Abstract
Chlamydia trachomatis causes STI and reproductive dysfunction worldwide which is not preventable with antibiotics. Identifying a population of endocervical T cells to target in vaccine development would enhance efficacy. Trafficking of murine CD4+ lymphocytes to Chlamydia muridarum infected genital tract (GT) tissue in vivo was measured using adoptive transfer studies of fluorescent CD4+ T cells from integrin β7-/- mice or mice which lack E-selectin on endothelial cells. Murine in vivo migration studies showed that lack of α4β7 or E-selectin significantly reduced trafficking of CD4 T cells to the GT of mice infected with C. muridarum. CD4+ T cells use at least two different adhesive mechanisms involving an integrin of the mucosal homing pathway and selectin pathway to accumulate in the GT during C. muridarum infection.
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