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Correlations between diacylglycerol metabolism and T cell anergy have been reported, but a causative relationship has not been established. The Gajewski and Koretzky groups (pp 1166 & 1174, News & Views by Mueller, p 1132) now link altered diacylglycerol metabolism with the anergic state. The original immunofluorescence image (bottom, by K. Praveen, Y. Zha and T.F. Gajewski) shows defective recruitment of RasGRP1 (green) to the contact site between a T cell overexpressing diacylglycerol kinase-α and an antigen-presenting cell (blue). Artwork by Lewis Long.
Contacts between T cell receptors and peptide–major histocompatibility complex molecules require specific amino acid interactions. However, some amino acids have no direct involvement in contact but nevertheless are critical for specificity.
How individual hematopoietic stem cells contribute to blood cell formation throughout a lifetime has remained a subject of debate. A new analysis suggests there is substantial variation in hematopoietic stem cell fate and self-renewal activity.
A pathway has been defined linking cell cycle inhibitor p27Kip1 to the inhibition of cyclin-dependent kinase 2 and its phosphorylation of transcription factor Smad3 in the induction of in vivo tolerance.
Understanding of the signaling networks regulating T cell anergy remains incomplete. Two reports now demonstrate that alterations in diacylglycerol metabolism regulate the adoption of an anergic versus an activated T cell fate.
The identification of a functionally distinct thymus-dependent lineage of mouse natural killer cells demonstrates the diversity of the natural killer cell population.