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Lymphocyte activation gene-3 (LAG-3) is an inhibitory receptor expressed by CD4 T cells and tempers their homeostatic expansion. Because CD4 T cell proliferation is tightly coupled to bioenergetics, we investigate the role of LAG-3 in modulating naive CD4 T cell metabolism. LAG-3 deficiency enhances the metabolic profile of naive CD4 T cells by elevating levels of mitochondrial biogenesis. In vivo, LAG-3 blockade partially restores expansion and the metabolic phenotype of wild-type CD4 T cells to levels of Lag3 CD4 T cells, solidifying that LAG-3 controls these processes. Lag3 CD4 T cells also demonstrate greater signal transducer and activator of transcription 5 (STAT5) activation, enabling resistance to interleukin-7 (IL-7) deprivation. These results implicate this pathway as a target of LAG-3-mediated inhibition. Additionally, enhancement of STAT5 activation, as a result of LAG-3 deficiency, contributes to greater activation potential in these cells. These results identify an additional mode of regulation elicited by LAG-3 in controlling CD4 T cell responses.
This article was published in the following journal.
Name: Cell reports
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Bioinformatics is the application of computer software and hardware to the management of biological data to create useful information. Computers are used to gather, store, analyze and integrate biological and genetic information which can then be applied...