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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.
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 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.
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.
Generation of B cell memory requires CD4+ T cell help and involves triggering of CD40 in target B cells. Several recent studies indicate that similar signals are involved in the generation of memory CD8+ T lymphocytes.
Experiments based on the requirement for immunoglobulin gene transcription provide new insights into the elusive role played by AID in immunoglobulin class switching and hypermutation.
Many infectious agents elicit a type I interferon response, but the molecular details that lead to IFN-α/β expression have remained obscure. New details are emerging about how specific TLRs signal IFN-α/β expression.
The transcription factor(s) controlling TReg cell development are not definitely known. The finding that these cells specifically express Foxp3 provides a better understanding of their development and function at the molecular level.
Peptide epitope generation for MHC class I presentation is normally dependent upon proteasome activity. Yet this pathway fails to generate critical HIV epitopes. Instead, the protease TPPII is required for this activity.
Terminal B cell differentiation requires a massive increase in the biosynthetic capacity to synthesize antibodies in response to infection. New data shows the ER stress response activates and commits B cells to this robust metabolic state.