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CD1a-autoreactive T cells are common in human skin, but their natural antigens have remained unknown. De Jong and colleagues show that apolar oils that naturally accumulate in epidermis and sebum nest within CD1a and are activatory.
Dendritic cell (DC) subsets show functional specialization. Singh and colleagues demonstrate that the transcription factor IRF4 enhances antigen presentation by MHC class II in CD11b+ DCs to promote the priming of CD4+ effector T cells.
IL-17 production by neutrophils has been reported in human psoriasis. Pearlman and colleagues identify a population of neutrophils that constitutively express the transcription factor RORγt and can produce and respond to IL-17A.
Pulendran and colleagues use a systems biology analysis to reveal distinct transcriptional signatures of antibody responses to different classes of human vaccines.
The kinase Csk inhibits basal TCR signaling. Weiss and colleagues reveal a requirement for CD28 costimulation upon Csk inhibition for facilitation of actin remodeling and activation of signaling pathways downstream of the phospholipase PLC-γ1.
The identity of the thymus-seeding progenitor cells has been a matter of debate. Cumano and colleagues report that early and late embryonic progenitor cells differ in their T cell–B cell lineage potential and capacity for population expansion and differentiation.
High-density lipoprotein (HDL) has beneficial effects in coronary artery disease. Latz and colleagues show that HDL's benefits stem at least in part by activating an anti-inflammatory program dependent on the transcription factor ATF3.
Dendritic cells (DCs) that orchestrate mucosal immunity have been studied in mice. Lahl and colleagues characterize human gut DC populations and define their relationship to previously described human and mouse DCs.
Plasmacytoid dendritic cells produce copious amounts of type I interferon in response to viral infection. Brown and colleagues show that the homeostasis and function of these cells are regulated by the microRNA miR-126.
Weninger and colleagues show that perivascular macrophages are critical for neutrophil migration into skin infected with Staphylococcus aureus and that the pathogen uses hemolysin-dependent killing of these cells as an immune evasion strategy.
RIG-I–like receptors are important inducers of innate immunity. Reinecker and colleagues find that activation of the microtubule-associated guanine nucleotide exchange factor GEF-H1 is essential for sensing of foreign RNA by these receptors.
T cell hyporesponsiveness is generally framed in terms of tolerance induction. Hayday and colleagues show that attenuating TCR responsiveness is also critical for the development of innate-like T cells that mediate the surveillance of dysregulated tissues.
Polymorphisms near genes encoding members of the IFN-λ family are associated with susceptibility or resistance to hepatitis C virus. Savan and colleagues show that differences in the stability of transcripts of those genes underlie the mechanism of resistance to that virus.
Paired immunoglobulin-like receptors (PIRs) recognize β2-microglobulin. Munitz and colleagues show that PIR-A and PIR-B have opposing roles in eosinophil development in response to interleukin 5 in the bone marrow.
The adaptor ASC is required for caspase-1 activation via the NLRP3 and AIM2 inflammasomes. Mitsuyama and colleagues show that signaling dependent on the kinases Syk and Jnk controls ASC speck formation through ASC phosphorylation.
Induction of type I interferon is a central event of antiviral immune responses. Fikrig and colleagues show that the transcription factor ELF4 is recruited by STING and translocates to the nucleus to control transcription of type I interferon genes.
Hematopoietic deficiency in the Notch target Hes1 results in severe defects in the T cell lineage. Bhandoola and colleagues show that Hes1 constrains myeloid gene-expression programs in T cell progenitors.
Lymphocyte function is regulated by phosphatidylinositol-dependent pathways. Uzel and colleagues identify a cohort of immunodeficient patients with hyperactive phosphatidylinositol-3-OH kinase activity due to mutant p110δ subunits, which results in enhanced senescence of cells of the immune system.
Jameson and colleagues show that the establishment of resident memory CD8+ T cells in nonlymphoid tissues requires transcriptional downregulation of the trafficking molecule S1P1, mediated by induced loss of the transcription factor KLF2.
Long-lived tissue-resident memory T cells (TRM cells) confer fast, robust protection after pathogen rechallenge. Gebhardt and colleagues show that skin TRM cells arise from KLRG1– cells that differentiate in situ in response to IL-15 and TGF-β.