Shuang Jia

TL;DR: In adoptive transfer immunotherapy of newborn Foxp3-deficient mice, iTreg cells are an essential nonredundant regulatory subset that supplements nTreg cells in part by expanding TCR diversity within regulatory responses.

TL;DR: A patient with an autoinflammatory disease in which the main clinical features are pustular rash, marked osteopenia, lytic bone lesions, respiratory insufficiency, and thrombosis is described, which contains a 175-kb homozygous deletion at chromosome 2q13, which encompasses several interleukin-1 family members.

TL;DR: This study supports prior investigations of serum that reflect disease processes associated with progression to T1DM and indicates that identification of unique inflammatory mediators may improve disease prediction beyond current islet autoantibodies.

TL;DR: Data are revealed that expression of EPCR and PAR1 on hematopoietic cells is required in mice for an aPC variant that mediates full cell signaling activity but only minimal anticoagulant function (5A-aPC) to reduce the mortality of endotoxemia, and E PCR-independent antiinflammatory effects of aPC on innate immune cells are documented.

TL;DR: A dynamic IL-10–dependent functional reciprocity between regulatory T cell subsets that maintains mucosal tolerance is identified and promoted by the niche supporting stable iTregs, which promotes a large population of ex-iTregs with pathogenic potential during immunotherapy.