IMMUNOLOGY: Sharing with the Needy

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Science  27 Aug 2004:
Vol. 305, Issue 5688, pp. 1214d-1215d
DOI: 10.1126/science.305.5688.1214d

When not responding to pathogens, naïve T cells survive with the aid of a variety of homeostatic influences. Dominant among these is the signal provided by the cytokine interleukin-7 (IL-7), which maintains the activity of anti-apoptotic (anti-death) pathways. However, the limiting amounts of IL-7 that are available relative to the large number of T cells suggests that a mechanism must exist that enables cells to compete successfully for this resource without risking the loss of antigenic diversity as represented by the whole T cell population.

Park et al.observed that expression of the IL-7 receptor (IL-7R) was reduced on T cells that had already received an IL-7 signal. This was traced to a decrease in transcription of the gene encoding the α chain of the IL-7R and was ascribed to activation of the transcriptional repressor GFI1. In transgenic mice with forced constitutive expression of the IL-7R α chain the T cell pool was reduced, rather than expanded, indicating that prolonged IL-7R expression in these animals had conferred an overall survival disadvantage. Thus, the survival benefit of IL-7 is spread across the pool of naïve T cells by reducing demand from those T cells that have already received their allotment: an efficient means by which cells share a scarce resource. — SJS

Immunity 21, 289 (2004).

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