Basophils control T-cell responses and limit disease activity in experimental murine colitis
| Autor: | Reich Barbara, Goebel Nicole, Dunger Nadja, Ketelsen Isabel, Mack Matthias, Rodriguez Gomez Manuel, Renner Kerstin, Hofmann Claudia, Talke Yvonne, Syed Shahzad-Nawaz, Bruehl Hilke, Hermann Fabian, Schmidbauer Kathrin |
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| Rok vydání: | 2014 |
| Předmět: |
Male
Adoptive cell transfer T-Lymphocytes T cell Immunology chemical and pharmacologic phenomena Biology medicine.disease_cause CCL5 Autoimmunity Disease activity Mice Lymphopenia parasitic diseases medicine Animals Murine colitis Immunology and Allergy Limit (mathematics) Colitis Mice Knockout business.industry Interleukin hemic and immune systems Th1 Cells medicine.disease Adoptive Transfer Basophils Interleukin 33 Disease Models Animal Phenotype medicine.anatomical_structure Cytokines Female Tumor necrosis factor alpha business |
| Zdroj: | Mucosal Immunology. 7:188-199 |
| ISSN: | 1933-0219 |
| DOI: | 10.1038/mi.2013.38 |
| Popis: | 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-γ, 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. |
| Databáze: | OpenAIRE |
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