One hundred years of (influenza) immunopathology
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The study of virus infections in experimental animals has led to the definition of the individual components of the host response, and their relative roles in the resolution of the infection. However, these immune responses can be perturbed by direct virus infection of immunocompetent cells, and effective responses may produce tissue damage for exmple by immune complex formation and T cell-mediated destruction of infected cells. This virus immunopathology assumes particular importance when the virus itself is relatively non-cytopathic and in the case of peristent infections.
Cytopathic effect
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Infection with influenza virus can result in massive pulmonary infiltration and potentially fatal immunopathology. Understanding the endogenous mechanisms that control immunopathology could provide a key to novel adjunct therapies for this disease. Here we show that the cytokine IL-27 plays a crucial role in protection from exaggerated inflammation during influenza virus infection. Using Il-27ra−/− mice, IL-27 was found to limit immunopathology, neutrophil accumulation, and dampened TH1 or TH17 responses via IL-10–dependent and -independent pathways. Accordingly, the absence of IL-27 signals resulted in a more severe disease course and in diminished survival without impacting viral loads. Consistent with the delayed expression of endogenous Il-27p28 during influenza, systemic treatment with recombinant IL-27 starting at the peak of virus load resulted in a major amelioration of lung pathology, strongly reduced leukocyte infiltration and improved survival without affecting viral clearance. In contrast, early application of IL-27 impaired virus clearance and worsened disease. These findings demonstrate the importance of IL-27 for the physiological control of immunopathology and the potential value of well-timed IL-27 application to treat life-threatening inflammation during lung infection.
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Rapid reaction to microbes invading mucosal tissues is key to protect the host against disease. Respiratory tissue-resident memory T (T
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Part 1 The pulmonary immune response determinants of T-cell motility in the lung immunopathology of acute pulmonary inflammation pulmonary macrophages dendritic cells in the lung immunology and immunotherapy of allergic diseases mechanisms of asthma implications for treatment immunology of idiopathic pulmonary fibrosis hypersensitivity pneumonitis in humans and experimental animals the pathogenesis of pulmonary manifestations of connective tissue diseases sardoidosis Langerham's cell granulomatosis pulmonary vasculitis immunopathology of tuberculosis host defences in pulmonary cryptococcosis lessons from a mouse model the spectrum of pulmonary responses to aspergillus immunopathology of pulmonary parasitic disease immunology of pneumocystis Carinii infection immunopathology of HIV infection and the lung immunopathology of asbestos-related lung disease immunopathogenesis of silicosis the immune response of lung tumours and the effects of cytokine administration on pulmonary immune cells the immunology and immunopathology of malignant mesothelioma the immunopathology of lung transplantation bronchoalveolar lavage new techniques for evaluating lung immunology and immunopathology.
Hypersensitivity pneumonitis
Allergic bronchopulmonary aspergillosis
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Respiratory syncytial virus (RSV), a member of the Paramyxoviridae family, is a major clinical problem causing yearly epidemics of severe lower airway disease in both infants and the elderly. Attempts at vaccination have been frustrated by both the poor immunogenicity of this virus, and the severe immunopathology observed in early vaccine trials. Primary infection generally occurs in infancy, with approximately 5% of infected infants requiring hospitalization. Equally problematic is the apparent link between severe RSV disease and the later development of allergy and asthma. While there is no evidence that natural infection promotes Th2 predominance, development of enhanced eosinophilic disease in children receiving inactivated virus administered with a commonly used adjuvant demonstrated how easily the balance between immune-mediated protection and immune- mediated pathology can be perturbed. In this review we have focused on studies carried out in the mouse model aimed at determining the correlates of RSV protection and explaining the mechanism of vaccine enhanced immunopathology.
Mononegavirales
Pneumovirus
Pneumovirinae
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Lymphoproliferative disease
Lymphoproliferative Disorders
Gammaherpesvirinae
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Priming (agriculture)
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PERSPECTIVES ON PEDIATRIC HUMAN IMMUNODEFICIENCY VIRUS INFECTIONS EDITED BY PHILIP A. PIZZO, M.D., AND CATHERINE M. WILFERT, M.D.: PDF Only
Pathogenesis
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