Table 2.

NKT cells in warm hepatic IRI.

Reference	Murine Models of IRI	Findings
[37]	30 min portal vein clamping, reperfusion times up to 50 h.	Reduction in liver injury (sALT) by 50% in NKT−/− mice. Serum IFN-γ reduced in NKT-/- mice.
[38]	72 min partial ischemia, reperfusion at 2, 24, and 48 h.	NKTc produce IFN-γ at 2 h. NK/NKTc depletion reduces sALT at 24 h. Adoptive transfer of NKTc from WT or A2AR KO restores IRI in RAG-1 mice.
[40]	90 min partial ischemia, reperfusion at 4 and 8 h.	NKTc (not NK) contribute to hepatic IRI by an anti-CD1d-dependent activationo of TCRs. NKTc depletion attenuated IRI.
[45]	60 min partial ischemia, 6 h reperfusion.	Selective activation of NKTc 1 h prior to ischemia reduced IRI. Protection is via an IL-13/A2AR-dependent mechanism.
Type II NKTc [56]	90 min partial ischemia. Reperfusion at 6 and 24 h.	Mice lacking Type I NKTc were protected from IRI. Type II NKTc activation reduced IFN-γ secretion by Type I NKTc and prevented IRI.

NKTc = natural killer T cell; IFN-γ = interferon gamma; sALT = serum alanine aminotransferase; TCR = T cell receptor; IRI = ischemia reperfusion injury; A2AR = adenosine 2A receptor.