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Natural killer cells and cytotoxic T lymphocytes kill targeted cells by releasing granzymes and perforin. Lieberman and colleagues show that these lethal molecules first accumulate in endocytic vesicles, where perforin generates pores that leak granzymes into the cytosol.
Inositol phosphates are widely produced in animal and plant tissues. Luo and colleagues demonstrate that the inositol phosphate InsP7 modulates membrane translocation of the kinase Akt and downstream phosphatidylinositol-(3,4,5)-trisphosphate signaling in neutrophils.
Type I natural killer T cells are characterized by an invariant Vα14-Jα18 T cell antigen receptor α-chain. Godfrey and colleagues describe a population of CD1d-restricted natural killer T cells that express a previously unidentified canonical Vα10-Jα50 α-chain.
Ectopic bronchus-associated lymphoid tissue can form in lungs after pulmonary infection. Randall and colleagues show that aerosolized lipopolysaccharide induces the formation of this tissue in neonatal mice by a process dependent on interleukin 17.
The antiviral protein IFIT1 is upregulated substantially in the cytoplasm of virus-infected cells. Superti-Furga and colleagues show that IFIT1 is part of a virus-recognition pathway that sequesters specific viral RNA.
The environmental cues involved in regulating germinal center size are not fully understood. Cyster and colleagues show that the sphingosine 1-phosphate receptor S1P2 controls the survival and localization of B cells in germinal centers by antagonizing signaling by the kinase Akt and follicular chemoattractants.
In quiescent T cells, the signaling adaptor Lat aggregates into cell-surface clusters. Gaus and colleagues demonstrate that pre-existing clusters of Lat do not participate in signaling from the T cell antigen receptor, which relies instead on recruitment of Lat from subsynaptic vesicles.
The transcriptional control of T cell exhaustion remains unclear. Wherry and colleagues show that the transcription factor T-bet regulates CD8+ T cell exhaustion and inhibitory receptor expression.
Innate lymphoid cells are present in the gut and support T helper type 2 responses. Umetsu and colleagues now identify these cells in the lung where they contribute to T cell– and B cell–independent asthma.
Cognate recognition by T cells drives the formation of immune synapses. Huse and colleagues show that a sequential cascade of distinct protein kinase C isoforms is needed to reorient microtubule-organizing centers and to establish T cell polarity.
Tumor necrosis factor promotes potent inflammatory immune responses that can result in pathological tissue damage. Ivashkiv and colleagues show that it induces a regulatory feedback pathway that dampens inflammatory signaling via the kinase GSK3.
The transcription factor BATF is known to control switched antibody responses. Murphy and colleagues show that BATF functions at multiple hierarchical levels in follicular helper T cells and B cells to regulate these responses.
The contribution of basophils to allergic and helminth immunity remains unclear. Locksley and colleagues use reporter strains and two-photon microscopy to demonstrate that basophils do not mediate T helper type 2 priming in vivo.
The molecular mechanisms that underlie T cell quiescence are poorly understood. Hu and co-workers show that the transcription factor Foxp1 has an essential cell-intrinsic role in regulating the quiescence of naive T cells.
IL-2 is well known for its effects on the proliferation of T cells. Leonard and colleagues demonstrate a mechanism in which IL-2 is critical for supporting TH1 differentiation but blocks TH17 differentiation.
The development of experimental autoimmune encephalomyelitis has been attributed to cells of the TH1 or TH17 subset of helper T cells. Becher and Rostami and their colleagues show that IL-23-induced production of the cytokine GM-CSF underlies disease development and severity.
The development of experimental autoimmune encephalomyelitis has been attributed to cells of the TH1 or TH17 subset of helper T cells. Becher and Rostami and their colleagues show that IL-23-induced production of the cytokine GM-CSF underlies disease development and severity.
Obesity is characterized by chronic inflammation, but the triggers for this remain unclear. Ting and colleagues demonstrate that a high fat diet activates the inflammasome, resulting in IL-1β release and insulin resistance.
The molecular machinery that regulates the self-renewal of hematopoietic stem cells remains elusive. Flavell and co-workers show that the type E3 ubiquitin ligase Itch negatively regulates the development and function of these cells.
Chronic stimulation of lymphocytes results in upregulation of immunomodulatory IL-10, but the molecular mechanisms of this process have remained unknown. Kubo and colleagues demonstrate that the transcription factor E4BP4 is responsible for this plasticity.