Wrage, Marius and Holland, Tim and Nuese, Bjoern and Kaltwasser, Johanna and Froehlich, Jessica and Arnold, Harald and Giessler, Claudia and Flamann, Cindy and Bruns, Heiko and Berges, Johannes and Daniel, Christoph and Hoffmann, Markus H. and Anish, Chakkumkal and Seeberger, Peter H. and Bogdan, Christian and Dettmer, Katja and Rauh, Manfred and Mattner, Jochen (2024) Cell type-specific fi c modulation of metabolic, immune-regulatory, and anti-microbial pathways by CD101. MUCOSAL IMMUNOLOGY, 17 (5). pp. 892-910. ISSN 1933-0219, 1935-3456
Full text not available from this repository. (Request a copy)Abstract
T lymphocytes and myeloid cells express the immunoglobulin-like glycoprotein cluster of differentiation (CD)101, notably in the gut. Here, we investigated the cell-specific functions of CD101 during dextran sulfate sodium (DSS)-induced colitis and Salmonella enterica Typhimurium infection. Similar to conventional CD101(-/-) mice, animals with a regulatory T cell-specific Cd101 deletion developed more severe intestinal pathology than littermate controls in both models. While the accumulation of T helper 1 cytokines in a CD101-deficient environment entertained DSS-induced colitis, it impeded the replication of Salmonella as revealed by studying CD101(-/-) x interferon-g(-/-) mice. Moreover, CD101-expressing neutrophils were capable to restrain Salmonella infection in vitro and in vivo. Both cell-intrinsic and -extrinsic mechanisms of CD101 contributed to the control of bacterial growth and spreading. The CD101-dependent containment of Salmonella infection required the expression of Irg-1 and Nox2 and the production of itaconate and reactive oxygen species. The level of intestinal microbial antigens in the sera of inflammatory bowel disease patients correlated inversely with the expression of CD101 on myeloid cells, which is in line with the suppression of CD101 seen in mice following DSS application or Salmonella infection. Thus, depending on the experimental or clinical setting, CD101 helps to limit inflammatory insults or bacterial infections due to cell type-specific modulation of metabolic, immune-regulatory, and anti-microbial pathways.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | SUSCEPTIBILITY GENE; T-CELLS; MICE; ITACONATE; NEUTROPHILS; ACTIVATION; INDUCTION; SUCCINATE; EXPANSION; EFFECTOR |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Institut für Funktionelle Genomik > Lehrstuhl für Funktionelle Genomik (Prof. Oefner) |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 27 Jan 2026 09:35 |
| Last Modified: | 27 Jan 2026 09:35 |
| URI: | https://pred.uni-regensburg.de/id/eprint/65367 |
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