To my thinking, control mechanisms always have the potential for a role for nutrition,somewhere nutrition will fit into the scheme. Adaptive immune responses depend on the activation and expansion of specific subsets of white blood cells such as T cells in response to antigens. Although it has long been known that such proliferative responses are linked to the uptake and de novo synthesis of cholesterol for membrane formation, whether cholesterol-efflux pathways can limit cell division has not been considered. Reporting in Cell, Bensinger et al: have produced evidence that cholesterol efflux inhibits the proliferation of resting T cells, T cells that have not yet encountered an antigen.
Intracellular cholesterol levels are tightly regulated by two complementary pathways that are mediated by the gene transcription factors SREBP and LXR. The SREBP-dependent pathway induces the expression of proteins that are required for cholesterol biosynthesis and uptake, such as HMG CoA reductase and the LDL receptor, thereby increasing cellular cholesterol levels. This pathway is regulated by feedback inhibition, but it cannot eliminate excess cholesterol once this lipid has accumulated. That task is in part accomplished by cholesterol-efflux pathways that are regulated by LXRα, and LXRβ, members of the nuclear-receptor superfamily Oxidized cholesterol derivatives (oxysterols) activate LXRs, which then control the transcription of genes that have diverse roles in cholesterol homeostasis and innate immunity.In many cell types LXRs promote a reduction in cellular cholesterol levels by inducing the expression of the ABCA1 and ABCG1 transporters, which mediate cholesterol efflux from the cell to extracellular acceptors.
Glass and Saijo 2008 Oxysterols hold T cells in check Nature vol 455 pp 40-41

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