ArticleProceedings of the National Academy of Sciences of the United States of America2014
Type I interferon suppresses de novo virus-specific CD4 Th1 immunity during an established persistent viral infection.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.
What it found
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Who cites it
74 citing papers in PubMed, 103 citations in OpenAlex.
- Beyond suppression: the paradox of JAK inhibitors as amplifiers of cancer immunotherapy.Nature reviews. Immunology · 2026Review
- Functional Type I and Type II interferon crosstalk restricts progenitor exhausted CD8 T cells through spatial exclusion and checkpoint enforcement.bioRxiv : the preprint server for biology · 2026Article
- Stepwise differentiation from precursor intermediates and distinct Th1 checkpoints promote CD4 Th1 cell differentiation during chronic viral infection.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Virus envelope glycoprotein targeting bispecific T cell engager protects mice from lethal severe fever with thrombocytopenia virus infection.Cell reports. Medicine · 2025Article
- Orf virus-based vectors induce potent germinal center B cell, Tfh cell, and CD8Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Context-dependent impact of type I interferon signaling in cancer.Molecular cancer · 2025Review
- Review
- Review
- Central tolerance shapes the neutralizing B cell repertoire against a persisting virus in its natural host.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Genetic diversity and seroprevalence of Toxoplasma gondii in COVID‑19 patients; a first case-control study in Iran.BMC infectious diseases · 2024Article
- Late-rising CD4 T cells resolve mouse cytomegalovirus persistent replication in the salivary gland.PLoS pathogens · 2024Article
- Cytomegalovirus viremia and advanced HIV disease: is there an argument for anti-CMV treatment?Expert review of anti-infective therapy · 2023Review
- Childhood-onset systemic lupus erythematosus: characteristics and the prospect of glucocorticoid pulse therapy.Frontiers in immunology · 2023Review
- A viral-specific CD4Frontiers in immunology · 2023Article
- Review
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- Autoantibodies in Neuropsychiatric Systemic Lupus Erythematosus (NPSLE): Can They Be Used as Biomarkers for the Differential Diagnosis of This Disease?Clinical reviews in allergy & immunology · 2022Review
- TRAF3 enhances type I interferon receptor signaling in T cells by modulating the phosphatase PTPN22.Science signaling · 2022Article
- Cytomegalovirus viremia as a risk factor for mortality in HIV-associated cryptococcal and tuberculous meningitis.International journal of infectious diseases : IJID : official publication of the International Society for Infectious Diseases · 2022Article
- Tfh-cell-derived interleukin 21 sustains effector CD8Immunity · 2022Article
14 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
8 authors at 3 institutions in 1 country.
Funding
Abstract
CD4 T cells are central to orchestrate, sustain, and potentially regenerate antiviral immunity throughout persistent viral infections. Although the evolving immune environment during persistent infection reshapes established CD4 T-cell responses, the fate of naïve CD4 T cells primed in the midst of persistent infection is unclear. We demonstrate that, in marked contrast to the onset of infection, virus-specific CD4 T cells primed during an established persistent infection have diminished ability to develop Th1 responses, to efficiently accumulate in peripheral tissues, and almost exclusively differentiate into T follicular helper cells. Consistent with suppressed Th1 and heightened Tfh differentiation, virus-specific CD4 T cells primed during the established persistent infection provide help to B cells, but only limited help to CD8 T cells. The suppression of de novo Th1 generation and tissue distribution was mediated by chronic type I IFN (IFN-I) production and was effectively restored by blocking IFN-I signaling during CD4 T-cell priming. Thus, we establish a suppressive function of chronic IFN-I signaling and mechanism of immunoregulation during an established persistent virus infection.
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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.