Gomez, M. Rodriguez and Talke, Y. and Hofmann, C. and Ketelsen, I. and Hermann, F. and Reich, B. and Goebel, N. and Schmidbauer, K. and Dunger, N. and Bruehl, H. and Renner, K. and Syed, S-N and Mack, M. (2014) Basophils control T-cell responses and limit disease activity in experimental murine colitis. MUCOSAL IMMUNOLOGY, 7 (1). pp. 188-199. ISSN 1933-0219, 1935-3456
Full text not available from this repository. (Request a copy)Abstract
Basophils have been recognized as important inducers of T helper type 2 (Th2) responses. Using the colitis model of adoptive transfer of CD4(+) CD62L(+) T cells into lymphopenic hosts, we have analyzed how basophils regulate T-cell responses and modulate disease activity. Transferred T cells rapidly proliferate, produce large amounts of interleukin (IL)-3, and expand the number of basophils in an IL-3-dependent manner. Depletion of basophils with two different antibodies substantially upregulated Th1 cytokines in transferred T cells at day 8. Increased Th1 cytokine expression persisted until the end of the experiment when basophil-depleted mice showed exacerbation of colitis with more severe loss of weight, histological damage, colonic leukocyte infiltration, and expression of pro-inflammatory cytokines. In vitro, we show that basophil-derived IL-4 and IL-6 downregulates expression of interferon-gamma, IL-2, and tumor necrosis factor in T cells. These data show a beneficial role of basophils in a T-cell driven model of autoimmunity.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | INFLAMMATORY-BOWEL-DISEASE; TRICHURIS-SUIS THERAPY; INDUCE WASTING DISEASE; IN-VIVO; CUTTING EDGE; INTERLEUKIN-10-DEFICIENT MICE; INTESTINAL INFLAMMATION; ALLERGIC INFLAMMATION; CYTOKINE PRODUCTION; HELMINTH INFECTION; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin I Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 02 Dec 2019 14:30 |
| Last Modified: | 02 Dec 2019 14:30 |
| URI: | https://pred.uni-regensburg.de/id/eprint/11109 |
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