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Nature Immunology

Joseph Chavarria-Smith, Wouter L W Hazenbos, Menno van Lookeren Campagne
No abstract text is available yet for this article.
September 19, 2018: Nature Immunology
Di Huang, Jianing Chen, Linbin Yang, Qian Ouyang, Jiaqian Li, Liyan Lao, Jinghua Zhao, Jiang Liu, Yiwen Lu, Yue Xing, Fei Chen, Fengxi Su, Herui Yao, Qiang Liu, Shicheng Su, Erwei Song
Activation-induced cell death (AICD) of T lymphocytes can be exploited by cancers to escape immunological destruction. We demonstrated that tumor-specific cytotoxic T lymphocytes (CTLs) and type 1 helper T (TH 1) cells, rather than type 2 helper T cells and regulatory T cells, were sensitive to AICD in breast and lung cancer microenvironments. NKILA, an NF-κB-interacting long noncoding RNA (lncRNA), regulates T cell sensitivity to AICD by inhibiting NF-κB activity. Mechanistically, calcium influx in stimulated T cells via T cell-receptor signaling activates calmodulin, thereby removing deacetylase from the NKILA promoter and enhancing STAT1-mediated transcription...
September 17, 2018: Nature Immunology
Jing-Ping Hsin, Yuheng Lu, Gabriel B Loeb, Christina S Leslie, Alexander Y Rudensky
Numerous microRNAs and their target mRNAs are coexpressed across diverse cell types. However, it is unknown whether they are regulated in a manner independent of or dependent on cellular context. Here, we explored transcriptome-wide targeting and gene regulation by miR-155, whose activation-induced expression plays important roles in innate and adaptive immunity. Through mapping of miR-155 targets through differential iCLIP, mRNA quantification with RNA-seq, and 3' untranslated region (UTR)-usage analysis with poly(A)-seq in macrophages, dendritic cells, and T and B lymphocytes either sufficient or deficient in activated miR-155, we identified numerous targets differentially bound by miR-155...
September 17, 2018: Nature Immunology
Pengda Chen, Kunyu Liao, Changchun Xiao
No abstract text is available yet for this article.
September 17, 2018: Nature Immunology
Vedrana Jelenčić, Marko Šestan, Inga Kavazović, Maja Lenartić, Sonja Marinović, Tim D Holmes, Michaela Prchal-Murphy, Berislav Lisnić, Veronika Sexl, Yenan T Bryceson, Felix M Wensveen, Bojan Polić
The activation of natural killer (NK) cells depends on a change in the balance of signals from inhibitory and activating receptors. The activation threshold values of NK cells are thought to be set by engagement of inhibitory receptors during development. Here, we found that the activating receptor NKG2D specifically set the activation threshold for the activating receptor NCR1 through a process that required the adaptor DAP12. As a result, NKGD2-deficient (Klrk1-/- ) mice controlled tumors and cytomegalovirus infection better than wild-type controls through the NCR1-induced production of the cytokine IFN-γ...
September 17, 2018: Nature Immunology
André Veillette, Yan Lu
No abstract text is available yet for this article.
September 17, 2018: Nature Immunology
Ryota Sato, Akihisa Kato, Takahiko Chimura, Shin-Ichiroh Saitoh, Takuma Shibata, Yusuke Murakami, Ryutaro Fukui, Kaiwen Liu, Yun Zhang, Jun Arii, Ge-Hong Sun-Wada, Yoh Wada, Tsuneo Ikenoue, Glen N Barber, Toshiya Manabe, Yasushi Kawaguchi, Kensuke Miyake
TLR3 is a sensor of double-stranded RNA that is indispensable for defense against infection with herpes simplex virus type 1 (HSV-1) in the brain. We found here that TLR3 was required for innate immune responses to HSV-1 in neurons and astrocytes. During infection with HSV-1, TLR3 recruited the metabolic checkpoint kinase complex mTORC2, which led to the induction of chemokines and trafficking of TLR3 to the cell periphery. Such trafficking enabled the activation of molecules (including mTORC1) required for the induction of type I interferons...
September 10, 2018: Nature Immunology
Jinfang Zhu
No abstract text is available yet for this article.
September 10, 2018: Nature Immunology
Roberto R Ricardo-Gonzalez, Steven J Van Dyken, Christoph Schneider, Jinwoo Lee, Jesse C Nussbaum, Hong-Erh Liang, Dedeepya Vaka, Walter L Eckalbar, Ari B Molofsky, David J Erle, Richard M Locksley
Group 2 innate lymphoid cells (ILC2s) are distributed systemically and produce type 2 cytokines in response to a variety of stimuli, including the epithelial cytokines interleukin (IL)-25, IL-33, and thymic stromal lymphopoietin (TSLP). Transcriptional profiling of ILC2s from different tissues, however, grouped ILC2s according to their tissue of origin, even in the setting of combined IL-25-, IL-33-receptor-, and TSLP-receptor-deficiency. Single-cell profiling confirmed a tissue-organizing transcriptome and identified ILC2 subsets expressing distinct activating receptors, including the major subset of skin ILC2s, which were activated preferentially by IL-18...
September 10, 2018: Nature Immunology
Dominik Aschenbrenner, Mathilde Foglierini, David Jarrossay, Dan Hu, Howard L Weiner, Vijay K Kuchroo, Antonio Lanzavecchia, Samuele Notarbartolo, Federica Sallusto
Different types of effector and memory T lymphocytes are induced and maintained in protective or pathological immune responses. Here we characterized two human CD4+ TH 17 helper cell subsets that, in the recently activated state, could be distinguished on the basis of their expression of the anti-inflammatory cytokine IL-10. IL-10+ TH 17 cells upregulated a variety of genes encoding immunoregulatory molecules, as well as genes whose expression is characteristic of tissue-resident T cells. In contrast, IL-10- TH 17 cells maintained a pro-inflammatory gene-expression profile and upregulated the expression of homing receptors that guide recirculation from tissues to blood...
September 10, 2018: Nature Immunology
Janko Nikolich-Žugich
In the version of this Review initially published, the type of cell in the final sentence of the legend to Figure 3 (group 2 innate lymphoid cells) was incorrect. The correct type of cell is group 3 innate lymphoid cells. The error has been corrected in the HTML and PDF versions of the article.
September 3, 2018: Nature Immunology
W Nicholas Haining, Sarah A Weiss
In the version of this article initially published, two sentences in the seventh paragraph (which begins "To delve more deeply") had incorrect text: the seventh sentence (which begins "Moreover, the decreased") stated "treatment of the mice with a blocking antibody"; the next sentence (which begins "These data") stated "that in turn has important consequences...". The correct text is as follows: "treatment of the cells with a blocking antibody" (in the seventh sentence); and "in turn might have important consequences" (in the next sentence)...
August 24, 2018: Nature Immunology
Tri Giang Phan, Stuart G Tangye
No abstract text is available yet for this article.
July 9, 2018: Nature Immunology
Ryan H Newton, Sharad Shrestha, Jenna M Sullivan, Kathleen B Yates, Ewoud B Compeer, Noga Ron-Harel, Bruce R Blazar, Steven J Bensinger, W Nicholas Haining, Michael L Dustin, Daniel J Campbell, Hongbo Chi, Laurence A Turka
Foxo transcription factors play an essential role in regulating specialized lymphocyte functions and in maintaining T cell quiescence. Here, we used a system in which Foxo1 transcription-factor activity, which is normally terminated upon cell activation, cannot be silenced, and we show that enforcing Foxo1 activity disrupts homeostasis of CD4 conventional and regulatory T cells. Despite limiting cell metabolism, continued Foxo1 activity is associated with increased activation of the kinase Akt and a cell-intrinsic proliferative advantage; however, survival and cell division are decreased in a competitive setting or growth-factor-limiting conditions...
July 9, 2018: Nature Immunology
Munir Akkaya, Javier Traba, Alexander S Roesler, Pietro Miozzo, Billur Akkaya, Brandon P Theall, Haewon Sohn, Mirna Pena, Margery Smelkinson, Juraj Kabat, Eric Dahlstrom, David W Dorward, Jeff Skinner, Michael N Sack, Susan K Pierce
B cells are activated by two temporally distinct signals, the first provided by the binding of antigen to the B cell antigen receptor (BCR), and the second provided by helper T cells. Here we found that B cells responded to antigen by rapidly increasing their metabolic activity, including both oxidative phosphorylation and glycolysis. In the absence of a second signal, B cells progressively lost mitochondrial function and glycolytic capacity, which led to apoptosis. Mitochondrial dysfunction was a result of the gradual accumulation of intracellular calcium through calcium response-activated calcium channels that, for approximately 9 h after the binding of B cell antigens, was preventable by either helper T cells or signaling via the receptor TLR9...
July 9, 2018: Nature Immunology
Fiamma Salerno, Sander Engels, Maartje van den Biggelaar, Floris P J van Alphen, Aurelie Guislain, Wanqi Zhao, Deborah L Hodge, Sarah E Bell, Jan Paul Medema, Marieke von Lindern, Martin Turner, Howard A Young, Monika C Wolkers
Memory T cells are critical for the immune response to recurring infections. Their instantaneous reactivity to pathogens is empowered by the persistent expression of cytokine-encoding mRNAs. How the translation of proteins from pre-formed cytokine-encoding mRNAs is prevented in the absence of infection has remained unclear. Here we found that protein production in memory T cells was blocked via a 3' untranslated region (3' UTR)-mediated process. Germline deletion of AU-rich elements (AREs) in the Ifng-3' UTR led to chronic cytokine production in memory T cells...
July 9, 2018: Nature Immunology
Dimitris L Kontoyiannis
No abstract text is available yet for this article.
July 9, 2018: Nature Immunology
Sudan He, Xiaodong Wang
Receptor-interacting protein (RIP) kinases, in particular RIPK1, RIPK2 and RIPK3, have emerged as pleiotropic modulators of inflammatory responses that act either by directly regulating intracellular inflammatory signaling pathways or by causing apoptotic or necrotic cell death. In this Review, we discuss the signaling pathways and immunological functions of these RIP kinases in the inflammatory response to microbial infection and tissue injury, as well as their potential roles in the pathogenesis of inflammatory disease and aging...
September 2018: Nature Immunology
Laurie A Dempsey
No abstract text is available yet for this article.
September 2018: Nature Immunology
Ioana Visan
No abstract text is available yet for this article.
September 2018: Nature Immunology
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