ArticleThe Journal of clinical investigation2011
Attenuation of HIV-associated human B cell exhaustion by siRNA downregulation of inhibitory receptors.
Article in The Journal of clinical investigation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 89 papers.
What it found
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Who cites it
89 citing papers in PubMed, 143 citations in OpenAlex.
- Circulating and intrahepatic antiviral B cells are defective in hepatitis B.The Journal of clinical investigation · 2018Trial
- PD-1 blockade partially recovers dysfunctional virus-specific B cells in chronic hepatitis B infection.The Journal of clinical investigation · 2018Trial
- Human CD21Journal of human immunity · 2026Review
- Immune Exhaustion in Chronic Infection and Cancer: Signaling Pathways and Therapeutic Interventions.MedComm · 2026Review
- Multifaceted B cell response to transient HIV viremia in elite controllers.PLoS pathogens · 2026Article
- Dysfunctional CD11cScience translational medicine · 2025Article
- FCRLs and atypical transcriptional pattern in tumor infiltrating B cells from lung and renal cancer.Frontiers in immunology · 2025Article
- Wip1 inhibitor CCT007093 alleviates immune exhaustion of lymphocytes via p65 NF-κB and YY1 in chronic hepatitis B virus infection in mice.Frontiers in immunology · 2025Article
- The Impact of HIV on B Cell Compartment and Its Implications for COVID-19 Vaccinations in People with HIV.Vaccines · 2024Review
- Siglec-6 as a therapeutic target for cell migration and adhesion in chronic lymphocytic leukemia.Nature communications · 2024Article
- Impact of HIV-Related Immune Impairment of Yellow Fever Vaccine Immunogenicity in People Living with HIV-ANRS 12403.Vaccines · 2024Article
- The role, relevance and management of immune exhaustion in bovine infectious diseases.Heliyon · 2024Review
- CD11cNeurology(R) neuroimmunology & neuroinflammation · 2024Observational
- Paired single-B-cell transcriptomics and receptor sequencing reveal activation states and clonal signatures that characterize B cells in acute myeloid leukemia.Journal for immunotherapy of cancer · 2024Article
- Tumor heterogeneity and immune-evasive T follicular cell lymphoma phenotypes at single-cell resolution.Leukemia · 2024Article
- Uncloaking the viral glycocalyx: How do viruses exploit glycoimmune checkpoints?Advances in virus research · 2024Review
- Dysfunction and regulatory interplay of T and B cells in chronic hepatitis B: immunotherapy and emerging antiviral strategies.Frontiers in cellular and infection microbiology · 2024Review
- Siglecs as potential targets of therapy in human mast cell- and/or eosinophil-associated diseases.Seminars in immunology · 2023Review
- Role of Siglecs in viral infections: A double-edged sword interaction.Molecular aspects of medicine · 2023Review
- Patient-derived Siglec-6-targeting antibodies engineered for T-cell recruitment have potential therapeutic utility in chronic lymphocytic leukemia.Journal for immunotherapy of cancer · 2022Article
29 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
13 authors at 1 institution in 1 country.
Funding
Abstract
Chronic immune activation in HIV-infected individuals leads to accumulation of exhausted tissue-like memory B cells. Exhausted lymphocytes display increased expression of multiple inhibitory receptors, which may contribute to the inefficiency of HIV-specific antibody responses. Here, we show that downregulation of B cell inhibitory receptors in primary human B cells led to increased tissue-like memory B cell proliferation and responsiveness against HIV. In human B cells, siRNA knockdown of 9 known and putative B cell inhibitory receptors led to enhanced B cell receptor-mediated (BCR-mediated) proliferation of tissue-like memory but not other B cell subpopulations. The strongest effects were observed with the putative inhibitory receptors Fc receptor-like-4 (FCRL4) and sialic acid-binding Ig-like lectin 6 (Siglec-6). Inhibitory receptor downregulation also led to increased levels of HIV-specific antibody-secreting cells and B cell-associated chemokines and cytokines. The absence of known ligands for FCRL4 and Siglec-6 suggests these receptors may regulate BCR signaling through their own constitutive or tonic signaling. Furthermore, the extent of FCLR4 knockdown effects on BCR-mediated proliferation varied depending on the costimulatory ligand, suggesting that inhibitory receptors may engage specific pathways in inhibiting B cell proliferation. These findings on HIV-associated B cell exhaustion define potential targets for reversing the deleterious effect of inhibitory receptors on immune responses against persistent viral infections.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.