Expression of B7-H1 and B7-DC on the airway epithelium is enhanced by double-stranded RNA

Biochem Biophys Res Commun. 2005 Apr 29;330(1):263-70. doi: 10.1016/j.bbrc.2005.02.161.

Abstract

Viral infection in the airway provokes various immune responses, including Th1 and Th2 responses, which are partly initiated by double-stranded RNA (dsRNA), a viral product for its replication. B7-H1 (PD-L1) and B7-DC (PD-L2) are B7-family molecules that bind to programmed death-1 (PD-1) on lymphocytes and are implicated in peripheral tolerance. We investigated the effect of dsRNA on the expression of B7-H1 and B7-DC on airway epithelial cell lines. B7-H1 and B7-DC were constitutively expressed on the cells, and their expression was profoundly upregulated by stimulation with an analog of viral dsRNA, polyinosinic-polycytidylic acid. B7-H1 and B7-DC were also upregulated by stimulation with IFN-gamma, IL-13, and the supernatant from T cell clones. A relatively high concentration of dexamethasone (1 microM) was required to suppress the upregulation of B7-H1 or B7-DC. These results suggest that epithelial B7-H1 and B7-DC play a role in virus-associated immune responses in the airways.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Antigens, CD
  • B7-1 Antigen / metabolism*
  • B7-H1 Antigen
  • Bronchi / cytology
  • Bronchi / metabolism*
  • Cell Line, Transformed
  • Clone Cells
  • Humans
  • Interferon-beta / metabolism
  • Interferon-gamma / metabolism
  • Interleukin-13 / metabolism
  • Membrane Glycoproteins / metabolism*
  • Peptides / metabolism*
  • Programmed Cell Death 1 Ligand 2 Protein
  • RNA, Double-Stranded / physiology*

Substances

  • Antigens, CD
  • B7-1 Antigen
  • B7-H1 Antigen
  • CD274 protein, human
  • Interleukin-13
  • Membrane Glycoproteins
  • PDCD1LG2 protein, human
  • Peptides
  • Programmed Cell Death 1 Ligand 2 Protein
  • RNA, Double-Stranded
  • Interferon-beta
  • Interferon-gamma