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Type 2 innate lymphoid cells (ILC2 cells) provide early immune responses to helminthes and contribute to allergic inflammation. Singh and colleagues show that the transcription factor Gfi1 controls the development, activation and specification of ILC2 cells.
Discriminating between harmless and pathogenic bacteria is a key challenge faced by the immune system. Ivanov and Roy demonstrate that virulent bacteria disrupt mTOR signaling, which then skews responses towards inflammatory cytokine production.
The cytidine deaminase AID mediates immunoglobulin class-switch recombination. Chaudhuri and colleagues show that a phosphorylation-dependent positive feedback loop regulates AID activity and is initiated by DNA breaks.
Mature invariant natural killer T cells (iNKT cells) are an early innate source of cytokines. Hogquist and colleagues classify three lineages of iNKT cells by their distinct transcription factors and cytokine profiles.
The transcription factor HIF is induced in response to hypoxic stress, TCR activation and cytokines. Goldrath and colleagues show that HIF signaling enhances CTL effector responses and can render cells refractory to immune exhaustion.
S1P1 is a sphingosine phosphate receptor expressed on lymphocytes. Han and colleagues show that phosphorylated S1P1 accumulates in brain lesions of patients with multiple sclerosis. Similarly, mice bearing mutant S1P1 develop more severe experimental autoimmune encephalomyelitis.
How γδ TCRs bind antigen presented by antigen-presenting molecules remains unclear. Godfrey and colleagues describe a population of human γδ T cells that interacts with CD1d and provide a molecular basis for how a γδ TCR binds CD1d–α-GalCer.
Clonal expansion of cytotoxic T lymphocytes entails profound energetic demands. Kallies and colleagues show that the transcription factor IRF4 is critical for the metabolic reprogramming, survival and effector function of these cells during clonal expansion.
Effector responses of NK cells occur via cytoxicity and cytokine secretion. Malarkannan and colleagues identify a signaling module that selectively controls the cytokine production of NK cells.
The transcription factor Ikaros, which is essential for lymphocyte development, contains multiple zinc fingers. Smale and colleagues show that mice lacking different zinc fingers develop distinct lymphocyte-developmental defects and tumor susceptibility.
Chronic inflammation is a fundamental aspect of metabolic disorders such as atherosclerosis. Freigang and colleagues report that fatty acids are potent inducers of IL-1α, which drives vascular inflammation.
The immunoregulatory effect of IL-27 is thought to act mainly on T cells. Quintana and colleagues show that IL-27 also converts conventional DCs into immunosuppressive cells.
Diffuse large B cell lymphomas can arise from dysregulation of BCL6 expression. Dalla-Favera and colleagues show that the transcription factor MEF2B regulates BCL6 and is commonly associated with the generation of such lymphomas.
Although GATA-3 is expressed in hematopoietic stem cells, its function there remains unclear. Iscove and colleagues show that GATA-3 inhibits the self-renewal potential of long-term hematopoietic stem cells downstream of p38 signaling.
Effector memory CD8+ T cells are capable of rapid IFN-γ production. Hess and colleagues show that antigenic reactivation triggers enhanced glycolytic flux, which is required for early IFN-γ recall responses.
Inflammation induces changes in the extracellular matrix density and composition. Fowell and colleagues show that CD4+ effector T cells use integrin αV for interstitial migration on fibronectin in inflamed tissues.
IL-23 is needed to protect mucosal surfaces from bacterial pathogens. Murphy and colleagues identify a Notch-2-dependent CD11b+ dendritic cell population that produces IL-23 and is required for survival after infection with Citrobacter.
The adaptor Nck is known for linking TCR signaling to cytoskeleton regulation. Batista and colleagues show that in B cells, Nck recruits the adaptor BCAP to the BCR to activate the PI(3)K pathway.
Failure to clear apoptotic cells can lead to autoinflammatory disease. Means and colleagues demonstrate that the receptor SCARF1 recognizes C1q-bound apoptotic cells, which leads to their clearance and prevents lupus-like symptoms.
The E3 ubiquitin ligases that modify the kinase RIP2 downstream of the receptor Nod2 remain unclear. Moynagh and colleagues show that Pellino3 ubiquitinates RIP2 for Nod2-induced activation of the transcription factor NF-κB.