Inhibition of Sphingosine-1-phosphate receptors in ischemia reperfusion injured autoimmunity-prone mice

Jess Edison, Sharon Frattalone, Christopher Tracy, Geoffrey E. Woodard, Melissa Butts, C. M. Moratz*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

2 Scopus citations


B6.MRL/lpr mice, an autoimmune strain, have an accelerated injury time course, increased intensity of tissue damage, and increased CD4+ T cell infiltration in the mesenteric ischemia/reperfusion injury model. In this study, the mechanism by which CD4+ T cells were recruited into injured tissue was addressed. Fingolimod (FTY720) was utilized to assess the role of infiltrating CD4+ T cells. FTY720 treatment was more effective in attenuating injury in B6.MRL/lpr mice then in control mice. Reduced CD4+ cell infiltration and tissue injury correlated with decreased neutrophil infiltration and pro-inflammatory cytokine generation. Inhibiting downstream Sphingosine-1-phosphate (S1P) receptor signaling, specifically GαI mediated signaling, did not inhibit injury, suggesting differential utilization of the S1P receptors between control and MRL/lpr strains. Analysis of S1P receptor expression exposed a predominance of S1P2 in the B6.MRL/lpr strain. Reliance on alternate S1P receptors in the autoimmune strain will alter the progress of inflammation and tissue injury.

Original languageEnglish
Pages (from-to)63-70
Number of pages8
JournalCellular Immunology
StatePublished - 1 Jan 2017


  • Autoimmunity
  • Inflammation: tissue injury T cells
  • Sphingosine-1-phosphate


Dive into the research topics of 'Inhibition of Sphingosine-1-phosphate receptors in ischemia reperfusion injured autoimmunity-prone mice'. Together they form a unique fingerprint.

Cite this