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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.
A diverse group of immunologists gathered recently at Asilomar, California, to discuss advances in the theory and practice of their field. The pristine setting and informal atmosphere have always made this a unique and memorable conference.
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.
A new study demonstrates that commitment to the CD8 lineage in the thymus requires sequential T cell antigen receptor (TCR) and interleukin 7 (IL-7) signaling. The TCR signal first induces IL-7 responsiveness, then recognition of IL-7 induces the nuclear factor Runx3, which specifies the CD8 lineage.
Hematopoietic stem cell self-renewal is tightly regulated. Regulation of the stability of c-Myc protein contributes to this control of hematopoietic stem cell quiescence and repopulation.
The signaling intermediates that activate inflammasomes are elusive. New data now show that reactive oxygen species causes TXNIP to associate with NLRP3 and activate the inflammasome.
