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Synaptotagmins are calcium-dependent regulators of intracellular vesicle fusion. Luster and colleagues show that synaptotagmins SYT2, SYTL5 and SYT7 also regulate leukocyte chemotaxis by triggering uropod de-adhesion via the fusion of lysosomes with plasma membranes.
Expression of the transcription factor Foxp3 is a hallmark of regulatory T cells. Li and co-workers find that Foxo1 and Foxo3 control thymic and TGF-β-induced Foxp3 expression.
PD-1 is commonly associated with inhibitory functions, yet it is highly expressed in follicular T cells. Shlomchik and colleagues find that PD-1 signaling in germinal centers is necessary for long-lived humoral immunity.
Intracellular nucleic acid sensors trigger the production of type I interferon. Cao and colleagues identify LRRFIP1 as a cytosolic nucleic acid–binding protein that mediates the production of type I interferon via a β-catenin-dependent pathway.
Interleukin 9 secretion contributes to allergic inflammation. Kaplan and colleagues identify the transcription factor PU.1 as being necessary for TH9 differentiation and as a contributing factor in allergic airway inflammation.
Infection elicits cytokine production that can alter hematopoiesis. Potocnik and colleagues identify a unique IL-7Rα+c-Kithi progenitor subset that arises during acute malaria infection and gives rise to predominantly myeloid cells.
Thymic selection requires that thymocytes transit through distinct anatomical compartments. Weiss and colleagues report that the G protein regulator GIT2 integrates T cell antigen receptor and chemokine receptor signaling necessary for proper migratory activity and positive selection.
Medullary thymic epithelial cells are essential to the establishment of central tolerance by expressing peripheral tissue antigens. Klein and co-workers now show that these cells also mediate clonal deletion of CD4+ T cells.
Cytokine signaling is thought to be tightly localized in lymphoid tissues. Mohrs and co-workers show that interferon-γ and interleukin 4 signal to most lymphocytes throughout the reactive lymph node.
The mechanism by which influenza virus activates the NLRP3 inflammasome is unknown. Iwasaki and colleagues show that the influenza virus M2 protein, a proton-selective ion channel, stimulates the NLRP3 inflammasome pathway.
How double-positive thymocytes enter the invariant natural killer T cell lineage is still unclear. Alberola-Ila and co-workers show that c-Myb has a central role in this process.
MAZR is an important negative regulator of CD8 expression. Ellmeier and colleagues now demonstrate that MAZR directly regulates the transcription factor Th-POK locus and is therefore involved in CD4 and CD8 cell-fate 'decisions'.
HIV-1 replication requires proviral production of full-length transcripts. Geijtenbeek and colleagues show that early Tat-independent HIV-1 replication coopts innate receptor signaling by DC-SIGN and TLR8 to promote RNA polymerase II elongation complexes at long terminal repeats.
Most antigenic peptides presented by MHC class I are produced by the proteasome. Van den Eynde and co-workers show that a MAGE-A3–derived peptide is produced directly by the cytosolic metallopeptidase IDE.
The transcription factor XBP1 is activated after endoplasmic reticulum stress. Glimcher and colleagues show that XBP1 can also be activated by TLR2 and TLR4 signaling pathways, in which it sustains proinflammatory cytokine production.
The AIM2 inflammasome induces maturation of the proinflammatory cytokines IL-1β and IL-18. Using AIM2-deficient mice, Fitzgerald and colleagues and Alnemri and colleagues show that the AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses.
The AIM2 inflammasome induces maturation of the proinflammatory cytokines IL-1β and IL-18. Using AIM2-deficient mice, Fitzgerald and colleagues and Alnemri and colleagues show that the AIM2 inflammasome is essential for host defense against cytosolic bacteria and DNA viruses.
Vaccines elicit neutralizing antibodies to protect organisms against viral infection. Carroll and colleagues show that medullary lymph node dendritic cells capture influenza virus via SIGN-R1 and are necessary for humoral antiviral immunity.
How and where invariant natural killer T cells encounter glycolipids in vivo remains unclear. Batista and colleagues use multiphoton microscopy to show that CD169+ macrophages present lipid antigens to invariant natural killer T cells in lymph nodes.
Surveillance for blood-borne pathogens by immune cells occurs chiefly in the spleen and liver. Kubes and colleagues show that liver Kupffer cells directly sample the bloodstream and are the predominant antigen-presenting cell for invariant natural killer T cells