Journal
JOURNAL OF IMMUNOLOGY
Volume 177, Issue 7, Pages 4311-4321Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.177.7.4311
Keywords
-
Categories
Funding
- NIDDK NIH HHS [DK 72381, DK 46267, DK 39773] Funding Source: Medline
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available