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Adoptive transfer of IFN-γ-induced M-MDSCs promotes immune tolerance to allografts through iNOS pathway. | LitMetric

Adoptive transfer of IFN-γ-induced M-MDSCs promotes immune tolerance to allografts through iNOS pathway.

Inflamm Res

Transplantation Biology Research Division, State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, University of Chinese Academy of Sciences, Beichen West Road 1-5, Chaoyang District, Beijing, 100101, China.

Published: July 2019

AI Article Synopsis

  • Efficient production of monocytic myeloid-derived suppressor cells (M-MDSCs) is important for therapies targeting transplant rejection and autoimmune diseases.
  • Researchers used M-CSF and IFN-γ to develop these cells in vitro, confirming their phenotypes and immunosuppressive functions through various methods, including animal models.
  • The study found that IFN-γ treatment enhances the immunosuppressive ability of M-MDSCs and that these cells effectively prolong graft survival and support immune tolerance in mice, presenting a potential strategy for preventing graft rejection.

Article Abstract

Aim And Objective: Efficient production of monocytic myeloid-derived suppressor cells (M-MDSCs) with stable immunosuppressive function is crucial for immunomodulatory cell therapy for many diseases such as transplant rejection, graft-versus-host disease and autoimmune diseases.

Methods: We used M-CSF as growth factor for myeloid progenitor cell differentiation and activated them with IFN-γ during early stage in vitro to produce M-MDSCs. The cell phenotypes were determined using flow cytometry, the immunosuppressive function and mechanisms were determined by skin grafted mouse models and genetic modified mice.

Results: IFN-γ treatment endows these cell strong immunosuppressive function by inhibition of T cell proliferation and cytokine productions. The phenotype of these cells also changed towards M-MDSCs. IFN-γ significantly upregulated iNOS expression in these M-MDSCs and inhibition of this molecule significantly reversed their immune regulatory function. The functional stability of induced M-MDSCs by IFN-γ was tested in vivo by transferring them to alloskin-grafted mice. Adoptive transfer of these cells significantly prolonged allograft survival and promoted immune tolerance, whereas iNOS deficiency in these cells reversed this effect.

Conclusions: We established one M-MDSCs-inducting protocol with the combination of M-CSF and IFN-γ in vitro. M-CSF+IFN-γ-induced M-MDSCs are promising to prevent graft rejection by immune regulation.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s00011-019-01237-9DOI Listing

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