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.
Abstract
Mechanisms of pulmonary IRIS in HIV-infected individuals recently initiated on ART are poorly defined http://ow.ly/AAOR301Bh36
Footnotes
Support statement. Funding was received from the US Department of Health and Human Science, the National Institutes of Health and the National Heart, Lung and Blood Institute with grant number R37 HL079142. Funding information for this article has been deposited with the Open Funder Registry.
Conflict of interest: Disclosures can be found alongside this article at err.ersjournals.com
Provenance: Submitted article, peer reviewed.
- Received April 25, 2016.
- Accepted June 9, 2016.
- Copyright ©ERS 2017.
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