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T Cell, Ig Domain, Mucin Domain-2 Gene-Deficient Mice Reveal a Novel Mechanism for the Regulation of Th2 Immune Responses and Airway Inflammation

2006; American Association of Immunologists; Volume: 177; Issue: 7 Linguagem: Inglês

10.4049/jimmunol.177.7.4311

1550-6606

Paul D. Rennert, Takaharu Ichimura, Irene Sizing, Véronique Bailly, Zhifang Li, Rachel Rennard, Patricia McCoon, Lourdes Pablo, Steven D. Miklasz, Leticia Tarilonte, Joseph V. Bonventre,

Glycosylation and Glycoproteins Research

Abstract 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.