دورية أكاديمية

Bacterial vaginosis-driven changes in vaginal T cell phenotypes and their implications for HIV susceptibility.

التفاصيل البيبلوغرافية
العنوان: Bacterial vaginosis-driven changes in vaginal T cell phenotypes and their implications for HIV susceptibility.
المؤلفون: MacLean F; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA., Tsegaye AT; Department of Global Health, University of Washington, Seattle, USA., Graham JB; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA., Swarts JL; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA., Vick SC; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA., Potchen N; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA., Talavera IC; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA., Warrier L; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA., Dubrulle J; Cellular Imaging Shared Resource, Fred Hutchinson Cancer Research Center, Seattle, USA., Schroeder LK; Cellular Imaging Shared Resource, Fred Hutchinson Cancer Research Center, Seattle, USA., Mar C; Department of Global Health, University of Washington, Seattle, USA., Thomas KK; Department of Global Health, University of Washington, Seattle, USA., Mack M; Department of Internal Medicine-Nephrology, University Hospital Regensburg, Regensburg, Germany., Sabo MC; Department of Medicine, University of Washington, Seattle, USA., Chohan BH; Department of Global Health, University of Washington, Seattle, USA.; Center for Virus Research, Kenya Medical Research Institute, Nairobi, Kenya., Ngure K; Department of Global Health, University of Washington, Seattle, USA.; School of Public Health, Jomo Kenyatta University of Agriculture and Technology, Nairobi, Kenya., Mugo N; Department of Global Health, University of Washington, Seattle, USA.; Center for Clinical Research, Kenya Medical Research Institute, Nairobi, Kenya., Lingappa JR; Department of Global Health, University of Washington, Seattle, USA.; Department of Medicine, University of Washington, Seattle, USA.; Department of Pediatrics, University of Washington, Seattle, USA., Lund JM; Vaccine and Infectious Disease Division, Fred Hutchinson Cancer Center, Seattle, USA.; Department of Global Health, University of Washington, Seattle, USA.
مؤلفون مشاركون: Kinga Study Team
المصدر: BioRxiv : the preprint server for biology [bioRxiv] 2024 Jul 05. Date of Electronic Publication: 2024 Jul 05.
نوع المنشور: Journal Article; Preprint
اللغة: English
بيانات الدورية: Country of Publication: United States NLM ID: 101680187 Publication Model: Electronic Cited Medium: Internet ISSN: 2692-8205 (Electronic) Linking ISSN: 26928205 NLM ISO Abbreviation: bioRxiv Subsets: PubMed not MEDLINE
مستخلص: Bacterial vaginosis (BV) is a dysbiosis of the vaginal microbiome that is prevalent in reproductive-age women worldwide. Adverse outcomes associated with BV include an increased risk of sexually acquired Human Immunodeficiency Virus (HIV), yet the immunological mechanisms underlying this association are not well understood. To investigate BV driven changes to cervicovaginal tract (CVT) and circulating T cell phenotypes, participants with or without BV provided vaginal tract (VT) and ectocervical (CX) tissue biopsies and peripheral blood mononuclear cells (PBMC). Immunofluorescence analysis of genital mucosal tissues revealed a reduced density of CD3 + CD4 + CCR5 + cells in the VT lamina propria of individuals with compared to those without BV (median 243.8 cells/mm 2 BV- vs 106.9 cells/mm 2 BV+, p=0.043). High-parameter flow cytometry of VT biopsies revealed an increased frequency in individuals with compared to those without BV of dysfunctional CD39 + conventional CD4 + T cells (Tconv) (median frequency 15% BV- vs 30% BV+, p adj =0.0331) and tissue-resident CD69 + CD103 + Tconv (median frequency 24% BV- vs 38% BV+, p adj =0.0061), previously reported to be implicated in HIV acquisition and replication. Our data suggests that BV elicits diverse and complex VT T cell alterations and expands on potential immunological mechanisms that may promote adverse outcomes including HIV susceptibility.
معلومات مُعتمدة: T32 AI007509 United States AI NIAID NIH HHS; T32 AI007140 United States AI NIAID NIH HHS; R01 AI131914 United States AI NIAID NIH HHS; R01 AI141435 United States AI NIAID NIH HHS; P30 CA015704 United States CA NCI NIH HHS; T32 AI083203 United States AI NIAID NIH HHS; R01 AI129715 United States AI NIAID NIH HHS
تواريخ الأحداث: Date Created: 20240715 Latest Revision: 20240722
رمز التحديث: 20240722
مُعرف محوري في PubMed: PMC11245000
DOI: 10.1101/2024.07.03.601916
PMID: 39005354
قاعدة البيانات: MEDLINE
الوصف
تدمد:2692-8205
DOI:10.1101/2024.07.03.601916