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T cell survival in the face of the immunosuppressive drug rapamycin depends on the expression of prosurvival proteins Pim-1 and Pim-2, according to a report by Fox et al. Pim-1 and Pim-2 transmit signals that compensate for those that are wiped out by rapamycin; without the Pim proteins, rapamycin is deadly.

Rapamycin, a drug used to prevent rejection of transplants in humans, blocks the activation of a protein kinase called TOR (target of rapamycin), a component of a T cell signaling pathway that is important for cell survival and activation. Rapamycin works in transplant patients, but treatment of T cells with this drug in vitro or elimination of a signaling protein upstream of TOR in mice has little effect on T cell activation or survival. This paradox, says senior author Craig Thompson, is ¡°rapamycin's dirty little secret.¡± The new work establishes the mechanism behind half of this secret.Thompson's group now shows that rapamycin's lack of effect in vitro and in mice is due to the expression of protein kinases Pim-1 and Pim-2, which are activated by growth-promoting cytokines and TCR ligation. T cells lacking both Pim proteins and treated with rapamycin failed in two respects: they did not turn on activation signals in response to TCR ligation and they were unable to respond to cytokine-driven survival signals. Wild-type cells, however, activated the TCR pathway and survived as well as untreated cells. Thus, the Pim proteins provide the only alternative signaling pathway that can bypass the defect inflicted by rapamycin.

The debilitating consequences of lacking Pim-1 and Pim-2 are in part due to an inability to phosphorylate and thus inactivate the proapoptotic protein Bad. Without the Pim proteins, Bad runs rampant. Whether activated Bad is the sole cause of the effects seen in the absence of Pim-1 and Pim-2 is not yet known, but future studies using Bad-deficient mice will reveal if other mechanisms are also at play. Why rapamycin works in patients who have no known defects in the Pim proteins remains a mystery

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Molecular Mechanisms of Dietary Restriction

DR reduces TOR signaling, and (like DR) reduced TOR signaling is sufficient to increase life span in yeast, worms, and flies.

Like many other labs studying DR, we are interested in the potential utility of "dietary restriction mimetics". Dietary restriction mimetics are (as yet hypothetical) compounds that mimic the physiological response to dietary restriction (including slowing aging) without requiring reduced consumption of food. Resveratrol, a compound found in red wine, has recieved much attention as a potential dietary restriction mimetic (Figure 1). However, it remains to be determined whether resveratrol indeed recapitulates the health and longevity benefits associated with DR. Given our interest in TOR signaling, we are excited about the potential of compounds that target this pathway as potential DR mimetics. One such compound is the TOR inhibitor rapamycin (Figure 1). We have previously shown that rapamycin treatment can increase life span in yeast, and other groups are testing rapamycin as a potential anti-cancer compound in humans (anti-cancer effects are one hallmark of DR). Rapamycin is also currenty being tested for its effects on life span in mice as part of the NIA Interventions Testing Program.


 


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