymphoid and myeloid cells in intestinal tissues, but absent from naïve splenic T cells. Here, we assessed the impact of CD101 on the course of inflammatory bowel disease (IBD). Using a T-cell transfer model of chronic colitis, we found that in recipients of naïve T cells from CD101(+/+) donors up to 30% of the recovered lymphocytes expressed CD101, correlating with an increased interleukin (IL)-2-mediated FoxP3 expression. Transfer of CD101(-/-) T cells caused more severe colitis and was associated with an expansion of IL-17-producing T cells and an enhanced expression of IL-2Rα/β independently of FoxP3. The co-transfer of naïve and regulatory T cells (Treg) protected most effectively from colitis, when both donor and recipient mice expressed CD101. Although the expression of CD101 on T cells was sufficient for Treg-function and the inhibition of T-cell proliferation, sustained IL-10 production required additional CD101 expression by myeloid cells. Finally, in patients with IBD a reduced CD101 expression on peripheral and intestinal monocytes and CD4(+) T cells correlated with enhanced IL-17 production and disease activity. Thus, CD101 deficiency is a novel marker for progressive colitis and potential target for therapeutic intervention.
Item Type: |
Journal Article (Original Article) |
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Division/Institute: |
04 Faculty of Medicine > Service Sector > Institute of Pathology > Clinical Pathology |
UniBE Contributor: |
Rau, Tilman |
ISSN: |
1933-0219 |
Publisher: |
Nature Publishing Group |
Language: |
English |
Submitter: |
Doris Haefelin |
Date Deposited: |
22 Dec 2016 15:48 |
Last Modified: |
05 Dec 2022 15:00 |
Publisher DOI: |
10.1038/mi.2015.139 |
PubMed ID: |
26813346 |
URI: |
https://boris.unibe.ch/id/eprint/92063 |