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.
Jasimuddin Ahamed (Mon,) studied this question.