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. Author manuscript; available in PMC: 2019 Oct 18.
Published in final edited form as: Immunity. 2014 May 15;40(5):633–635. doi: 10.1016/j.immuni.2014.05.001

Figure 1. The Tumor Suppressor p53 Blocks Bystander T Cell Proliferation Triggered by IL-2.

Figure 1.

(upper left) In response to a pathogenic challenge, CD4+ T cells that are not specific for antigen are exposed to mitogenic cytokines such as IL-2. In normal animals, IL-2-dependent signals increase the abundance of p53 protein, blocking the proliferation of these “bystander” T cells.

(upper right) T cells that lack functional p53 proliferate when exposed to IL-2, even in the absence of TCR signaling, confirming the essential role of p53 in the enforcement of this checkpoint.

(bottom right) The specific recognition of antigen (pMHC) by the TCR increases the concentration of the mRNA encoding Mdm2, a ubiquitin ligase that targets p53 for proteasomal degradation. The ensuing degradation of p53 enables the expansion of antigen-specific T cell clones while ensuring that potentially self-reactive “bystander” cells do not participate in the immune response.