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Chronic stimulation of lymphocytes results in upregulation of immunomodulatory IL-10, but the molecular mechanisms of this process have remained unknown. Kubo and colleagues demonstrate that the transcription factor E4BP4 is responsible for this plasticity.
Developing B cells show enhanced sensitivity to negatively selecting signals. Weiss and colleagues show that calcium signals arising from activation of the calcium sensor STIM1 lead to activation of Erk and apoptosis via a protein kinase C-δ and the guanine nucleotide-exchange factor RasGRP1-dependent pathway in transitional self-reactive B cells.
MHC class II is typically involved in the presentation of peptide antigen to CD4+ T cells. Cao and colleagues identify a previously unknown intracellular function for MHC class II in promoting Toll-like receptor signaling.
The chemokine CXCL12 is essential for hematopoietic stem cell function. Lapidot and colleagues report that secretion of CXCL12 from bone marrow stromal cells is a cell contact–dependent event, mediated by connexin-43 and connexin-45 gap junctions.
The development and function of TCRαβ+CD8αα+ intraepithelial lymphocytes remain poorly understood. These cells are now shown to require transforming growth factor-β for development and proper expression of characteristic surface homodimers of CD8α.
Analysis of the serine-threonine phosphoproteome leads to the intriguing find that phosphorylation of the histone deacetylase HDAC7 is key to cytotoxic T lymphocyte function.
Regulatory T cells adopt specialized differentiation programs controlled by transcription factors. The transcription factors Blimp-1 and IRF4 are now shown to be pivotal in the maturation of effector regulatory T cells.
Helminth parasites are adept at dampening immunity. New data showing that intracellular degradative pathways are manipulated have important implications for therapy.
Chronic inflammatory diseases represent a major challenge for both clinical research and patient care, and evidence indicates that these disorders develop as a result of complex gene-environment interactions. Better understanding of their cause-and-effect relationship is the basis for emerging proposals for therapy and prevention.
B cells arise via a precise developmental pathway. Goodnow and Beutler report that mice bearing mutations in Atp11c, which encodes a phosphatidylserine 'flippase', have defective B cell generation in the adult bone marrow.
B cells arise via a precise developmental pathway. Goodnow and Beutler report that mice bearing mutations in Atp11c, which encodes a phosphatidylserine 'flippase', have defective B cell generation in the adult bone marrow.
The NF-κB subunit RPS3 can contribute to the selection of nuclear targets by NF-κB. Lenardo and colleagues show that the kinase IκBβ phosphorylates RPS3 to promote its nuclear translocation, a process targeted by enteropathogenic Escherichia coli.
TCR ligation triggers multiple signaling cascades. Cantrell and colleagues provide an unbiased phosphoproteomics analysis of CD8+ T cells showing that phosphorylation of the histone deacetylase HDAC7 is needed to maintain the identity of cytotoxic T lymphoctyes.
Regulatory T cells can adopt specialized differentiation programs in the periphery. Kallies and co-workers show that IRF4 and Blimp-1 control the acquisition of regulatory T cell effector functions, such as IL-10 production.
The kinase mTOR has emerged as an important regulator of helper T cell differentiation. Powell and co-workers show that the mTOR complex mTORC1 selectively regulates TH1 and TH17 differentiation, whereas mTORC2 signaling is required for TH2 differentiation.
Parasites use multifarious means to manipulate and avoid sterilizing immunity. Melendez and colleagues show that a nematode product triggers macrophage autophagocytosis to degrade the adaptor MyD88 and suppress inflammatory responses.