Antiinflammatory effects of CD95 ligand (FasL)-induced apoptosis

Yakun Gao, John M. Herndon, Hui Zhang, Thomas S. Griffith, Thomas A. Ferguson

Research output: Contribution to journalArticlepeer-review

184 Scopus citations

Abstract

Apoptosis is critical to homeostasis of multicellular organisms. In immune privileged sites such as the eye, CD95 ligand (FasL)-induced apoptosis controls dangerous inflammatory reactions that can cause blindness. Recently, we demonstrated that apoptotic cell death of inflammatory cells was a prerequisite for the induction of immune deviation after antigen presentation in the eye. In this report, we examine the mechanism by which this takes place. Our results show that Fas-mediated apoptosis of lymphoid cells leads to rapid production of interleukin (IL)-10 in these cells. The apoptotic cells containing IL-10 are responsible for the activation of immune deviation through interaction with antigen-presenting cells (APC). In support of this, we found that apoptotic cells from IL-10(+/+) animals fed to APC in vitro promote Th2 cell differentiation, whereas apoptotic IL-10(-/-) cells, as well as nonapoptotic cells, favor Th1 induction. Thus, apoptotic cell death and tolerance are linked through the production of an antiinflammatory cytokine to prevent dangerous and unwanted immune responses that might compromise organ integrity.

Original languageEnglish (US)
Pages (from-to)887-896
Number of pages10
JournalJournal of Experimental Medicine
Volume188
Issue number5
DOIs
StatePublished - Sep 7 1998

Keywords

  • Apoptosis
  • FasL
  • Immune privilege
  • Inflammation
  • Interleukin-10

Fingerprint Dive into the research topics of 'Antiinflammatory effects of CD95 ligand (FasL)-induced apoptosis'. Together they form a unique fingerprint.

Cite this