Cytokine-Induced Myeloid-Derived Suppressor Cells Demonstrate Their Immunoregulatory Functions to Prolong the Survival of Diabetic Mice

Tung Teng Li, Chun Liang Lin, Meihua Chiang, Jie Teng He, Chien Hui Hung, Ching Chuan Hsieh*

*Corresponding author for this work

Research output: Contribution to journalJournal Article peer-review

2 Scopus citations

Abstract

Type 1 diabetes is an inflammatory state. Myeloid-derived suppressive cells (MDSCs) originate from immature myeloid cells and quickly expand to control host immunity during infection, inflammation, trauma, and cancer. This study presents an ex vivo procedure to develop MDSCs from bone marrow cells propagated from granulocyte–macrophage-colony-stimulating factor (GM-CSF), interleukin (IL)-6, and IL-1β cytokines expressing immature morphology and high immunosuppression of T-cell proliferation. The adoptive transfer of cytokine-induced MDSCs (cMDSCs) improved the hyperglycemic state and prolonged the diabetes-free survival of nonobese diabetic (NOD) mice with severe combined immune deficiency (SCID) induced by reactive splenic T cells harvested from NOD mice. In addition, the application of cMDSCs reduced fibronectin production in the renal glomeruli and improved renal function and proteinuria in diabetic mice. Moreover, cMDSCs use mitigated pancreatic insulitis to restore insulin production and reduce the levels of HbA1c. In conclusion, administering cMDSCs propagated from GM-CSF, IL-6, and IL-1β cytokines provides an alternative immunotherapy protocol for treating diabetic pancreatic insulitis and renal nephropathy.

Original languageEnglish
Article number1507
JournalCells
Volume12
Issue number11
DOIs
StatePublished - 29 05 2023

Bibliographical note

Publisher Copyright:
© 2023 by the authors.

Keywords

  • cytokine
  • diabetic nephropathy
  • immunotherapy
  • myeloid-derived suppressor cells
  • pancreatic insulitis
  • Myeloid-Derived Suppressor Cells
  • Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
  • Animals
  • Diabetes Mellitus, Experimental/therapy
  • Mice, Inbred NOD
  • Mice
  • Cytokines/pharmacology

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