Role of PD-L1 in licensing immunoregulatory function of dental pulp mesenchymal stem cells

Stem Cell Res Ther. 2021 Dec 4;12(1):598. doi: 10.1186/s13287-021-02664-4.

Abstract

Background: Dental pulp stem cells (DPSCs) are low immunogenic and hold immunomodulatory properties that, along with their well-established multi-potency, might enhance their potential application in autoimmune and inflammatory diseases. The present study focused on the ability of DPSCs to modulate the inflammatory microenvironment through PD1/PD-L1 pathway.

Methods: Inflammatory microenvironment was created in vitro by the activation of T cells isolated from healthy donors and rheumatoid arthritis (RA) patients with anti-CD3 and anti-CD28 antibodies. Direct and indirect co-cultures between DPSCs and PBMCs were carried out to evaluate the activation of immunomodulatory checkpoints in DPSCs and the inflammatory pattern in PBMCs.

Results: Our data suggest that the inflammatory stimuli trigger DPSCs immunoregulatory functions that can be exerted by both direct and indirect contact. As demonstrated by using a selective PD-L1 inhibitor, DPSCs were able to activate compensatory pathways targeting to orchestrate the inflammatory process by modulating pro-inflammatory cytokines in pre-activated T lymphocytes. The involvement of PD-L1 mechanism was also observed in autologous inflammatory status (pulpitis) and after direct exposure to pre-activated T cells from RA patients suggesting that immunomodulatory/anti-inflammatory properties are strictly related to their stemness status.

Conclusions: Our findings point out that the communication with the inflammatory microenvironment is essential in licensing their immunomodulatory properties.

Keywords: DPSCs; Immunomodulatory functions; Neural crest stem cells; PD1/PD-L1 pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • B7-H1 Antigen* / physiology
  • Cell Differentiation
  • Cell Proliferation
  • Cells, Cultured
  • Dental Pulp* / immunology
  • Humans
  • Immunomodulation*
  • Mesenchymal Stem Cells* / immunology

Substances

  • B7-H1 Antigen
  • CD274 protein, human