Research shows TGF-β1 influences Treg maintenance in ITP, suggesting other sources may contribute.
Mei et al. suggest platelet-derived-TGF-β1 is critical to ITP tolerance via Treg modulation, but their implausibly high TGF-β1 levels likely reflect ex vivo artifacts. We couldn't confirm platelet-derived TGF-β1-driven Treg deficiency using knock-out mice; remission maintenance likely involves extra-platelet TGF-β1 sources.
No takes yet. Share an insight, caveat, or question.
Jasimuddin Ahamed (2026) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: