ArticleThe Journal of clinical investigation2014
An unexpected role for platelets in blocking Th17 differentiation.
Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 10 citations in OpenAlex.
- Proteomic signatures of COVID-19 Post-Vaccination/Post-Infection Syndrome (PV/PIS): insights into immune dysregulation and coagulopathy.Frontiers in cellular and infection microbiology · 2026Article
- Platelet Factor 4: A Mysterious Chemokine in Inflammatory Regulation Diseases.Journal of inflammation research · 2025Review
- Proteoforms in Peripheral Blood Mononuclear Cells as Novel Rejection Biomarkers in Liver Transplant Recipients.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2017Article
- Hematopoietic stem and multipotent progenitor cells produce IL-17, IL-21 and other cytokines in response to TLR signals associated with late apoptotic products and augment memory Th17 and Tc17 cells in the bone marrow of normal and lupus mice.Clinical immunology (Orlando, Fla.) · 2016Article
- Human megakaryocyte progenitors derived from hematopoietic stem cells of normal individuals are MHC class II-expressing professional APC that enhance Th17 and Th1/Th17 responses.Immunology letters · 2015Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
It is well known that platelets interact with cells of the innate immune system to promote tissue repair. In contrast, it is less clear whether these links extend to cells of the adaptive immune system, such as T cells. In this issue of the JCI, Morrell and colleagues provide compelling evidence that platelets are required to limit CD4+ Th17 differentiation through the actions of the chemokine platelet factor 4 (PF4). Absence of PF4 in the host leads to exaggerated Th17 differentiation after transplantation and rapid graft rejection. The authors' findings argue that platelets are not bit part players, but rather fully fledged, critical members of the adaptive immune system.
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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.