| First Author | Davila SJ | Year | 2014 |
| Journal | J Immunol | Volume | 192 |
| Issue | 9 | Pages | 4284-93 |
| PubMed ID | 24659687 | Mgi Jnum | J:209989 |
| Mgi Id | MGI:5569208 | Doi | 10.4049/jimmunol.1303238 |
| Citation | Davila SJ, et al. (2014) Integrin alpha4beta1 is necessary for CD4+ T cell-mediated protection against genital Chlamydia trachomatis infection. J Immunol 192(9):4284-93 |
| abstractText | 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-gamma 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 alpha4beta1. Interfering with alpha4beta1, but not alpha4beta7, function resulted in defective CD4(+) T cell trafficking to the uterus and high bacterial load. We conclude that integrin alpha4beta1 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. |
