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      Viral infection of the lung: Host response and sequelae

      , PhD a , , , PhD a , c , , , PhD a , b , , , , MD, PhD a , b , c ,

      The Journal of Allergy and Clinical Immunology

      American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc.

      Viral sensor molecules, innate immunity, adaptive immunity, T-cell immunity, B-cell immunity, viral clearance, tissue repair, stem cells, AIM2, Absent in melanoma 2, APC, Antigen-presenting cell, ASC, Apoptosis-associated speck-like protein containing CARD, CTL, Cytotoxic CD8+ T-cell, DAMP, Damage-associated molecular pattern, DC, Dendritic cell, GC, Germinal center, HMGB1, High-mobility group box 1, IAV, Influenza A virus, ILC, Innate lymphoid cell, ILC-II, Type II innate lymphoid cell, IRF, Interferon regulatory factor, LAPC, Late activator antigen-presenting cell, MAVS, Mitochondrial anti-viral signaling, MLN, Mediastinal lymph node, NK, Natural killer, NLRP3, Nod-like receptor family protein 3, PAMP, Pathogen-associated molecular pattern, PRR, Pattern recognition receptor, RIG-I, Retinoic acid–inducible gene I, RLR, RIG-I–like receptor, RSV, Respiratory syncytial virus, TFH, Follicular helper T, TLR, Toll-like receptor, Treg, Regulatory T

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          Abstract

          Because of its essential role in gas exchange and oxygen delivery, the lung has evolved a variety of strategies to control inflammation and maintain homeostasis. Invasion of the lung by pathogens (and in some instances exposure to certain noninfectious particulates) disrupts this equilibrium and triggers a cascade of events aimed at preventing or limiting colonization (and more importantly infection) by pathogenic microorganisms. In this review we focus on viral infection of the lung and summarize recent advances in our understanding of the triggering of innate and adaptive immune responses to viral respiratory tract infection, mechanisms of viral clearance, and the well-recognized consequences of acute viral infection complicating underlying lung diseases, such as asthma.

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          Most cited references 179

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          Complement: a key system for immune surveillance and homeostasis.

          Nearly a century after the significance of the human complement system was recognized, we have come to realize that its functions extend far beyond the elimination of microbes. Complement acts as a rapid and efficient immune surveillance system that has distinct effects on healthy and altered host cells and foreign intruders. By eliminating cellular debris and infectious microbes, orchestrating immune responses and sending 'danger' signals, complement contributes substantially to homeostasis, but it can also take action against healthy cells if not properly controlled. This review describes our updated view of the function, structure and dynamics of the complement network, highlights its interconnection with immunity at large and with other endogenous pathways, and illustrates its multiple roles in homeostasis and disease.
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            Follicular helper CD4 T cells (TFH).

             Shane Crotty (2010)
            T cell help to B cells is a fundamental aspect of adaptive immunity and the generation of immunological memory. Follicular helper CD4 T (T(FH)) cells are the specialized providers of B cell help. T(FH) cells depend on expression of the master regulator transcription factor Bcl6. Distinguishing features of T(FH) cells are the expression of CXCR5, PD-1, SAP (SH2D1A), IL-21, and ICOS, among other molecules, and the absence of Blimp-1 (prdm1). T(FH) cells are important for the formation of germinal centers. Once germinal centers are formed, T(FH) cells are needed to maintain them and to regulate germinal center B cell differentiation into plasma cells and memory B cells. This review covers T(FH) differentiation, T(FH) functions, and human T(FH) cells, discussing recent progress and areas of uncertainty or disagreement in the literature, and it debates the developmental relationship between T(FH) cells and other CD4 T cell subsets (Th1, Th2, Th17, iTreg).
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              Mechanisms of type-I- and type-II-interferon-mediated signalling.

              Interferons are cytokines that have antiviral, antiproliferative and immunomodulatory effects. Because of these important properties, in the past two decades, major research efforts have been undertaken to understand the signalling mechanisms through which these cytokines induce their effects. Since the original discovery of the classical JAK (Janus activated kinase)-STAT (signal transducer and activator of transcription) pathway of signalling, it has become clear that the coordination and cooperation of multiple distinct signalling cascades - including the mitogen-activated protein kinase p38 cascade and the phosphatidylinositol 3-kinase cascade - are required for the generation of responses to interferons. It is anticipated that an increased understanding of the contributions of these recently identified pathways will advance our current thinking about how interferons work.
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                Author and article information

                Contributors
                Journal
                J Allergy Clin Immunol
                J. Allergy Clin. Immunol
                The Journal of Allergy and Clinical Immunology
                American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc.
                0091-6749
                1097-6825
                1 August 2013
                December 2013
                1 August 2013
                : 132
                : 6
                : 1263-1276
                Affiliations
                [a ]Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, Va
                [b ]Department of Microbiology, Immunology and Cancer Biology, University of Virginia, Charlottesville, Va
                [c ]Department of Pathology and Molecular Medicine, University of Virginia, Charlottesville, Va
                Author notes
                []Corresponding author: Thomas J. Braciale, MD, PhD, Beirne B. Carter Center for Immunology Research, University of Virginia, Charlottesville, VA 22908. tjb2r@ 123456virginia.edu
                [∗]

                These authors contributed equally to this work.

                [‡]

                Dr Hufford is currently affiliated with the Department of Pediatrics and Department of Microbiology and Immunology, Indiana University School of Medicine, HB Wells Center for Pediatric Research, Indianapolis, Ind.

                Article
                S0091-6749(13)00917-2
                10.1016/j.jaci.2013.06.006
                3844062
                23915713
                Copyright © 2013 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.

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