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    Immune reconstitution inflammatory syndrome associated with pulmonary pathogens

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    Author
    Gopal, R.
    Rapaka, R.R.
    Kolls, J.K.
    Date
    2017
    Journal
    European Respiratory Review
    Publisher
    European Respiratory Society
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://doi.org/10.1183/16000617.0042-2016
    Abstract
    Immune reconstitution inflammatory syndrome (IRIS) is an exaggerated immune response to a variety of pathogens in response to antiretroviral therapy-mediated recovery of the immune system in HIV-infected patients. Although IRIS can occur in many organs, pulmonary IRIS, associated with opportunistic infections such as Mycobacterium tuberculosis and Pneumocystis jirovecii, is particularly associated with high morbidity and mortality. The pathology of IRIS is associated with a variety of innate and adaptive immune factors, including CD4+ T-cells, CD8+ T-cells, γδ T-cells, natural killer cells, macrophages, the complement system and surfactant proteins, Toll-like receptors and pro-inflammatory cytokines and chemokines. Although there are numerous reports about the immune factors involved in IRIS, the mechanisms involved in the development of pulmonary IRIS are poorly understood. Here, we propose that studies using gene-deficient murine and nonhuman primate models will help to identify the specific molecular targets associated with the development of IRIS. An improved understanding of the mechanisms involved in the pathology of pulmonary IRIS will help to identify potential biomarkers and therapeutic targets in this syndrome.
    Sponsors
    Funding was received from the US Department of Health and Human Science, the National Institutes of HealthNIH and the National Heart, Lung and Blood Institute with grant number R37 HL079142.
    Keyword
    Immune Reconstitution Inflammatory Syndrome
    HIV Infections
    Mycobacterium tuberculosis
    Pneumocystis carinii
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85008705105&doi=10.1183%2f16000617.0042-2016&partnerID=40&md5=2caa1b88e9f77c4650473a65357e9fc5; http://hdl.handle.net/10713/11001
    ae974a485f413a2113503eed53cd6c53
    10.1183/16000617.0042-2016
    Scopus Count
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    UMB Open Access Articles 2017

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