ArticleBlood2014
CLEC-2 is required for development and maintenance of lymph nodes.
Article in Blood, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 97 citations in OpenAlex.
- Beyond Hemostasis: Platelets' Multifaceted Functions in Immune Responses.Life (Basel, Switzerland) · 2026Review
- Integrated machine learning and multi-dataset analysis identify SDS as a diagnostic and immune-related hub gene in hepatoblastoma.Frontiers in oncology · 2026Article
- Review
- Mice with lymphatic dysfunction develop pathogenic lung tertiary lymphoid organs that model an autoimmune emphysema phenotype of COPD.American journal of physiology. Lung cellular and molecular physiology · 2025Article
- Reduction in disialyl-T antigen levels in mice deficient for both St6galnac3 and St6galnac4 results in blood filling of lymph nodes.Scientific reports · 2023Article
- Comprehensive analysis identifies CLEC1B as a potential prognostic biomarker in hepatocellular carcinoma.Cancer cell international · 2023Article
- Lessons of Vascular Specialization From Secondary Lymphoid Organ Lymphatic Endothelial Cells.Circulation research · 2023Review
- C-type lectin receptor expression is a hallmark of neutrophils infiltrating the skin in epidermolysis bullosa acquisita.Frontiers in immunology · 2023Article
- OIT3 mediates macrophage polarization and facilitates hepatocellular carcinoma progression.Cancer immunology, immunotherapy : CII · 2022Article
- Intratumoral Platelets: Harmful or Incidental Bystanders of the Tumor Microenvironment?Cancers · 2022Review
- Fibroblastic reticular cell response to dendritic cells requires coordinated activity of podoplanin, CD44 and CD9.Journal of cell science · 2021Article
- Role of Podoplanin-Positive Cells in Cardiac Fibrosis and Angiogenesis After Ischemia.Frontiers in physiology · 2021Review
- Low-dose Btk inhibitors selectively block platelet activation by CLEC-2.Haematologica · 2021Article
- Role of Platelets in Detection and Regulation of Infection.Arteriosclerosis, thrombosis, and vascular biology · 2021Review
- Article
- Lymphatic impairment leads to pulmonary tertiary lymphoid organ formation and alveolar damage.The Journal of clinical investigation · 2019Article
- Ontogeny of platelet function.Blood advances · 2019Review
- Functional significance of the platelet immune receptors GPVI and CLEC-2.The Journal of clinical investigation · 2019Review
- Translational Implications of Platelets as Vascular First Responders.Circulation research · 2018Review
- C-Type Lectin-Like Receptors As Emerging Orchestrators of Sterile Inflammation Represent Potential Therapeutic Targets.Frontiers in immunology · 2018Review
Corrections and comments
- Commented on byLymphomania.2014
Authors and funding
11 authors at 1 institution in 1 country.
Funding
Abstract
The importance of CLEC-2, a natural ligand/receptor for Gp38/Podoplanin, in the formation of the lymphatic vasculature has recently been demonstrated. As the development and maintenance of lymph nodes (LNs) is dependent on the formation of the lymphatic vasculature and the differentiation of Gp38/Podoplanin(+) stromal cells, we investigated the role of CLEC-2 in lymphoneogenesis and LN homeostasis. Using constitutive Clec1b(-/-) mice, we showed that while CLEC-2 was not necessary for initiation of the LN anlage, it was required at late stages of development. Constitutive deletion of CLEC-2 induced a profound defect in lymphatic endothelial cell proliferation, resulting in lack of LNs at birth. In contrast, conditional deletion of CLEC-2 in the megakaryocyte/platelet lineage in Clec1b(fl/fl)PF4-Cre mice led to the development of blood-filled LNs and fibrosis, in absence of a proliferative defect of the lymphatic endothelial compartment. This phenotype was also observed in chimeric mice reconstituted with Clec1b(fl/fl)PF4-Cre bone marrow, indicating that CLEC-2 expression in platelets was required for LN integrity. We demonstrated that LNs of Clec1b(fl/fl)PF4-Cre mice are able to sustain primary immune responses but show a defect in immune cell recirculation after repeated immunizations, thus suggesting CLEC-2 as target in chronic immune response.
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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.