Immunity Enabled by Sibling Cells that Feast and Fast

Immunology Interest Group Seminar Series It has become increasingly clear that sustaining clonal regeneration of a lymphocyte during the immune response requires a B cell or a T cell to renew itself while also producing its differentiated cellular progeny (plasma cells or effector cells). I will present data showing that activated lymphocytes immediately competent to differentiate will divide to yield sibling cells with unequal metabolic behaviors. One cell undergoes terminal differentiation driven by an anabolic constellation of aerobic glycolysis, mitochondrial stasis, and ROS production. Conversely, its sibling cell undergoes self-renewal maintained by a catabolic constellation of autophagy, mitochondrial turnover, oxidative metabolism, and maintenance of parental transcription factor network. I will also present data tracing the fate of determined effector T cells and their immediate progenitors during infection. Asymmetric division and self-renewal by progenitors, but not effector cells, allows them to become quiescent and enter the memory cell pool after acute infection. In persistent, sub-clinical infections, self-renewal of progenitors sustains the regeneration of effector cells over decades. T cell regeneration, however, appears to be rate-limiting, but remediable, in chronic active infections and cancer. Immunity may become more easily manipulated by targeting the ways in which a progenitor cell tells its progeny, " you feast but I'll fast " .Air date: 11/9/2016 4:1...
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