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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.
Medullary thymic epithelial cells maintain tolerance by expressing peripheral self antigens. New data show that they also present these antigens, which leads to the deletion of conventional CD4+ T cells and the induction of regulatory T cells.
Chemoattractants direct the extravasation of leukocytes to the site of immune response. New data highlight the role of synaptotagmins and Rab proteins in leukocyte chemotaxis.
The 'choice' between the CD4+CD8− and CD4−CD8+ T cell lineage involves genomic specification via a set of transcription factors. A new study shows that the zinc-finger protein MAZR is another member of this transcription factor network.
Dendritic cells can internalize and degrade invading pathogens in phagosomes, yet some HIV-1 particles can evade this degradation process and productively infect dendritic cells. New data show that HIV-1 replication is triggered by signal-transduction events through Toll-like receptor 8 and DC-SIGN.
A critical aspect of innate immune function is the coordinated regulation of inflammatory gene expression. Now an unexpected discovery shows that certain signaling components of the unfolded protein response are required for optimal gene induction by Toll-like receptors.
Intracellular pathogens face a diverse array of innate immune receptors. New data show that a single receptor, AIM2, functions to detect bacterial or viral DNA in the cytosol, inducing a protective inflammasome response.
The mechanisms that enforce T cell quiescence are incompletely understood. Slfn2 has now been identified as another participant in this process, functioning as a critical regulator of T cell– and monocyte-mediated immunity.
The ability of natural killer cells to eliminate abnormal cells has been shown to be enhanced by triggering of certain inhibitory receptors during their maturation. New data show that sometimes the opposite can happen.
Neutrophils and other cells secrete the pentraxin PTX3, which promotes innate immunity by binding to pathogens and activating complement. PTX3 can also limit neutrophil recruitment by inhibiting rolling on P-selectin in inflamed venules.
The cross-priming of antigen-specific CD8+ T cells requires help. The mechanism by which natural killer T cells provide such help is now characterized.
Members of the transient receptor potential vanilloid ion-channel family are expressed in a wide variety of cells and function as sensors of mechanical stress. The second such family member, TVRP2, is now also linked to phagocytosis in macrophages.
Transient formation of reactive oxygen species (ROS) accompanies B cell signaling and activation. Now the voltage-gated proton channel HVCN1 has been linked to ROS formation and B cell activation.
