| First Author | Rennert PD | Year | 2006 |
| Journal | J Immunol | Volume | 177 |
| Issue | 7 | Pages | 4311-21 |
| PubMed ID | 16982865 | Mgi Jnum | J:125054 |
| Mgi Id | MGI:3723404 | Doi | 10.4049/jimmunol.177.7.4311 |
| Citation | Rennert PD, et al. (2006) T cell, Ig domain, mucin domain-2 gene-deficient mice reveal a novel mechanism for the regulation of Th2 immune responses and airway inflammation. J Immunol 177(7):4311-21 |
| abstractText | The development of asthma and other atopic diseases is influenced by cytokines produced by Th2 effector T cells. How effector T cell responses are regulated once these cell populations are established remains unclear. The recently described T cell and airway phenotype regulator locus, containing the T cell, Ig domain, mucin domain (TIM) genes, is genetically associated with Th2 cytokine production and Th2-dependent immune responses. In this study, we report the phenotype of the TIM-2 gene-deficient mouse, and demonstrate exacerbated lung inflammation in an airway atopic response model. Immune responses in the TIM-2-deficient mouse reveal disregulated expression of Th2 cytokines, and adoptive transfer experiments show that the T cell compartment is responsible for the heightened inflammatory phenotype. These studies show that TIM-2 is a novel and critical regulator of effector T cell activity. |
