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In addition to participating in the regulation of T cell proliferation, survival, and TCR

signaling,autophagy has recently been shown to control CD8+ T cell memory generation

[ 10, 84]. Mice bearing Atg7-deficient CD8+ T cells showed impaired memory formation

using influenza or murine cytomegalovirus models, as well as diminished recall responses to secondary influenza infection [84]. Similarly, in a granzyme-Cre Atg7fl/fl mouse model,

CD8+ T cells had cell-intrinsic defects in memory formation in response to lymphocytic

Figure 2. Roles of autophagy in T cells

Engagement of the TCR and CD28 signaling pathways is required for full activation of T cells, which can be further augmented by signaling through the IL-2r. Autophagy is

maintained at basal levels innaïve and resting T cells and the cargo of autophagosomes

largely consists of organelles, such as mitochondria (1), which is an important quality

control mechanism. TCR- and IL-2r-signaling induce autophagy. Upon activation the cargo nature switches to mostly cytosolic components, and activation-induced degradation of

specific proteins (p27, caspases, Bim or Bcl10) has been described to control proliferation, survival and activation. Important roles of Autophagy have been reported in the regulation of cell homeostasis (2); TCR signaling transduction (3); the breakdown of macromolecules to recycle cellular building blocks and generate signaling metabolites (4); and the regulation of T cell metabolism (5). In addition, macroautophagy has been shown to be necessary for

CD4+ T cell activation, cell survival, and proliferation (6), differentiation of specific CD4+ T helper sucdfts, (7), enforcing Treg lineage stability (8), and for generation of CD8+

memory T cells (9).