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, 2006 Oct 01.
Article
em En
| MEDLINE
| ID: mdl-16982865
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.
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Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Células Th2
/
Inflamação
/
Pulmão
/
Proteínas de Membrana
Limite:
Animals
Idioma:
En
Revista:
J Immunol
Ano de publicação:
2006
Tipo de documento:
Article
País de afiliação:
Estados Unidos
País de publicação:
Estados Unidos