Death by Consumption

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Science  09 Nov 2007:
Vol. 318, Issue 5852, pp. 888
DOI: 10.1126/science.318.5852.888b

Regulatory T (Treg) cells continue to command attention in the minds of immunologists, not least because the mechanisms by which they exert their suppressive effects remain obscure. Although one possibility is that Treg cells paralyze particular functions in effector T cells, Pandiyan et al. present evidence that they can starve their targets to death. When the two types of T cells were placed in culture together, the effector (also called the responder) CD4+ T cell population eventually underwent cell death in a manner reminiscent of that seen when T cells are deprived of cytokines. It emerged that the Treg cells were consuming the growth factor interleukin 2 (IL-2), and possibly other cytokines as well. This depletion appeared to operate only when the two types of cells were in close proximity, suggesting that the balance between the supply of secreted cytokines and the voraciousness of the Treg cells might be an important factor. Cell death by cytokine withdrawal was controlled by intracellular mediators, such as the pro-apoptotic protein Bim, and Bim-deficient responder T cells were able to resist suppression by Treg cells. Cytokine consumption by Treg cells was also found to block pathogenic T cells in a mouse colitis model, suggesting that this mechanism might be broadly involved in regulating pro-inflammatory T cells. — SJS

Nat. Immunol. 8, 1353 (2007).

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