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The cytidine deaminase AID is essential for the immunoglobulin-diversification processes. Chaudhuri and colleagues identify the splicing factor PTBP2, which promotes the binding of AID to switch-region DNA.
Ldb1 functions as a core component of various multiprotein transcription complexes. Love and co-workers show a continuous requirement for Ldb1 in the maintenance of both fetal and adult HSC.
Pathways dependent on the transcription factor NF-κB provide innate immunity against microbes. Karin and colleagues show that mice lacking the kinase IKKβ have IL-1-dependent neutrophilia. Loss of IL-1 signaling restores blood cellularity but severely compromises antimicrobial defense.
Against a backdrop of some of the most savage spending cuts in the developed world, the UK science budget has emerged relatively unscathed, but funding priorities may yet prove problematic.
NF-κB is a critical transcription factor that is regulated by several post-transcriptional modifications. The characterization of their roles would help in the design of new therapeutic targets in cancer and inflammation.
The molecular mechanisms that control Treg and TH17 development and the precise role of TGF-β in this process are complex and imperfectly understood. New findings indicate that the helix-loop-helix proteins E2A and Id3 are also critically involved in some of these processes.
TH2 cells control immune responses to helminth infection and contribute to the development of allergic asthma. A single intronic enhancer element in Il4 can regulate TH2 differentiation and susceptibility to allergic asthma via interaction with the transcription factor GATA-3.
The fields of immunology, microbiology, nutrition and metabolism are rapidly converging. Here we expand on a diet-microbiota model as the basis for the greater incidence of asthma and autoimmunity in developed countries.
Transcription factors specific for helper T cell lineages, such as T-bet, counter-regulate helper T cell development, but the details of this remain unclear. Glimcher and colleagues unravel the molecular basis of the regulation of TH17 cells by T-bet.
Immunoglobulin genes are further diversified by the cytidine deaminase AID. Gearhart and colleagues show immunoglobulin genes accumulate AID-dependent uracil residues within the first 24 hours of B cell stimulation.
Peptides presented to cytotoxic T lymphocytes are typically generated by proteasome action. Kessler and colleagues show that the cytosolic endopeptidases nardilysin and thimet oligopeptidase generate the C termini of tumor-relevant epitopes.
Autophagy is a physiological process that involves the engulfment and degradation of organelles. Choi and colleagues demonstrate that autophagy is important for the removal of damaged mitochondria and thus the control of inflammation.
TGF-β and Foxp3 are required for the development of regulatory T cells. Chen and colleagues show that the helix-loop-helix proteins E2A and Id3 enhance Foxp3 expression and relieve it from inhibition by other transcription factors.
HLA-DM activity ensures that only high-affinity peptides are displayed on MHC class II molecules. Wucherpfennig and colleagues show that interaction of HLA-DR with the N terminus of bound peptides determines susceptibility to HLA-DM.
The molecular basis of TH2 lineage commitment is poorly understood. Kubo and colleagues identify the Il4 enhancer HS2 as a target of the transcription factor GATA-3 and show it to be critical for IL-4 production and TH2 functional commitment.
Binding of the transcription factor NF-κB subunit RelA activates proinflammatory gene expression. Gozani and colleagues show that basal expression of RelA target genes is suppressed by methylation of RelA by SETD6, which triggers repressive histone methylation by GLP.