ReviewBlood vessels, thrombosis & hemostasis2026
Inflammatory cytokines, inflammasomes, and neutrophil extracellular traps in primary immune thrombocytopenia pathogenesis.
Review in Blood vessels, thrombosis & hemostasis, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- Autophagy, NET formation, and inflammation crosstalk in thrombotic autoimmune diseases.Frontiers in immunology · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary immune thrombocytopenia (ITP) is a disorder characterized by enhanced platelet clearance and impaired production due to immune dysregulation. Central to its pathogenesis are platelet autoantibodies, T-cell-mediated processes, and altered cytokine profiles, which exacerbate clearance and hinder production. These mechanisms mirror other immune-mediated diseases and contribute to symptoms such as fatigue and thromboembolism. Despite extensive research, the inflammatory role in ITP remains unclear, with variability across studies underscoring the need for further investigation to optimize therapies. This study aims to summarize the evidence on inflammatory cytokines, inflammasomes, and neutrophil extracellular traps (NET) in adult primary ITP. A systematic literature review was conducted using Embase and MEDLINE (search date 9 January 2024), covering publications from the past decade. Observational studies and clinical trials reporting inflammatory markers were included (79 studies). Most studies were case-control (69.7%) and conducted in China (77.2%). Activation of multiple immune and inflammatory pathways was observed. T helper 17 (Th17; n = 21) and T follicular helper cells (n = 4) demonstrated involvement, with Th17-derived interleukin-17 (IL-17) contributing prominently to the inflammatory milieu. NLRP3 inflammasome hyperactivity/increased expression (n = 6 studies) emerged as a significant pathway, and strongly associated markers (IL-18 [n = 4]) were elevated. Additionally, NET and neutrophil activation promoted inflammation and thrombosis (n = 2). In conclusion, immune dysregulation from Th17 cell pathways and NLRP3 inflammasome strongly contribute to inflammation in adults with primary ITP, with IL-18 and IL-17 linked to disease activity/progression. The findings suggest a need for novel therapies to target immune dysregulation and clarify their roles in ITP.
Identifiers
What Socratic holds
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 Socratic graph.