| First Author | Gomez MR | Year | 2014 |
| Journal | Mucosal Immunol | Volume | 7 |
| Issue | 1 | Pages | 188-99 |
| PubMed ID | 23757302 | Mgi Jnum | J:347215 |
| Mgi Id | MGI:7616592 | Doi | 10.1038/mi.2013.38 |
| Citation | Gomez MR, et al. (2014) Basophils control T-cell responses and limit disease activity in experimental murine colitis. Mucosal Immunol 7(1):188-99 |
| abstractText | 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. |
