ArticleImmunologic research2016
Elevated expression of NLRP3 in patients with immune thrombocytopenia.
Article in Immunologic research, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 22 citations in OpenAlex.
- Efficacy and Safety Results With Rilzabrutinib, an Oral Bruton Tyrosine Kinase Inhibitor, in Patients With Immune Thrombocytopenia: Phase 2 Part B Study.American journal of hematology · 2025Trial
- Inflammatory cytokines, inflammasomes, and neutrophil extracellular traps in primary immune thrombocytopenia pathogenesis.Blood vessels, thrombosis & hemostasis · 2026Review
- Evaluating rilzabrutinib in the treatment of immune thrombocytopenia.Immunotherapy · 2025Review
- Pyroptosis in platelets: Thrombocytopenia and inflammation.Journal of clinical laboratory analysis · 2023Review
- Novel Biomarkers for Diagnosis and Monitoring of Immune Thrombocytopenia.International journal of molecular sciences · 2023Review
- COVID-19-induced immune thrombocytopenic purpura; Immunopathogenesis and clinical implications.Le infezioni in medicina · 2022Review
- NF-Journal of immunology research · 2018Article
- Imbalanced expression of Bcl-xL and Bax in platelets treated with plasma from immune thrombocytopenia.Immunologic research · 2016Article
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Authors and funding
12 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune thrombocytopenia (ITP) is a heterogeneous autoimmune disease, which is characterized by dysregulation of T cell-mediated autoimmunity. NLRP3, a largest and mostly well-studied inflammasome, has been shown to be important in the regulation of adaptive immune response, especially in T cell response. Given the closely association of imbalance of T cell response with ITP, whether NLRP3 is involved in the pathogenesis of ITP remains poorly understood. In this study, 69 active ITP patients, 21 ITP in remission and 24 age- and gender-matched healthy controls were included. Peripheral blood mononuclear cells (PBMCs) were isolated from ITP and control for isolation of RNA and plasma, which were used to measure mRNA level of NLRP3 and adaptor protein ASC by quantitative real-time PCR and IL-18 plasma level by ELISA. Meanwhile, protein was also extracted from PBMCs for Western blot analysis of NLRP3 expression. Our results showed a significantly higher expression of NLRP3, ASC and plasma IL-18 level in patients with active ITP when compared to control. The expression of NLRP3, ASC and plasma IL-18 level was significantly lower in patients in remission than that in active ITP, and no difference was observed when compared to control. Furthermore, a significantly positive correlation of NLRP3 with ASC was observed in patients with active ITP. In conclusion, increased expression of NLRP3 was associated with the pathogenesis of ITP and therapeutically targeting it might be a new strategy in the treatment of ITP.
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