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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.
Mucosal-associated invariant T cells are evolutionarily conserved T lymphocytes with undefined antigen specificity. These cells are now shown to have a unique role in host defense by targeting highly conserved microbial antigens.
Type I interferons are produced by almost all nucleated cells in response to virus infection. MafB is now shown to modulate the efficiency of interferon production by setting a threshold for IRF3-dependent transcription.
Notch1 has an indispensable role in T cell development and NOTCH1 acts as a potent oncogene in T cell leukemia. New data now reveal the role of RNA-binding proteins in regulating the stability of Notch1 mRNA and the induction of T cell leukemia.
Hematopoietic lineage schemes commonly show two distinct lymphoid and myeloid branches arising from the hematopoietic stem cell early during blood cell development. A new study of human hematopoiesis demonstrates that, similar to findings in mice, this split is not as dichotomous as is often presented.
Lineage specification and development require a hierarchy of transcription factors. A genome-wide view of transcription factor binding provides new insights into early B lineage development.
B cell–T cell interactions in germinal centers are needed to generate high-affinity antibodies. PD-1 signaling is now shown to influence the quality of germinal center responses.
Many pathogens induce a type I interferon response via a pathway dependent on the kinase TBK1 and transcription factor IRF3. However, LRRFIP1, a cytosolic sensor of DNA and RNA, triggers interferon production by a β-catenin-dependent signal.
