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December 8, 2025BloodOpen Access

Joint injury induces a robust proinflammatory cytokine response in hemophilia A mice: Implications for immune-mediated arthropathy

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Authors

MRMeera Rao

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Overview

Joint injury triggers proinflammatory cytokine increases in hemophilia A mice, suggesting biomarkers for arthropathy.

Key Points

  • To define the systemic inflammatory cytokine profile triggered by joint injury in hemophilia A mice.
  • Collected plasma samples from FVIII-deficient mice 72 hours post joint injury and naïve controls.
  • Performed cytokine profiling using a 32-plex mouse cytokine array.
  • Conducted statistical analysis with unpaired t-tests and Mann-Whitney U-test.
  • Joint injury led to a robust proinflammatory cytokine response compared to controls.
  • Significant increases in IL-9, IL-17, and TNF-α, implicating vigorous T-cell immune activation.
  • Suppressed IL-13 indicates a shift from regulatory to inflammatory responses.

Cite This Study

Meera Rao (2025) studied this question.

synapsesocial.com/papers/69362f4e4fa91c937236d8dfhttps://doi.org/10.1182/blood-2025-6606
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1Neutrophil-dependent interferonopathy contributes to joint damage in hemophilia2026
  2. 2Impact of secondary FVIII prophylaxis on joint bleeding and arthropathy in a Hemophilia A mouse model lacking inhibitor response2025
  3. 3Mechanisms of blood-induced joint disease in hemophilia and potential novel targets for interventions2026
  4. 4Characterization of a mouse model to study mechanisms of hemophilia A pain2026
  5. 5Quantitative assessment of CD4/CD8 ratio and its impact among pediatric and adolescent patients with hemophilia A2025