ArticleEuropean journal of immunology2014
PD-1 modulates steady-state and infection-induced IL-10 production in vivo.
Article in European journal of immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- The impact of immune checkpoint inhibitors on infection in patients with solid malignancies: a systematic review and meta-analysis of randomised controlled trials.EClinicalMedicine · 2026Article
- PD-L1 is an intrinsic switch for natural killer cell-mediated, TRAIL-dependent antiviral function.Cell reports · 2026Article
- Adoptive cell therapy for cancer: combination strategies and biomarkers.Frontiers in immunology · 2025Review
- PD-L1-PD-1 interactions limit effector regulatory T cell populations at homeostasis and during infection.Nature immunology · 2022Article
- Characterization of a novel cysteine protease inhibitor inFrontiers in immunology · 2022Article
- Role of the PD-1/PD-L1 Pathway in ExperimentalFrontiers in immunology · 2022Article
- Characteristics of Infection Immunity Regulated byFrontiers in immunology · 2018Article
- Stress exacerbates infectivity and pathogenicity of Blastocystis hominis: in vitro and in vivo evidences.PloS one · 2014Article
- The regulation of the PD-1/PD-L1 pathway in imiquimod-induced chronic psoriasis itch and itch sensitization in mouse.Molecular painArticle
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
Programmed death-1 (PD-1) plays an important role in mediating immune tolerance through mechanisms that remain unclear. Herein, we investigated whether PD-1 prevents excessive host tissue damage during infection with the protozoan parasite, Toxoplasma gondii. Surprisingly, our results demonstrate that PD-1-deficient mice have increased susceptibility to T. gondii, with increased parasite cyst counts along with reduced type-1 cytokine responses (IL-12 and IFN-γ). PD-1⁻/⁻ DCs showed no cell intrinsic defect in IL-12 production in vitro. Instead, PD-1 neutralization via genetic or pharmacological approaches resulted in a striking increase in IL-10 release, which impaired type-1-inflammation during infection. Our results indicate that the absence of PD-1 increases IL-10 production even in the absence of infection. Although the possibility that such increased IL-10 protects against autoimmune damage is speculative, our results show that IL-10 suppresses the development of protective Th1 immune response after T. gondii infection.
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