T Cell, Ig Domain, Mucin Domain-2 Gene-Deficient Mice Reveal a Novel Mechanism for the Regulation of Th2 Immune Responses and Airway Inflammation
| Autor: | Zhifang Li, Steven D. Miklasz, Joseph V. Bonventre, Takaharu Ichimura, Lourdes Pablo, Patricia Mccoon, Irene Sizing, Veronique Bailly, Paul D. Rennert, Leticia Tarilonte, Rachel Rennard |
|---|---|
| Rok vydání: | 2006 |
| Předmět: |
Adoptive cell transfer
Ovalbumin Recombinant Fusion Proteins T-Lymphocytes T cell Cellular differentiation Immunology Cell Inflammation Biology Mice Th2 Cells Immune system medicine Animals Immunology and Allergy Lung Mice Inbred BALB C Reverse Transcriptase Polymerase Chain Reaction Effector Membrane Proteins Cell Differentiation Flow Cytometry Phenotype Asthma Mice Mutant Strains Rats Disease Models Animal medicine.anatomical_structure medicine.symptom |
| Zdroj: | The Journal of Immunology. 177:4311-4321 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.177.7.4311 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|