Showing papers in "Immunity in 2017"
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University of Hamburg1, Brigham and Women's Hospital2, University of Massachusetts Medical School3, Medical University of Vienna4, Icahn School of Medicine at Mount Sinai5, German Center for Neurodegenerative Diseases6, Washington University in St. Louis7, Harvard University8, Boston University9, Charité10
TL;DR: The TREM2-APOE pathway is identified as a major regulator of microglial functional phenotype in neurodegenerative diseases and serves as a novel target that could aid in the restoration of homeostatic microglia.
1,535 citations
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TL;DR: Recent studies that demonstrate that different initiating CNS injuries can elicit at least two types of "reactive" astrocytes with strikingly different properties, one type being helpful and the other harmful are summarized.
1,324 citations
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TL;DR: The dominant cellular mediators of these interactions are reviewed and emerging themes associated with the current understanding of the homeostatic immunological dialogue between the host and its microbiota are discussed.
728 citations
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TL;DR: The central role played by the P2X7 receptor in promoting inflammation and driving innate and adaptive immunity is discussed, with an in‐depth knowledge of its structure and of the associated signal transduction mechanisms needed for an effective therapeutic development.
714 citations
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TL;DR: Recent data that support intriguing models of disease pathogenesis allude to the possibility of restoration of immunologic homeostasis and thus a state of tolerance associated with drug-free remission of RA, and represents a bold vision for the future of RA therapeutics.
685 citations
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TL;DR: A scalable mono‐allelic strategy for profiling the HLA peptidome is implemented and a strategy for systematically learning the rules of endogenous antigen presentation is demonstrated, providing an updated portrait of antigen processing rules.
477 citations
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TL;DR: Unexpectedly, significant portions of pancreas‐resident macrophages originated from embryonic development and expanded through in situ proliferation during tumor progression and demonstrate a unique pro‐fibrotic transcriptional profile distinct from that of their monocyte‐derived counterparts.
467 citations
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TL;DR: The results suggest that highly prevalent genital bacteria increase HIV risk by inducing mucosal HIV target cells, and specific taxa highly prevalent in young healthy South African women that increase their HIV risk might be leveraged to reduce HIV acquisition in women.
447 citations
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TL;DR: The recent discoveries of tissue-resident NK cell developmental intermediates, non-NK innate lymphoid cells, and the capacity for NK cells to adapt and differentiate into long-lived memory cells has added further complexity to this field.
429 citations
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TL;DR: Overall, CD49a expression delineates CD8+ Trm cell specialization in human epithelial barriers and correlates with the effector cell balance found in distinct inflammatory skin diseases.
413 citations
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TL;DR: It is demonstrated that RAS can drive cell‐intrinsic PD‐L1 expression, thus presenting therapeutic opportunities to reverse the innately immunoresistant phenotype of RAS mutant cancers and a post‐transcriptional mechanism whereby oncogenic RAS signaling increases PD‐l1 expression.
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TL;DR: Mechanisms related to cellular cholesterol, phenotypic plasticity, metabolism, and aging play key roles in affecting these responses.
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TL;DR: Mechanisms of peripheral sensory neuronal function in response to immune challenges, the neural regulation of immunity and inflammation, and the therapeutic implications of those mechanistic insights are reviewed.
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TL;DR: In this near‐complete response to PD‐1 blockade in a mesenchymal tumor, PTEN mutations and reduced expression of genes encoding neoantigens as potential mediators of resistance to immune checkpoint therapy are identified.
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TL;DR: Lambda interferons (IFN&lgr;s) or type III IFNs share homology, expression patterns, signaling cascades, and antiviral functions with type I IFNs, and are shown to provide front‐line antiviral protection without activating inflammation.
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TL;DR: The analysis shows that human ILCs are highly heterogeneous cell types between individuals and tissues, and provides a global, comprehensive, and detailed description of ILC heterogeneity in humans across patients and tissues.
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Frederick Arce Vargas1, Andrew Furness1, Andrew Furness2, Isabelle Solomon1 +247 more•Institutions (7)
TL;DR: Use of an anti‐CD25 antibody with enhanced binding to activating Fc&ggr;Rs led to effective depletion of tumor‐infiltrating Treg cells, increased effector to Treg cell ratios, and improved control of established tumors.
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University of Toronto1, University Health Network2, Braunschweig University of Technology3, University of Luxembourg4, Australian National University5, Tokyo Medical and Dental University6, Yale University7, University of Marburg8, University of Southern Denmark9, University of Düsseldorf10, Harvard University11
TL;DR: It is reported that GSH is essential for T cell effector functions through its regulation of metabolic activity and plays an unexpected role in metabolic integration and reprogramming during inflammatory T cell responses.
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TL;DR: Recent advances such as the discovery that a broad complement of immune cells play a role in immunometabolism and the emerging evidence that nutrients and metabolites modulate inflammatory pathways are described.
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TL;DR: The emerging literature that the ENS is essential for important aspects of microbe-induced immune responses in the gut is highlighted, suggesting that novel paradigms for nervous system function await discovery.
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TL;DR: This review focuses on emerging functions of neutrophils in homeostasis, immunity, and disease and identifies transcriptional and phenotypic diversity that endows them with regulatory properties that extend beyond their lifetime in the circulation.
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TL;DR: A transcriptional module consisting of the TCR‐induced transcription factors IRF4, BATF, and NFATc1 that drives T cell exhaustion and impairs memory T cell development is identified.
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TL;DR: It is demonstrated that lymphocyte trafficking through lymph nodes and lymph occurs in a circadian manner and that adaptive immune responses are also time‐of‐day dependent and are ablated when circadian clock function is lost in T cells.
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TL;DR: How plasticity, i.e. the capacity to adapt to demands encountered in early life, also provides the potential to leverage protection of the young against infection and disease through a number of interventions is discussed.
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TL;DR: A coordinated epithelium‐intrinsic inflammasome response was sufficient to protect against Salmonella tissue invasion and involved a previously reported IEC expulsion that was coordinated with lipid mediator and cytokine production and lytic IEC death.
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TL;DR: It is suggested that release of phosphorylated MLKL within extracellular vesicles serves as a mechanism for self‐restricting the necroptotic activity of this protein, and apparently withholding death mediation by MLKl.
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Scripps Research Institute1, La Jolla Institute for Allergy and Immunology2, Beth Israel Deaconess Medical Center3, Massachusetts Institute of Technology4, Emory University5, Yerkes National Primate Research Center6, Discovery Institute7, University of California, San Diego8, University of Amsterdam9, Duke University10, Cornell University11
TL;DR: This study identifies protocols for rapid and consistent generation of tier 2 nAbs, providing a framework for future pre‐clinical and clinical vaccine studies targeting nAb elicitation and identified immunogens that minimized non‐neutralizing V3 responses and demonstrated that continuous immunogen delivery could enhance nAb responses.
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TL;DR: The balance of GMP and MDP differentiation shapes the myeloid cell repertoire during homeostasis and following infection, and shows that functionally distinct inflammatory monocytes, including those producing monocyte‐derived DCs and a “neutrophil‐like” subset, arise from bone marrow progenitors via two independent pathways
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TL;DR: The gene expression signatures revealed that CD4+ T cell help during priming optimized CTLs in expression of cytotoxic effector molecules and many other functions that ensured efficacy of C TLs throughout their life cycle.
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TL;DR: It is established that mo-DCs and mo-Macs are controlled by distinct transcription factors and show that AHR acts as a molecular switch for monocyte fate specification in response to micro-environmental factors.