ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Peripheral blood CCR4+CCR6+ and CXCR3+CCR6+CD4+ T cells are highly permissive to HIV-1 infection.
Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 210 papers, 1 of them a synthesis that pooled it.
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Who cites it
210 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Identification of novel HIV-1 dependency factors in primary CCR4(+)CCR6(+)Th17 cells via a genome-wide transcriptional approach.Retrovirology · 2015Pooled it
- Initiating Intramuscular Depot Medroxyprogesterone Acetate Increases Frequencies of Th17-like Human Immunodeficiency Virus Target Cells in the Genital Tract of Women in South Africa: A Randomized Trial.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2022Trial
- Cofilin hyperactivation in HIV infection and targeting the cofilin pathway using an anti-αScience advances · 2019Trial
- Trial
- Chemokine Levels in the Penile Coronal Sulcus Correlate with HIV-1 Acquisition and Are Reduced by Male Circumcision in Rakai, Uganda.PLoS pathogens · 2016Trial
- Phenotype and susceptibility to HIV infection of CD4+ Th17 cells in the human female reproductive tract.Mucosal immunology · 2014Trial
- The Th17/Treg ratio, IL-1RA and sCD14 levels in primary HIV infection predict the T-cell activation set point in the absence of systemic microbial translocation.PLoS pathogens · 2013Trial
- HCV-specific CD4EBioMedicine · 2026Article
- Immunodominant Tuberculosis Antigens Recognized by Human CD4Cold Spring Harbor perspectives in medicine · 2026Article
- Pre-Human Immunodeficiency Virus (HIV) infection Th17 CD4+ T cells as predictors of early HIV disease progression.PLoS pathogens · 2026Article
- Deleterious germline CARD11 gain-of-function variants alter human B-cell and CD4+ T-cell differentiation and function.Clinical and experimental immunology · 2026Article
- Decoding Treg diversity and dysfunction to advance Treg-based therapies in autoimmune and inflammatory diseases.Frontiers in immunology · 2026Review
- Integrated cellular, proteomic and metabolomic profiling of immune-related adverse events in non-small cell lung cancer.Frontiers in immunology · 2026Article
- Article
- Concurrent TB and HIV therapies control TB reactivation during co-infection but not chronic immune activation.Nature communications · 2025Article
- The tuberculosis-associated microenvironment promotes HIV-1 persistence by impairing CD8+ T cell-mediated viral control.bioRxiv : the preprint server for biology · 2025Article
- Single cell technologies and the biology of HIV-infected CD4 T-cell reservoirs.Current opinion in HIV and AIDS · 2025Review
- Article
- Human LY9 governs CD4Science immunology · 2025Article
- Multi-layered deep immune profiling, SARS-CoV-2 RNAemia and inflammation in unvaccinated COVID-19 individuals with persistent symptoms.Communications medicine · 2025Article
150 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
12 authors.
Funding
Abstract
There is limited knowledge on the identity of primary CD4(+) T cell subsets selectively targeted by HIV-1 in vivo. In this study, we established a link between HIV permissiveness, phenotype/homing potential, and lineage commitment in primary CD4(+) T cells. CCR4(+)CCR6(+), CCR4(+)CCR6(-), CXCR3(+)CCR6(+), and CXCR3(+)CCR6(-) T cells expressed cytokines and transcription factors specific for Th17, Th2, Th1Th17, and Th1 lineages, respectively. CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells expressed the HIV coreceptors CCR5 and CXCR4 and were permissive to R5 and X4 HIV replication. CCR4(+)CCR6(-) T cells expressed CXCR4 but not CCR5 and were permissive to X4 HIV only. CXCR3(+)CCR6(-) T cells expressed CCR5 and CXCR4 but were relatively resistant to R5 and X4 HIV in vitro. Total CCR6(+) T cells compared with CCR6(-) T cells harbored higher levels of integrated HIV DNA in treatment-naive HIV-infected subjects. The frequency of total CCR6(+) T cells and those of CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells were diminished in chronically infected HIV-positive subjects, despite viral-suppressive therapy. A high-throughput analysis of cytokine profiles identified CXCR3(+)CCR6(+) T cells as a major source of TNF-alpha and CCL20 and demonstrated a decreased TNF-alpha/IL-10 ratio in CXCR3(+)CCR6(-) T cells. Finally, CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells exhibited gut- and lymph node-homing potential. Thus, we identified CCR4(+)CCR6(+) and CXCR3(+)CCR6(+) T cells as highly permissive to HIV replication, with potential to infiltrate and recruit more CCR6(+) T cells into anatomic sites of viral replication. It is necessary that new therapeutic strategies against HIV interfere with viral replication/persistence in discrete CCR6(+) T cell subsets.
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