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Prosurvival cytokines prevent activation and mitochondrial localization of the apoptosis-inducing factor Bax. Malter and colleagues (p 257) find that the peptidyl-prolyl isomerase Pin1 is integral to this process. The original confocal image shows activated Bax (green) partially colocalized (yellow) with mitochondria (red). Original image by Z.-J. Shen. Artwork by Lewis Long.
Is it possible to return from the industrial sector back to academia? Although academic scientists have traditionally perceived this to be akin to winning the Nobel prize, the personal experience of Ross Kedl suggests that the reality is something quite different altogether.
Although the development of natural killer T cells is a T cell antigen receptor–dependent process, the signaling pathways involved are poorly defined. New data demonstrate that the calcineurin–transcription factor NFAT pathway exerts a critical influence on this process by controlling the transcription factor Egr2.
The intrinsic stability of mRNA is important in the regulation of gene expression. New data show that the intrinsic stability of tumor necrosis factor–induced mRNA transcripts strongly influences the coordinated expression of genes that promote distinct phases of the inflammatory response.
Factors influencing progenitor cell 'choice' between lymphoid and myeloid lineage fates are incompletely understood. New work implicates the transcription factor Mef2c as one component needed to promote lymphoid and suppress myeloid lineage differentiation.
Interleukin 23 is tightly associated with TH-17 cell–mediated inflammation and autoimmunity. A new study of mice deficient in its receptor shows that interleukin 23 is required for the terminal differentiation of TH-17 cells in vivo.
In worms, antimicrobial peptides contribute to the defense against pathogen infection. Ewbank and colleagues describe a noncanonical signaling pathway required for the induction of one particular family of antimicrobial peptides.
The mechanism by which cytokines suppress Bax activation and eosinophil apoptosis are not well understood. Malter and colleagues pinpoint a function for the peptidyl-prolyl isomerase Pin1 in mediating cytokine-induced suppression of Bax activation.
The identity of the cytoplasmic DNA receptor that activates the inflammasome has remained elusive. Superti-Furga and colleagues use a proteomics screen to identity AIM2 as the DNA sensor for the inflammasome.
CD40 signals induce the production of interleukin 12 and interleukin 10 in uninfected and Leishmania major–infected macrophages, respectively. Saha and colleagues suggest that L. major–induced cholesterol depletion facilitates the assembly of distinct CD40 signalosomes.
Genes induced by inflammatory stimuli are expressed in a precise temporal order. Baltimore and colleagues show that mRNA stability exerts strong influence over the kinetics of the induction of genes encoding inflammatory molecules.
Myeloid and lymphoid cells are derived from the same multipotent progenitor cell. Camargo and colleagues show that the transcription factor Mef2c restricts myeloid differentiation to favor production of B, T and natural killer cells.
The biological function of the SLAM family receptor CRACC is not known. Using a CRACC-deficient mouse, Veillette and colleagues show that CRACC can activate or inhibit natural killer cells, depending on the availability of the adaptor EAT-2.
The signals that regulate the development of natural killer T cells are not completely understood. Glimcher and colleagues document an essential function for the transcription factor Egr2 in the maturation of these cells.
Whether interleukin 23 (IL-23) affects the differentiation of or simply the maintenance of IL-17–producing helper T cells (TH-17 cells) is unclear. Cua and colleagues show that IL-23 is required for the full differentiation and proliferation of effector TH-17 cells in vivo.