Tick saliva-induced programmed death-1 and PD-ligand 1 and its related host immunosuppression

Sci Rep. 2021 Jan 13;11(1):1063. doi: 10.1038/s41598-020-80251-y.

Abstract

The tick Rhipicephalus microplus is a harmful parasite of cattle that causes considerable economic losses to the cattle breeding industry. Although R. microplus saliva (Rm-saliva) contains several immunosuppressants, any association between Rm-saliva and the expression of immunoinhibitory molecules, such as programmed death (PD)-1 and PD-ligand 1 (PD-L1), has not been described. In this study, flow cytometric analyses revealed that Rm-saliva upregulated PD-1 expression in T cells and PD-L1 expression in CD14+ and CD11c+ cells in cattle. Additionally, Rm-saliva decreased CD69 expression in T cells and Th1 cytokine production from peripheral blood mononuclear cells. Furthermore, PD-L1 blockade increased IFN-γ production in the presence of Rm-saliva, suggesting that Rm-saliva suppresses Th1 responses via the PD-1/PD-L1 pathway. To reveal the upregulation mechanism of PD-1/PD-L1 by Rm-saliva, we analyzed the function of prostaglandin E2 (PGE2), which is known as an inducer of PD-L1 expression, in Rm-saliva. We found that Rm-saliva contained a high concentration of PGE2, and PGE2 treatment induced PD-L1 expression in CD14+ cells in vitro. Immunohistochemical analyses revealed that PGE2 and PD-L1 expression was upregulated in tick-attached skin in cattle. These data suggest that PGE2 in Rm-saliva has the potential to induce the expression of immunoinhibitory molecules in host immune cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • B7-H1 Antigen / metabolism*
  • Cattle / metabolism
  • Cattle / parasitology
  • Dinoprostone / metabolism
  • Flow Cytometry
  • Host-Parasite Interactions*
  • Immune Tolerance*
  • Metabolic Networks and Pathways
  • Programmed Cell Death 1 Receptor / metabolism*
  • Rhipicephalus / physiology*
  • Saliva / physiology*
  • Th1 Cells / physiology
  • Tick Bites / immunology
  • Tick Bites / metabolism
  • Tick Bites / veterinary*

Substances

  • B7-H1 Antigen
  • Programmed Cell Death 1 Receptor
  • Dinoprostone