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Inhibition of cholesterol esterification in T cells by genetic ablation or pharmacological inhibition of ACAT1 (a key cholesterol esterase) can lead to potentiated effector function and enhanced proliferation of CD8(+) T cells by increasing plasma membrane cholesterol levels, which causes enhanced T-cell receptor clustering and signaling as well as more efficient formation of the immunological synapse, thereby controlling the growth and metastasis of mouse melanoma (284)

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(2002) Oxidant stress mechanism of homocysteine potentiating Con A-induced proliferation in murine splenic T lymphocytes

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