| First Author | Curtiss ML | Year | 2012 |
| Journal | Eur J Immunol | Volume | 42 |
| Issue | 3 | Pages | 651-61 |
| PubMed ID | 22144095 | Mgi Jnum | J:187793 |
| Mgi Id | MGI:5438195 | Doi | 10.1002/eji.201141581 |
| Citation | Curtiss ML, et al. (2012) Tim-1 regulates Th2 responses in an airway hypersensitivity model. Eur J Immunol 42(3):651-61 |
| abstractText | T-cell immunoglobulin mucin-1 (Tim-1) is a transmembrane protein postulated to be a key regulator of Th2-type immune responses. This hypothesis is based in part upon genetic studies associating Tim-1 polymorphisms in mice with a bias toward airway hyperrespon-siveness (AHR) and the development of Th2-type CD4(+) T cells. Tim-1 expressed by Th2 CD4(+) T cells has been proposed to function as a co-stimulatory molecule. Tim-1 is also expressed by B cells, macrophages, and dendritic cells, but its role in responses by these cell types has not been firmly established. Here, we generated Tim-1-deficient mice to determine the role of Tim-1 in a murine model of allergic airway disease that depends on the development and function of Th2 effector cells and results in the generation of AHR. We found antigen-driven recruitment of inflammatory cells into airways is increased in Tim-1-deficient mice relative to WT mice. In addition, we observed increased antigen-specific cytokine production by splenocytes from antigen-sensitized Tim-1-deficient mice relative to those from controls. These data support the conclusion that Tim-1 functions in pathways that suppress recruitment of inflammatory cells into the airways and the generation or activity of CD4(+) T cells. |
