4.3 Article

IL-17 down-regulates the immunosuppressive capacity of olfactory ecto-mesenchymal stem cells in murine collagen-induced arthritis

Journal

ONCOTARGET
Volume 7, Issue 28, Pages 42953-42962

Publisher

IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.10261

Keywords

olfactory ecto-mesenchymal stem cells; IL-17; suppressive capacity; Treg; collagen-induced arthritis; Immunology and Microbiology Section; Immune response; Immunity

Funding

  1. National Natural Science Foundation of China [31470881, 31100648]
  2. Specialized Research Fund for the Doctoral Program of Higher Education [20133227110008]
  3. Jiangsu Province 333 Project [BRA2015197]
  4. Specialized Project for Clinical Medicine of Jiangsu Province [BL2014065]
  5. Natural Science Foundation of Jiangsu [BK20150533]
  6. China Postdoctoral Science Foundation [2016M590423]
  7. Health Department Foundation of Jiangsu Province [Z201312]
  8. Science and Technology Support Program (Social Development) of Zhenjiang [SH2014039]
  9. Summit of the Six Top Talents Program of Jiangsu Province [2015-WSN-116]
  10. Jiangsu University Science Foundation [15JDG070, 11JDG093, FCJJ2015022]
  11. Priority Academic Program Development of Jiangsu Higher Education Institutions

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Olfactory ecto-mesenchymal stem cells (OE-MSCs) are a population of cells which has been recognized as a new resident stem cell type in the olfactory lamina propria. OE-MSCs have been shown to exert their immunosuppressive capacity by modulating T cell responses, including up-regulation of regulatory T cells (Tregs) and down-regulation of Th1/Th17 cells. As an inflammatory cytokine, IL-17 plays a critical role in orchestrating the inflammatory response during the development of collagen-induced arthritis (CIA). However, it is unclear whether the increased level of IL-17 may affect the immunosuppressive function of OE-MSCs under inflammatory condition. In this study, we found that IL-17 could significantly reduce the suppressive capacity of OE-MSCs on CD4+ T cells and down-regulate the suppressive factors produced by OE-MSCs. Notably, IL-17 treatment abolished the capacity of OE-MSCs in inducing Treg expansion. In addition, knockdown of IL-17R in OE-MSCs significantly enhanced their therapeutic effect in ameliorating CIA upon adoptive transfer. Moreover, IL-17R knockdown-OE-MSCs could efficiently induce Tregs expansion and reduce Th1 and Th17 responses. Taken together, all these data suggest that IL-17R knockdown in OE-MSCs may provide a novel strategy in maintaining their immunosuppressive properties for the treatment of autoimmune diseases.

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