Integrin α4ß1 is necessary for CD4+ T cell-mediated protection against genital Chlamydia trachomatis infection.
J Immunol
; 192(9): 4284-93, 2014 May 01.
Article
em En
| MEDLINE
| ID: mdl-24659687
ABSTRACT
Chlamydia trachomatis infection is the most common sexually transmitted bacterial infection in the United States and a significant health burden worldwide. Protection from Chlamydia infection in the genital mucosa is dependent on IFN-γ derived from CD4(+) Th1 cells. These CD4(+) T cells must home successfully to the genital tract to exert their effector function and decrease C. trachomatis burden. Although adhesion receptors expressed by CD4(+) T cells in the genital tract have been characterized, the integrin receptor required for Chlamydia-specific CD4(+) T cell-mediated protection has not been explored. In this study, we demonstrate that C. trachomatis infection of the upper genital tract results in recruitment of Chlamydia-specific CD4(+) T cells robustly expressing the integrin α4ß1. Interfering with α4ß1, but not α4ß7, function resulted in defective CD4(+) T cell trafficking to the uterus and high bacterial load. We conclude that integrin α4ß1 is necessary for CD4(+) T cell-mediated protection against C. trachomatis infection in the genital mucosa. By identifying homing molecules required for successful CD4(+) T cell trafficking to C. trachomatis-infected tissues, we will be better equipped to design vaccines that elicit sterilizing, long-lasting immunity without inducing immune pathologies in the upper genital tract.
Texto completo:
1
Bases de dados:
MEDLINE
Assunto principal:
Linfócitos T CD4-Positivos
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Infecções por Chlamydia
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Chlamydia trachomatis
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Integrina alfa4beta1
Limite:
Animals
Idioma:
En
Revista:
J Immunol
Ano de publicação:
2014
Tipo de documento:
Article