MacLean, Finn and Tsegaye, Adino Tesfahun and Graham, Jessica B. and Swarts, Jessica L. and Vick, Sarah C. and Potchen, Nicole B. and Talavera, Irene Cruz and Warrier, Lakshmi and Dubrulle, Julien and Schroeder, Lena K. and Saito, Ayumi and Mar, Corinne and Thomas, Katherine K. and Mack, Matthias and Sabo, Michelle C. and Chohan, Bhavna H. and Ngure, Kenneth and Mugo, Nelly Rwamba and Lingappa, Jairam R. and Lund, Jennifer M. (2025) Bacterial vaginosis associates with dysfunctional T cells and altered soluble immune factors in the cervicovaginal tract. JOURNAL OF CLINICAL INVESTIGATION, 135 (10): e184609. ISSN 0021-9738, 1558-8238
Full text not available from this repository. (Request a copy)Abstract
BACKGROUND. Bacterial vaginosis (BV) is a dysbiosis of the vaginal microbiome that is prevalent among reproductive-age females worldwide. Adverse health outcomes associated with BV include an increased risk of sexually acquired HIV, yet the immunological mechanisms underlying this association are not well understood. METHODS. To investigate BV-driven changes to cervicovaginal tract (CVT) and circulating T cell phenotypes, Kinga Study participants with or without BV provided vaginal tract (VT) and ectocervical (CX) tissue biopsies and PBMC samples. RESULTS. High-parameter flow cytometry revealed an increased frequency of cervical CD4+ conventional T (Tconv) cells expressing CCR5 in BR+ versus BR-women. However, we found no difference in the number of CD3+CD4+CCR5+ cells in the CX or VT of BV+ versus BV-individuals, suggesting that BV-driven increased HIV susceptibility may not be solely attributed to increased CVT HIV target cell abundance. Flow cytometry also revealed that individuals with BV had an increased frequency of dysfunctional CX and VT CD39+ Tconv and CX tissue-resident CD69+CD103+ Tconv cells, reported to be implicated in HIV acquisition risk and replication. Many soluble immune factor differences in the CVT further support that BV elicits diverse and complex CVT immune alterations. CONCLUSION. Our comprehensive analysis expands on potential immunological mechanisms that may underlie the adverse health outcomes associated with BV, including increased HIV susceptibility. TRIAL REGISTRATION. ClinicalTrials.gov NCT03701802. FUNDING. This work was supported by National Institutes of Health grants R01AI131914, R01AI141435, and R01AI129715.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | SEXUALLY-TRANSMITTED INFECTIONS; HUMAN T(H)17 CELLS; TRANSCRIPTION FACTOR; HIV ACQUISITION; CYTOKINE LEVELS; TH17 CELLS; IFN-GAMMA; DIFFERENTIATION; RESPONSES; WOMEN; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Abteilung für Nephrologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 20 Apr 2026 06:54 |
| Last Modified: | 20 Apr 2026 06:54 |
| URI: | https://pred.uni-regensburg.de/id/eprint/67639 |
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