ArticleHaematologica2016
A distinct plasmablast and naïve B-cell phenotype in primary immune thrombocytopenia.
Article in Haematologica, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 15 citations in OpenAlex.
- Inflammatory cytokines, inflammasomes, and neutrophil extracellular traps in primary immune thrombocytopenia pathogenesis.Blood vessels, thrombosis & hemostasis · 2026Review
- Phenotypic, functional and metabolic features of B cells from a small cohort of breast cancer patients.Frontiers in oncology · 2026Article
- Age-related and disease-specific changes in B-cell profiles in older adults with immune thrombocytopenia.Frontiers in immunology · 2026Article
- Identification of ORM1, vWF, SPARC, and PPBP as immune-related proteins involved in immune thrombocytopenia by quantitative LC-MS/MS.Clinical proteomics · 2023Article
- Increasing numbers of CD19 + CD24International journal of hematology · 2021Article
- Atypical phenotype and response of B cells in patients with seropositive rheumatoid arthritis.Clinical and experimental immunology · 2021Article
- Serum B-Cell Maturation Antigen (BCMA) Levels Differentiate Primary Antibody Deficiencies.The journal of allergy and clinical immunology. In practice · 2020Article
- Widespread B cell perturbations in HIV-1 infection afflict naive and marginal zone B cells.The Journal of experimental medicine · 2019Article
- Reversing Autoimmunity Combination of Rituximab and Intravenous Immunoglobulin.Frontiers in immunology · 2018Article
- The Extensive Regulation of MicroRNA in Immune Thrombocytopenia.Clinical and applied thrombosis/hemostasis : official journal of the International Academy of Clinical and Applied Thrombosis/HemostasisReview
Corrections and comments
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Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary immune thrombocytopenia is an autoimmune disorder in which platelet destruction is a consequence of both B- and T-cell dysregulation. Flow cytometry was used to further characterize the B- and T-cell compartments in a cross-sectional cohort of 26 immune thrombocytopenia patients including antiplatelet antibody positive (n=14) and negative (n=12) patients exposed to a range of therapies, and a cohort of matched healthy volunteers. Markers for B-cell activating factor and its receptors, relevant B-cell activation markers (CD95 and CD21) and markers for CD4(+) T-cell subsets, including circulating T-follicular helper-like cells, were included. Our results indicate that an expanded population of CD95(+) naïve B cells correlated with disease activity in immune thrombocytopenia patients regardless of treatment status. A population of CD21-naïve B cells was specifically expanded in autoantibody-positive immune thrombocytopenia patients. Furthermore, the B-cell maturation antigen, a receptor for B-cell activating factor, was consistently and strongly up-regulated on plasmablasts from immune thrombocytopenia patients. These observations have parallels in other autoantibody-mediated diseases and suggest that loss of peripheral tolerance in naïve B cells may be an important component of immune thrombocytopenia pathogenesis. Moreover, the B-cell maturation antigen represents a potential target for plasma cell directed therapies in immune thrombocytopenia.
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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.