Adipose-mesenchymal stromal cells suppress experimental Sjogren syndrome by IL-33-driven expansion of ST2+ regulatory T cells

Adipose-derived mesenchymal stromal cells (ADSCs) play important roles in the alleviation of inflammation and autoimmune diseases. Interleukin-33 (IL-33), a member of the IL-1 family, has been shown to regulate innate and adaptive immunity. However, it is still unknown whether ADSCs regulate immune responses via IL-33. We show here that ADSCs produced IL-33 in response to IL-1 beta stimulation, which depended on TAK1, ERK, and p38 pathways. ADSCs-derived IL-33 drove the proliferation of CD4(+)Foxp3(+)ST2(+) regulatory T cells (Tregs) and alleviated experimental autoimmune Sjogren syndrome in mice. Importantly, human ADSCs also produced IL-33 in response to IL-1 beta. Thus, we have revealed a previously unrecognized immunoregulatory function of ADSCs by IL-33 production in experimental autoimmunity, which may have clinical applications for human immunopathology.

Automated summary

Research has shown that ADSCs can produce IL-33 in response to stimulation, which alleviates autoimmune diseases by promoting the proliferation of regulatory T cells (Tregs). This previously unrecognized immunoregulatory function of ADSCs through IL-33 production may have potential clinical applications.