Table 1.

CD4+ T Lymphocytes and Warm Liver IRI.

Reference	Murine Models of IRI	Findings
[15]	30, 60 and 90 min partial ischemia. Reperfusion from 0–36 h.	Similar IRI in acute phase (3–6 h) btwn BALB/c and nu/nu mice. At 16–20 h enzymes/necrosis reduced in nu/nu (10-fold reduction in neutrophil accumulation). CD4+-depletion in BALB/c reduced IRI.
[16]	90 min partial ischemia. Reperfusion at 4 and 20 h.	IRI significantly reduced in T-cell deficiency, disruption of CD154 signaling, or CD154 blockade.
[17]	90 min partial ischemia. Reperfusion at 1, 4, and 8 h.	CD4+ lymphocytes were recruited to the liver within 1 h of reperfusion. CD4−/− had greater injury and less neutrophil accumulation.
[18]	90 min partial ischemia. Reperfusion at 30–140 min.	CD4 deficiency, CD40-CD40L and CD28-B7 disruption attenuates platelet adherence, reduces neutrophil transmigration, sinusoidal perfusion failure, and transaminase activities.
[19]	90 min partial ischemia. Reperfusion at 8 h.	CD4−/− and CD4 depletion protect from IRI. CD154 blockade protects from IRI. CD4 T cells function in IRI without de novo Ag-specific activation.
[20]	60 min partial ischemia. Reperfusion 0–24 h.	Anti-CD25 mAb protects from IRI via reducing CD4+ T cells (less expression of TNF-∝, IFN-γ, IL-2, and IL-6).

IFN-γ = interferon gamma; TNF-α = tumor necrosis factor-α; IL-2 = interleukin-2; IL-6 = interleukin-6; IRI = ischemia reperfusion injury.