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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.
Developing B cells show enhanced sensitivity to negatively selecting signals. Weiss and colleagues show that calcium signals arising from activation of the calcium sensor STIM1 lead to activation of Erk and apoptosis via a protein kinase C-δ and the guanine nucleotide-exchange factor RasGRP1-dependent pathway in transitional self-reactive B cells.
MHC class II is typically involved in the presentation of peptide antigen to CD4+ T cells. Cao and colleagues identify a previously unknown intracellular function for MHC class II in promoting Toll-like receptor signaling.
The chemokine CXCL12 is essential for hematopoietic stem cell function. Lapidot and colleagues report that secretion of CXCL12 from bone marrow stromal cells is a cell contact–dependent event, mediated by connexin-43 and connexin-45 gap junctions.