PROBLEM: Differences in circulating (peripheral) and mucosal T-cell phenotypes in chlamydia-infected women remain largely unknown. METHOD OF STUDY: Thirteen paired mononuclear cell specimens from blood and cervicovaginal lavages collected from chlamydia-infected women were stained and analyzed using ten-color cell surface flow cytometry for T-cell distribution, activation status, homing, and T helper (Th)-associated chemokine receptors (CKRs). RESULTS: A higher proportion of genital mucosal T-cells were activated (CD38+ HLA-DR+ ) and expressed CCR5 and Th1-associated CKR CXCR3+ CCR5+ compared to peripheral T-cells, but a lower proportion of mucosal T-cells expressed homing CKR CCR7, Th-2 associated CKR CCR4, and CXCR3+ CCR4+ for both T-cell subsets. CONCLUSION: T-cell phenotypes differed in the peripheral vs genital mucosa compartments in chlamydia-infected women. As chlamydia infects mucosal epithelial cells, the finding of a higher frequency of activated T-cells and Th-1 phenotypes in the mucosa likely reflects an adaptive immune response to infection.
PROBLEM: Differences in circulating (peripheral) and mucosal T-cell phenotypes in chlamydia-infected women remain largely unknown. METHOD OF STUDY: Thirteen paired mononuclear cell specimens from blood and cervicovaginal lavages collected from chlamydia-infected women were stained and analyzed using ten-color cell surface flow cytometry for T-cell distribution, activation status, homing, and T helper (Th)-associated chemokine receptors (CKRs). RESULTS: A higher proportion of genital mucosal T-cells were activated (CD38+ HLA-DR+ ) and expressed CCR5 and Th1-associated CKR CXCR3+ CCR5+ compared to peripheral T-cells, but a lower proportion of mucosal T-cells expressed homing CKR CCR7, Th-2 associated CKR CCR4, and CXCR3+ CCR4+ for both T-cell subsets. CONCLUSION: T-cell phenotypes differed in the peripheral vs genital mucosa compartments in chlamydia-infected women. As chlamydia infects mucosal epithelial cells, the finding of a higher frequency of activated T-cells and Th-1 phenotypes in the mucosa likely reflects an adaptive immune response to infection.
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