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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.
Regulatory T cells come in many different forms depending on their mode of action or developmental origin. Data now show that interleukin 35, an immunomodulatory cytokine secreted by regulatory T cells, and interleukin 10 induce so-called 'iTR35 cells', which may have an important role in the phenomenon of infectious tolerance.
Human CD4+ T cells that produce interleukin 22 are an essential component of skin defense and repair. New evidence shows that these T cells recognize CD1a-lipid complexes on Langerhans cells.
Natural killer cells have emerged as key components of innate immunity with critical antimicrobial functions. New work showing that they can also be accessed by vaccination to deliver antigen-specific memory responses and protect against subsequent viral infections challenges the traditional distinctions made between innate and adaptive immunity.
Innate immune responses to pathogens are often triggered by nucleic acids, including DNA delivered to the cytoplasm of cells. IFI16 is a newly identified cytoplasmic DNA sensor that induces the transcription of genes involved in the innate response.
Neutrophils can function as chief effector cells in inflammation but can also regulate excessive inflammatory responses by secreting anti-inflammatory cytokines. The acute-phase reactant SAA-1 seems to be pivotal in the control of such plasticity.
Human immunodeficiency virus type 1 (HIV-1) seems to avoid detection by nucleic acid sensors. This is probably due to the host exonuclease TREX1, which degrades HIV DNA generated during HIV-1 infection.
Induction of the microRNA miR-182 by interleukin 2 in helper T lymphocytes targets the transcription factor Foxo1 and promotes clonal expansion. Targeting this process opens new possibilities for adjuvancy, immunosuppression and anti-inflammatory therapeutics.
IAPP, a hormone secreted together with insulin and deposited in pancreatic islets in type 2 diabetes, can induce macrophage processing of interleukin 1 linked to beta-cell destruction in type 2 diabetes.
The regulation of gene expression through changes in chromatin structure is increasingly recognized as a chief component of activation of cells of the immune response. It now seems that histone demethylation of the promoter of the gene encoding the transcription factor IRF4 contributes to alternative macrophage activation.
IL-1 signaling requires a heterotrimeric complex of IL-1 receptor, its homolog IL-1RAcP and ligand. The crystal structure of this complex has now been solved, with implications for signaling by many IL-1 family members.
The transcription factor TOX has been shown to influence adaptive T cell development. Further analysis of TOX-deficient mice now demonstrates previously unknown roles for TOX in innate immunity.
The mechanisms driving IL-10 production by human T helper type 1 effector cells are poorly defined. New data link the complement regulator protein CD46 to this process and suggest an important role in autoimmune arthritis.
Mucosal IgA regulates the composition of gut microbiota. IgT in bony fish is now shown to have—via convergent evolution—the same properties as IgA, demonstrating strong evolutionary pressure to preserve both systemic and mucosal immunity.
Although nickel allergy is very common, the specific receptor for nickel has not been identified. TLR4 is now shown to bind nickel and cause inflammation, an interaction that is specific to humans.
Immunohomeostasis prevents pathology resulting from immune activation. Two new studies link its regulation with the activation of the aryl hydrocarbon receptor, a known mediator of the toxic effects of xenobiotic ligands, in a subset of T lymphocytes.
Regulation of the inflammatory response is necessary for limiting tissue destruction and preventing autoimmunity. A recent discovery shows that CD11b activated by Toll-like receptors via inside-out signaling mediates degradation of the Toll-like receptor adaptors MyD88 and TRIF.
