Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Lymphocyte development depends on appropriate expression of transcription activators and regulators, as illustrated by two reports in this issue. Wakabayashi et al. now report that Bcl11b-deficient mice had abnormal thymic development and Liu et al. find that Bcl11a mice have disrupted B and T cell maturation. Micrograph from Wakabayashi et al. and artwork by Lewis Long.
Although immunologists have found the dichotomous helper T cell subset model a useful construct, it is beginning to show its age. Some suggest that proponents of the TH1-TH2 dichotomy are overzealous in making the data conform to the scheme, like Procrustes who stretched or truncated his guests so that they would fit his guest bed.
Overexpression studies suggest that SOCS3 is a pleiotropic negative regulator of cytokines. The generation of Socs3−/− mice indicates that SOCS3 actually functions in a remarkably specific manner.
The ability of NKG2D to trigger costimulation in CD8+ T cells and cytotoxicity in NK cells is thought to arise from its differential association with the intracellular signaling molecules DAP10 and DAP12, respectively. This model has now been refined to include the ability of DAP10 to mediate cytotoxic signals.
The mechanisms that regulate self-renewal of hematopoietic stem cells have remained elusive. Recent papers in Nature point to an important role of the Wnt–β-catenin signaling pathway in promoting this process.
Lymphocyte development is a complex process that involves the coordinated action of many transcription factors. The puzzle of B cell and T cell development gains an additional clue with the discovery of two critical factors.