Tim-1 regulates Th2 responses in an airway hypersensitivity model
| Autor: | Thomas R. Businga, Paul B. Rothman, David M. Valenzuela, Joel N. Kline, John D. Colgan, Suzanne L. Cassel, Melody Singh, Miranda L. Curtiss, Geri L. Traver, Andrew J. Murphy, David K. Meyerholz, Jacob V. Gorman |
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| Rok vydání: | 2012 |
| Předmět: |
Cell type
medicine.medical_treatment T cell Immunology Mice Transgenic Biology Article Mice Interleukin 21 Th2 Cells Immune system medicine Animals Immunology and Allergy Hepatitis A Virus Cellular Receptor 1 IL-2 receptor Antigen-presenting cell Cell Proliferation Mice Inbred BALB C Interleukin-13 ZAP70 Interleukin-17 Membrane Proteins Mice Inbred C57BL Disease Models Animal Cytokine medicine.anatomical_structure Bronchial Hyperreactivity Interleukin-5 |
| Zdroj: | European Journal of Immunology. 42:651-661 |
| ISSN: | 0014-2980 |
| Popis: | 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 hyperresponsiveness and the development of Th2-type CD4+ T cells. Tim-1 is expressed by Th2 CD4+ T cells on which it 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. 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 wild-type 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. |
| Databáze: | OpenAIRE |
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