@entity20630 Regulates the Ratio of XXXX to Eomesodermin in @entity405 + T Cells Responding to Persistent @entity57265 Infection.

@entity15636 @entity5 @entity20630 @entity10071 @entity281 @entity1800 @entity57265 @entity405
UNASSIGNED: @entity405 + T cell exhaustion commonly occurs in @entity5 . During T cell exhaustion there is a progressive and hierarchical loss of effector cytokine production, up-regulation of inhibitory co-stimulatory molecules, and eventual deletion of antigen specific cells by apoptosis. A key factor that regulates T cell exhaustion is persistent TCR stimulation. Loss of this interaction results in restoration of @entity405 + T cell effector functions in previously exhausted @entity405 + T cells. TCR stimulation is also important for the differentiation of Eomeshi anti-viral @entity405 + effector T cells from T-bethi precursors, both of which are required for optimal viral control. However, the molecular mechanisms regulating the differentiation of these two cell subsets and the relative ratios required for viral clearance have not been described. We show that TCR signal strength regulates the relative expression of @entity10071 and @entity15636 in antigen-specific @entity405 + T cells by modulating levels of @entity20630 . Reduced @entity20630 expression results in skewing of this ratio in the favor of @entity15636 , leading to lower proportions and numbers of @entity10071 + @entity15636 - precursors and poor control of @entity57265 -clone 13 @entity281 . Manipulation of this ratio in the favor of @entity10071 restores the differentiation of @entity10071 + @entity15636 - precursors and the protective balance of @entity10071 to @entity15636 required for efficient viral control. These data highlight a critical role for @entity20630 in regulating protective anti-viral @entity405 + T cell responses by ensuring a balanced ratio of @entity10071 to @entity15636 , leading to the ultimate control of this chronic @entity1800 .
