ArticleProceedings of the National Academy of Sciences of the United States of America2013
Programmed cell death 1 inhibits inflammatory helper T-cell development through controlling the innate immune response.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 47 citations in OpenAlex.
- Harnessing tumor immune checkpoints for autoimmune disease therapeutics.Frontiers in immunology · 2026Review
- CRISPR/Cas9-Mediated Knockout and Overexpression Studies Unveil the Role of PD-L1 in Immune Modulation in a Psoriasis-like Mouse Model.Inflammation · 2025Article
- Altered memory CCR6EBioMedicine · 2024Article
- Dectin-1 signaling in neutrophils up-regulates PD-L1 and triggers ROS-mediated suppression of CD4Journal of leukocyte biology · 2022Article
- Divergent roles of PD-L1 in immune regulation during ischemia-reperfusion injury.Frontiers in immunology · 2022Review
- Regulatory Effect of Mesenchymal Stem Cells on T Cell Phenotypes in Autoimmune Diseases.Stem cells international · 2021Review
- Immune Checkpoint Inhibitors and Neurotoxicity.Current neuropharmacology · 2021Review
- The role of Th17 immunity in chronic ocular surface disorders.The ocular surface · 2021Review
- Paraneoplastic dermatomyositis appearing after nivolumab therapy for gastric cancer: a case report.Journal of medical case reports · 2019Article
- Impact of early inflammatory cytokine elevation after commencement of PD-1 inhibitors to predict efficacy in patients with non-small cell lung cancer.Medical oncology (Northwood, London, England) · 2019Article
- A comprehensive review on the role of co-signaling receptors and Treg homeostasis in autoimmunity and tumor immunity.Journal of autoimmunity · 2018Review
- Inflammatory CNS disease caused by immune checkpoint inhibitors: status and perspectives.Nature reviews. Neurology · 2017Review
- Case-control Association Study of Autoimmunity Associated Variants in PDCD1 and Juvenile Idiopathic Arthritis.Current rheumatology reviews · 2017Article
- Programmed Death-1 Culls Peripheral Accumulation of High-Affinity Autoreactive CD4 T Cells to Protect against Autoimmunity.Cell reports · 2016Article
- Basics of PD-1 in self-tolerance, infection, and cancer immunity.International journal of clinical oncology · 2016Review
- Genetic and Epigenetic Regulation of PD-1 Expression.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
- The anticancer immune response of anti-PD-1/PD-L1 and the genetic determinants of response to anti-PD-1/PD-L1 antibodies in cancer patients.Oncotarget · 2015Review
- NF-κB regulates PD-1 expression in macrophages.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Both PD-1 ligands protect the kidney from ischemia reperfusion injury.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Phosphorylated STAT3 and PD-1 regulate IL-17 production and IL-23 receptor expression in Mycobacterium tuberculosis infection.European journal of immunology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Programmed cell death 1 (PD-1) is an inhibitory coreceptor on immune cells and is essential for self-tolerance because mice genetically lacking PD-1 (PD-1(-/-)) develop spontaneous autoimmune diseases. PD-1(-/-) mice are also susceptible to severe experimental autoimmune encephalomyelitis (EAE), characterized by a massive production of effector/memory T cells against myelin autoantigen, the mechanism of which is not fully understood. We found that an increased primary response of PD-1(-/-) mice to heat-killed mycobacteria (HKMTB), an adjuvant for EAE, contributed to the enhanced production of T-helper 17 (Th17) cells. Splenocytes from HKMTB-immunized, lymphocyte-deficient PD-1(-/-) recombination activating gene (RAG)2(-/-) mice were found to drive antigen-specific Th17 cell differentiation more efficiently than splenocytes from HKMTB-immunized PD-1(+/+) RAG2(-/-) mice. This result suggested PD-1's involvement in the regulation of innate immune responses. Mice reconstituted with PD-1(-/-) RAG2(-/-) bone marrow and PD-1(+/+) CD4(+) T cells developed more severe EAE compared with the ones reconstituted with PD-1(+/+) RAG2(-/-) bone marrow and PD-1(+/+) CD4(+) T cells. We found that upon recognition of HKMTB, CD11b(+) macrophages from PD-1(-/-) mice produced very high levels of IL-6, which helped promote naive CD4(+) T-cell differentiation into IL-17-producing cells. We propose a model in which PD-1 negatively regulates antimycobacterial responses by suppressing innate immune cells, which in turn prevents autoreactive T-cell priming and differentiation to inflammatory effector T cells.
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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.