Consistent with our previous studies indicating that endogenous memory CD4 + T cell proliferation within high-ischemic allografts is dependent on memory CD8 + T cell activation ( 17 ), CD4 + T cell proliferation within the highly ischemic IL-15Rα–deficient allografts was also compromised, though the decrease did not achieve significance.
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p40 homodimers bridge ischemic tissue inflammation and heterologous alloimmunity in mice via IL-15 transpresentation.
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