4,153 results match your criteria Nature Immunology[Journal]


CARD9 microglia promote antifungal immunity via IL-1β- and CXCL1-mediated neutrophil recruitment.

Nat Immunol 2019 05 17;20(5):559-570. Epub 2019 Apr 17.

Fungal Pathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy & Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

The C-type lectin receptor-Syk (spleen tyrosine kinase) adaptor CARD9 facilitates protective antifungal immunity within the central nervous system (CNS), as human deficiency in CARD9 causes susceptibility to fungus-specific, CNS-targeted infection. CARD9 promotes the recruitment of neutrophils to the fungus-infected CNS, which mediates fungal clearance. In the present study we investigated host and pathogen factors that promote protective neutrophil recruitment during invasion of the CNS by Candida albicans. Read More

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http://www.nature.com/articles/s41590-019-0377-2
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http://dx.doi.org/10.1038/s41590-019-0377-2DOI Listing
May 2019
3 Reads

Macrophages light the way.

Authors:
Zoltan Fehervari

Nat Immunol 2019 May;20(5):517

Nature Immunology, .

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http://www.nature.com/articles/s41590-019-0394-1
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May 2019
1 Read

Signaling platforms.

Authors:
Ioana Visan

Nat Immunol 2019 May;20(5):517

Nature Immunology, .

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http://www.nature.com/articles/s41590-019-0391-4
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May 2019
1 Read

Heterogeneity in the retina.

Authors:
Ioana Visan

Nat Immunol 2019 May;20(5):517

Nature Immunology, .

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http://www.nature.com/articles/s41590-019-0390-5
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May 2019
1 Read

Functional degradation.

Authors:
Laurie A Dempsey

Nat Immunol 2019 May;20(5):517

Nature Immunology, .

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http://www.nature.com/articles/s41590-019-0392-3
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http://dx.doi.org/10.1038/s41590-019-0392-3DOI Listing
May 2019
1 Read

Distinct S1PR roles.

Authors:
Laurie A Dempsey

Nat Immunol 2019 May;20(5):517

Nature Immunology, .

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http://www.nature.com/articles/s41590-019-0393-2
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May 2019
1 Read

Old dog PU.1 reveals new tricks.

Authors:
Richard Dahl

Nat Immunol 2019 05;20(5):520-522

Department of Microbiology and Immunology, Indiana University School of Medicine, South Bend, IN, USA.

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http://dx.doi.org/10.1038/s41590-019-0380-7DOI Listing

IL-17 metabolically reprograms activated fibroblastic reticular cells for proliferation and survival.

Nat Immunol 2019 05 8;20(5):534-545. Epub 2019 Apr 8.

Department of Medicine, University of Pittsburgh, Pittsburgh, PA, USA.

Lymph-node (LN) stromal cell populations expand during the inflammation that accompanies T cell activation. Interleukin-17 (IL-17)-producing helper T cells (T17 cells) promote inflammation through the induction of cytokines and chemokines in peripheral tissues. We demonstrate a critical requirement for IL-17 in the proliferation of LN and splenic stromal cells, particularly fibroblastic reticular cells (FRCs), during experimental autoimmune encephalomyelitis and colitis. Read More

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http://dx.doi.org/10.1038/s41590-019-0367-4DOI Listing
May 2019
5 Reads

IL-17 instructs lymphoid stromal cells.

Authors:
Scott N Mueller

Nat Immunol 2019 05;20(5):524-526

Department of Microbiology and Immunology, The University of Melbourne, The Peter Doherty Institute for Infection and Immunity, Melbourne, Victoria, Australia.

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http://dx.doi.org/10.1038/s41590-019-0375-4DOI Listing

SUCNR1 controls an anti-inflammatory program in macrophages to regulate the metabolic response to obesity.

Nat Immunol 2019 05 8;20(5):581-592. Epub 2019 Apr 8.

Unitat de Recerca, Hospital Universitari de Tarragona Joan XXIII, Institut d´Investigació Sanitària Pere Virgili, Tarragona, Spain.

Succinate is a signaling metabolite sensed extracellularly by succinate receptor 1 (SUNCR1). The accumulation of succinate in macrophages is known to activate a pro-inflammatory program; however, the contribution of SUCNR1 to macrophage phenotype and function has remained unclear. Here we found that activation of SUCNR1 had a critical role in the anti-inflammatory responses in macrophages. Read More

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Transcriptome networks identify mechanisms of viral and nonviral asthma exacerbations in children.

Nat Immunol 2019 05 8;20(5):637-651. Epub 2019 Apr 8.

University of Wisconsin School of Medicine and Public Health, Madison, WI, USA.

Respiratory infections are common precursors to asthma exacerbations in children, but molecular immune responses that determine whether and how an infection causes an exacerbation are poorly understood. By using systems-scale network analysis, we identify repertoires of cellular transcriptional pathways that lead to and underlie distinct patterns of asthma exacerbation. Specifically, in both virus-associated and nonviral exacerbations, we demonstrate a set of core exacerbation modules, among which epithelial-associated SMAD3 signaling is upregulated and lymphocyte response pathways are downregulated early in exacerbation, followed by later upregulation of effector pathways including epidermal growth factor receptor signaling, extracellular matrix production, mucus hypersecretion, and eosinophil activation. Read More

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6472965PMC

Innate immunity to intracellular LPS.

Nat Immunol 2019 05 8;20(5):527-533. Epub 2019 Apr 8.

National Institute of Biological Sciences, Beijing, China.

Monitoring of the cytosolic compartment by the innate immune system for pathogen-encoded products or pathogen activities often enables the activation of a subset of caspases. In most cases, the cytosolic surveillance pathways are coupled to activation of caspase-1 via canonical inflammasome complexes. A related set of caspases, caspase-11 in rodents and caspase-4 and caspase-5 in humans, monitors the cytosol for bacterial lipopolysaccharide (LPS). Read More

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http://dx.doi.org/10.1038/s41590-019-0368-3DOI Listing
May 2019
1 Read

Author Correction: Deciphering CD4 T cell specificity using novel MHC-TCR chimeric receptors.

Nat Immunol 2019 May;20(5):663

Institute of Molecular Health Sciences, ETH Zürich, Zürich, Switzerland.

In the version of this article initially published, a reference (23) was cited incorrectly and two references were not included in the second sentence of the first paragraph of the second Results subsection ('Screening for gp61 mimotopes with different functional properties'). The correct citation is as follows: ".. Read More

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http://dx.doi.org/10.1038/s41590-019-0383-4DOI Listing

Dynamic changes to lipid mediators support transitions among macrophage subtypes during muscle regeneration.

Nat Immunol 2019 05 1;20(5):626-636. Epub 2019 Apr 1.

Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.

Muscle damage elicits a sterile immune response that facilitates complete regeneration. Here, we used mass spectrometry-based lipidomics to map the mediator lipidome during the transition from inflammation to resolution and regeneration in skeletal muscle injury. We observed temporal regulation of glycerophospholipids and production of pro-inflammatory lipid mediators (for example, leukotrienes and prostaglandins) and specialized pro-resolving lipid mediators (for example, resolvins and lipoxins) that were modulated by ibuprofen. Read More

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http://dx.doi.org/10.1038/s41590-019-0356-7DOI Listing
May 2019
20.004 Impact Factor

Adaptive plasticity of IL-10 and IL-35 T cells cooperatively promotes tumor T cell exhaustion.

Nat Immunol 2019 Apr 1. Epub 2019 Apr 1.

Department of Immunology, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

Regulatory T cells (T cells) maintain host self-tolerance but are a major barrier to effective cancer immunotherapy. T cells subvert beneficial anti-tumor immunity by modulating inhibitory receptor expression on tumor-infiltrating lymphocytes (TILs); however, the underlying mediators and mechanisms have remained elusive. Here, we found that the cytokines IL-10 and IL-35 (Ebi3-IL-12α heterodimer) were divergently expressed by T cell subpopulations in the tumor microenvironment (TME) and cooperatively promoted intratumoral T cell exhaustion by modulating several inhibitory receptor expression and exhaustion-associated transcriptomic signature of CD8 TILs. Read More

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http://dx.doi.org/10.1038/s41590-019-0346-9DOI Listing
April 2019
8 Reads

The lung environment controls alveolar macrophage metabolism and responsiveness in type 2 inflammation.

Nat Immunol 2019 05 1;20(5):571-580. Epub 2019 Apr 1.

Lydia Becker Institute of Immunology and Inflammation, Manchester Collaborative Centre for Inflammation Research, Faculty of Biology, Medicine and Health, University of Manchester, Manchester Academic Health Science Centre, Manchester, UK.

Fine control of macrophage activation is needed to prevent inflammatory disease, particularly at barrier sites such as the lungs. However, the dominant mechanisms that regulate the activation of pulmonary macrophages during inflammation are poorly understood. We found that alveolar macrophages (AlvMs) were much less able to respond to the canonical type 2 cytokine IL-4, which underpins allergic disease and parasitic worm infections, than macrophages from lung tissue or the peritoneal cavity. Read More

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http://dx.doi.org/10.1038/s41590-019-0352-yDOI Listing
May 2019
4 Reads

Translate less, prime better, to improve anti-tumor responses.

Nat Immunol 2019 05;20(5):518-520

Institut Curie, PSL Research University, INSERM U932, Paris, France.

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http://dx.doi.org/10.1038/s41590-019-0371-8DOI Listing

The IFN-λ Pony Express.

Nat Immunol 2019 05;20(5):522-524

Department of Biomedicine, University Hospital Basel, University of Basel, Basel, Switzerland.

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http://dx.doi.org/10.1038/s41590-019-0362-9DOI Listing

Safeguard function of PU.1 shapes the inflammatory epigenome of neutrophils.

Nat Immunol 2019 05 25;20(5):546-558. Epub 2019 Mar 25.

Institute of Molecular Tumor Biology, University of Muenster, Muenster, Germany.

Neutrophils are essential first-line defense cells against invading pathogens, yet when inappropriately activated, their strong immune response can cause collateral tissue damage and contributes to immunological diseases. However, whether neutrophils can intrinsically titrate their immune response remains unknown. Here we conditionally deleted the Spi1 gene, which encodes the myeloid transcription factor PU. Read More

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http://www.nature.com/articles/s41590-019-0343-z
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May 2019
2 Reads

Regulatory T cell adaptation in the intestine and skin.

Nat Immunol 2019 04 19;20(4):386-396. Epub 2019 Mar 19.

University of Oxford, Kennedy Institute of Rheumatology, Oxford, UK.

The intestine and skin are distinct microenvironments with unique physiological functions and are continually exposed to diverse environmental challenges. Host adaptation at these sites is an active process that involves interaction between immune cells and tissue cells. Regulatory T cells (T cells) play a pivotal role in enforcing homeostasis at barrier surfaces, illustrated by the development of intestinal and skin inflammation in diseases caused by primary deficiency in T cells. Read More

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Activation of naïve CD4 T cells re-tunes STAT1 signaling to deliver unique cytokine responses in memory CD4 T cells.

Nat Immunol 2019 04 19;20(4):458-470. Epub 2019 Mar 19.

Division of Infection & Immunity, School of Medicine, Cardiff University, Cardiff, Wales, UK.

The cytokine IL-6 controls the survival, proliferation and effector characteristics of lymphocytes through activation of the transcription factors STAT1 and STAT3. While STAT3 activity is an ever-present feature of IL-6 signaling in CD4 T cells, prior activation via the T cell antigen receptor limits IL-6's control of STAT1 in effector and memory populations. Here we found that phosphorylation of STAT1 in response to IL-6 was regulated by the tyrosine phosphatases PTPN2 and PTPN22 expressed in response to the activation of naïve CD4 T cells. Read More

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http://dx.doi.org/10.1038/s41590-019-0350-0DOI Listing

STING-ing insights.

Authors:
Laurie A Dempsey

Nat Immunol 2019 Apr;20(4):377

Nature Immunology, .

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Tumor adaptations.

Authors:
Laurie A Dempsey

Nat Immunol 2019 Apr;20(4):377

Nature Immunology, .

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http://dx.doi.org/10.1038/s41590-019-0369-2DOI Listing
April 2019
3 Reads

Inflammation-induced remodeling.

Authors:
Ioana Visan

Nat Immunol 2019 Apr;20(4):377

Nature Immunology, .

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http://dx.doi.org/10.1038/s41590-019-0364-7DOI Listing
April 2019
1 Read

Vpu broadens its effects.

Authors:
Zoltan Fehervari

Nat Immunol 2019 Apr;20(4):377

Nature Immunology, .

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http://dx.doi.org/10.1038/s41590-019-0366-5DOI Listing
April 2019
1 Read

Digest to diverge.

Authors:
Zoltan Fehervari

Nat Immunol 2019 Apr;20(4):377

Nature Immunology, .

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http://dx.doi.org/10.1038/s41590-019-0365-6DOI Listing
April 2019
2 Reads

Hacking the 'Cellular Immunology Agency': T cells caught in the act.

Nat Immunol 2019 04;20(4):382-383

Department of Otolaryngology-Head and Neck Surgery, Department of Microbiology and Immunology, Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA, USA.

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Infection drives meningeal engraftment by inflammatory monocytes that impairs CNS immunity.

Nat Immunol 2019 04 18;20(4):407-419. Epub 2019 Mar 18.

Viral Immunology and Intravital Imaging Section, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD, USA.

Tissue macrophages have an embryonic origin and can be replenished in some tissues under steady-state conditions by blood monocytes. However, little is known about the residency and properties of infiltrating monocytes after an inflammatory challenge. The meninges of the central nervous system (CNS) are populated by a dense network of macrophages that act as resident immune sentinels. Read More

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http://dx.doi.org/10.1038/s41590-019-0344-yDOI Listing
April 2019
1 Read

Lymph node conduits transport virions for rapid T cell activation.

Nat Immunol 2019 05 18;20(5):602-612. Epub 2019 Mar 18.

Viral Immunity and Pathogenesis Unit, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.

Despite intense interest in antiviral T cell priming, the routes by which virions move in lymph nodes (LNs) are imperfectly understood. Current models fail to explain how virus-infected cells rapidly appear within the LN interior after viral infection. To better understand virion trafficking in the LN, we determined the locations of virions and infected cells after administration to mice of vaccinia virus or Zika virus. Read More

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http://www.nature.com/articles/s41590-019-0342-0
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May 2019
8 Reads

Interferon-λ enhances adaptive mucosal immunity by boosting release of thymic stromal lymphopoietin.

Nat Immunol 2019 05 18;20(5):593-601. Epub 2019 Mar 18.

Institute of Virology, Medical Center University of Freiburg, Freiburg, Germany.

Interferon-λ (IFN-λ) acts on mucosal epithelial cells and thereby confers direct antiviral protection. In contrast, the role of IFN-λ in adaptive immunity is far less clear. Here, we report that mice deficient in IFN-λ signaling exhibited impaired CD8 T cell and antibody responses after infection with a live-attenuated influenza virus. Read More

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http://dx.doi.org/10.1038/s41590-019-0345-xDOI Listing

Publisher Correction: Clonal analysis of Salmonella-specific effector T cells reveals serovar-specific and cross-reactive T cell responses.

Nat Immunol 2019 Apr;20(4):514

MRC Human Immunology Unit, MRC Weatherall Institute of Molecular Medicine, University of Oxford, Oxford, UK.

In the version of this article initially published, the first affiliation lacked 'MRC'; the correct name of the institution is 'MRC Weatherall Institute of Molecular Medicine'. Two designations (SP110Y and ST110H) were incorrect in the legend to Fig. 6f,h,i. Read More

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http://dx.doi.org/10.1038/s41590-019-0357-6DOI Listing
April 2019
2 Reads
20.004 Impact Factor

Publisher Correction: Self-renewing resident cardiac macrophages limit adverse remodeling following myocardial infarction.

Nat Immunol 2019 May;20(5):664

Toronto General Hospital Research Institute, University Health Network (UHN), Toronto, Canada.

In the version of this article initially published, the equal contribution of the third author was omitted. The footnote links for that author should be "Sara Nejat" and the correct statement is as follows: "These authors contributed equally: Sarah A. Dick, Jillian A. Read More

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http://www.nature.com/articles/s41590-019-0363-8
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May 2019
3 Reads
20.004 Impact Factor

Publisher Correction: Uncoupling protein 2 reprograms the tumor microenvironment to support the anti-tumor immune cycle.

Nat Immunol 2019 Apr;20(4):515-516

Department of Fundamental Oncology, University of Lausanne, Lausanne, Switzerland.

In the version of this article initially published, the bars were not aligned with the data points or horizontal axis labels in Fig. 5d, and the labels along each horizontal axis of Fig. 5j-l indicating the presence (+) or absence (-) of doxycycline (Dox) were incorrectly included with the labels below that axis. Read More

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http://dx.doi.org/10.1038/s41590-019-0359-4DOI Listing
April 2019
1 Read

SLAM-ing the brakes on iNKT cell selection.

Nat Immunol 2019 04;20(4):378-379

Division of Gastroenterology, Hepatology and Endoscopy, Department of Medicine, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.

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http://www.nature.com/articles/s41590-019-0355-8
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6444350PMC
April 2019
6 Reads

NAD-biosynthetic pathways regulate innate immunity.

Nat Immunol 2019 04;20(4):380-382

Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, USA.

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http://dx.doi.org/10.1038/s41590-019-0353-xDOI Listing

Deciphering CD4 T cell specificity using novel MHC-TCR chimeric receptors.

Nat Immunol 2019 05 11;20(5):652-662. Epub 2019 Mar 11.

Institute of Molecular Health Sciences, ETH Zürich, Zürich, Switzerland.

αβ T cell antigen receptors (TCRs) bind complexes of peptide and major histocompatibility complex (pMHC) with low affinity, which poses a considerable challenge for the direct identification of αβ T cell cognate peptides. Here we describe a platform for the discovery of MHC class II epitopes based on the screening of engineered reporter cells expressing novel pMHC-TCR (MCR) hybrid molecules carrying cDNA-derived peptides. This technology identifies natural epitopes of CD4 T cells in an unbiased and efficient manner and allows detailed analysis of TCR cross-reactivity that provides recognition patterns beyond discrete peptides. Read More

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http://dx.doi.org/10.1038/s41590-019-0335-zDOI Listing

Inflammasome activation: a monocyte lineage privilege.

Nat Immunol 2019 04;20(4):383-385

Institut Curie, PSL Research University, Immunity and Cancer Department, INSERM U932, Paris, France.

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http://www.nature.com/articles/s41590-019-0348-7
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April 2019
5 Reads

Inflammatory macrophage dependence on NAD salvage is a consequence of reactive oxygen species-mediated DNA damage.

Nat Immunol 2019 04 11;20(4):420-432. Epub 2019 Mar 11.

Department of Immunometabolism, Max Planck Institute of Immunobiology and Epigenetics, Freiburg im Breisgau, Germany.

The adoption of Warburg metabolism is critical for the activation of macrophages in response to lipopolysaccharide. Macrophages stimulated with lipopolysaccharide increase their expression of nicotinamide phosphoribosyltransferase (NAMPT), a key enzyme in NAD salvage, and loss of NAMPT activity alters their inflammatory potential. However, the events that lead to the cells' becoming dependent on NAD salvage remain poorly defined. Read More

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http://dx.doi.org/10.1038/s41590-019-0336-yDOI Listing

Publisher Correction: SERPINB1-mediated checkpoint of inflammatory caspase activation.

Nat Immunol 2019 May;20(5):664

Department of Molecular Microbiology and Immunology, Keck School of Medicine, University of Southern California, Los Angeles, CA, USA.

In the version of this article initially published, the label (CASP4-CA-HA) above the second and fifth lanes in the right blot in Fig. 1e is incorrect; the correct label is CASP4-CA-HA. Also, the two labels at right above the plot in Fig. Read More

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May 2019
1 Read

Author Correction: Hobit- and Blimp-1-driven CD4 tissue-resident memory T cells control chronic intestinal inflammation.

Nat Immunol 2019 Apr;20(4):514

Department of Medicine 1, Kussmaul Campus for Medical Research and Translational Research Center, Friedrich-Alexander-Universität (FAU) Erlangen-Nürnberg, Erlangen, Germany.

In the version of this article initially published, a portion of the Acknowledgements section ("the Clinical Research Group CEDER of the German Research Council (DFG)") was incorrect. The correct statement is as follows: ".. Read More

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http://dx.doi.org/10.1038/s41590-019-0360-yDOI Listing
April 2019
2 Reads

BCR affinity differentially regulates colonization of the subepithelial dome and infiltration into germinal centers within Peyer's patches.

Nat Immunol 2019 04 4;20(4):482-492. Epub 2019 Mar 4.

Department of Immunology, Weizmann Institute of Science, Rehovot, Israel.

Gut-derived antigens trigger immunoglobulin A (IgA) immune responses that are initiated by cognate B cells in Peyer's patches (PPs). These cells colonize the subepithelial domes (SEDs) of the PPs and subsequently infiltrate pre-existing germinal centers (GCs). Here we defined the pre-GC events and the micro-anatomical site at which affinity-based B cell selection occurred in PPs. Read More

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http://dx.doi.org/10.1038/s41590-019-0325-1DOI Listing
April 2019
2 Reads

A protein-interaction network of interferon-stimulated genes extends the innate immune system landscape.

Nat Immunol 2019 04 4;20(4):493-502. Epub 2019 Mar 4.

Innate Immunity Laboratory, Max-Planck Institute of Biochemistry, Munich, Germany.

Interferon-stimulated genes (ISGs) form the backbone of the innate immune system and are important for limiting intra- and intercellular viral replication and spread. We conducted a mass-spectrometry-based survey to understand the fundamental organization of the innate immune system and to explore the molecular functions of individual ISGs. We identified interactions between 104 ISGs and 1,401 cellular binding partners engaging in 2,734 high-confidence interactions. Read More

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http://dx.doi.org/10.1038/s41590-019-0323-3DOI Listing
April 2019
3 Reads

SLAM receptors foster iNKT cell development by reducing TCR signal strength after positive selection.

Nat Immunol 2019 04 4;20(4):447-457. Epub 2019 Mar 4.

Laboratory of Molecular Oncology, Institut de recherches cliniques de Montréal, Montréal, Québec, Canada.

Invariant natural killer T cells (iNKT cells) develop through an incompletely understood process that requires positive selection by CD4CD8 double-positive thymocytes and SLAM family receptors (SFRs). Here we found that SFRs promoted the development of iNKT cells by reducing the strength of the T cell antigen receptor (TCR) signal after positive selection. This effect improved the survival of iNKT cells and their responses to antigen. Read More

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http://dx.doi.org/10.1038/s41590-019-0334-0DOI Listing
April 2019
3 Reads
20.004 Impact Factor

Publisher Correction: γδ TCR ligands: the quest to solve a 500-million-year-old mystery.

Nat Immunol 2019 Apr;20(4):516

Institute of Immunology and Immunotherapy, Cancer Immunology and Immunotherapy Centre, Cancer Research UK Birmingham Centre, University of Birmingham, Birmingham, UK.

In the version of this article initially published, the affiliations were incorrect. The correct affiliations are as follows: "Institute of Immunology and Immunotherapy, University of Birmingham, Birmingham, UK. Institute of Immunology and Immunotherapy, Cancer Immunology and Immunotherapy Centre, Cancer Research UK Birmingham Centre, University of Birmingham, Birmingham, UK. Read More

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http://dx.doi.org/10.1038/s41590-019-0358-5DOI Listing
April 2019
2 Reads

Publisher Correction: The transcription factor c-Maf is essential for the commitment of IL-17-producing γδ T cells.

Nat Immunol 2019 May;20(5):663

Department of Immunology, Duke University Medical Center, Durham, NC, USA.

In the version of this article initially published, the top right plot in Figure 4a was aligned incorrectly. The error has been corrected in the HTML and PDF versions of the article. The original and corrected figures are provided in the accompanying Publisher Correction. Read More

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http://dx.doi.org/10.1038/s41590-019-0349-6DOI Listing
May 2019
3 Reads

Listeria hijacks host mitophagy through a novel mitophagy receptor to evade killing.

Nat Immunol 2019 04 25;20(4):433-446. Epub 2019 Feb 25.

CAS Key Laboratory of Tissue Microenvironment and Tumor, CAS Center for Excellence in Molecular Cell Science, Shanghai Institute of Nutrition and Health, Shanghai Institutes for Biological Sciences, University of the Chinese Academy of Sciences, Chinese Academy of Sciences, Shanghai, China.

Cells use mitophagy to remove damaged or unwanted mitochondria to maintain homeostasis. Here we report that the intracellular bacterial pathogen Listeria monocytogenes exploits host mitophagy to evade killing. We found that L. Read More

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http://www.nature.com/articles/s41590-019-0324-2
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April 2019
7 Reads

Subsets of exhausted CD8 T cells differentially mediate tumor control and respond to checkpoint blockade.

Nat Immunol 2019 03 18;20(3):326-336. Epub 2019 Feb 18.

Department of Pediatric Oncology, Dana-Farber Cancer Institute, Boston, MA, USA.

T cell dysfunction is a hallmark of many cancers, but the basis for T cell dysfunction and the mechanisms by which antibody blockade of the inhibitory receptor PD-1 (anti-PD-1) reinvigorates T cells are not fully understood. Here we show that such therapy acts on a specific subpopulation of exhausted CD8 tumor-infiltrating lymphocytes (TILs). Dysfunctional CD8 TILs possess canonical epigenetic and transcriptional features of exhaustion that mirror those seen in chronic viral infection. Read More

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http://www.nature.com/articles/s41590-019-0312-6
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March 2019
33 Reads
20.004 Impact Factor

The transcription factor c-Myb regulates CD8 T cell stemness and antitumor immunity.

Nat Immunol 2019 03 18;20(3):337-349. Epub 2019 Feb 18.

Experimental Transplantation and Immunology Branch, Center for Cancer Research, National Cancer Institute, Bethesda, MD, USA.

Stem cells are maintained by transcriptional programs that promote self-renewal and repress differentiation. Here, we found that the transcription factor c-Myb was essential for generating and maintaining stem cells in the CD8 T cell memory compartment. Following viral infection, CD8 T cells lacking Myb underwent terminal differentiation and generated fewer stem cell-like central memory cells than did Myb-sufficient T cells. Read More

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http://www.nature.com/articles/s41590-018-0311-z
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http://dx.doi.org/10.1038/s41590-018-0311-zDOI Listing
March 2019
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Inhibition of the dipeptidyl peptidase DPP4 (CD26) reveals IL-33-dependent eosinophil-mediated control of tumor growth.

Nat Immunol 2019 03 18;20(3):257-264. Epub 2019 Feb 18.

Department of Cancer Immunology, Genentech, South San Francisco, CA, USA.

Post-translational modification of chemokines mediated by the dipeptidyl peptidase DPP4 (CD26) has been shown to negatively regulate lymphocyte trafficking, and its inhibition enhances T cell migration and tumor immunity by preserving functional chemokine CXCL10. By extending those initial findings to pre-clinical models of hepatocellular carcinoma and breast cancer, we discovered a distinct mechanism by which inhibition of DPP4 improves anti-tumor responses. Administration of the DPP4 inhibitor sitagliptin resulted in higher concentrations of the chemokine CCL11 and increased migration of eosinophils into solid tumors. Read More

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http://dx.doi.org/10.1038/s41590-019-0321-5DOI Listing
March 2019
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