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dc.contributor.authorOliver, B.
dc.contributor.authorElliott, J.
dc.contributor.authorSaphonn, V.
dc.contributor.authorVun, M.
dc.contributor.authorFrench, M.
dc.contributor.authorPrice, Patricia
dc.date.accessioned2017-01-30T10:35:28Z
dc.date.available2017-01-30T10:35:28Z
dc.date.created2016-09-12T08:36:58Z
dc.date.issued2010
dc.identifier.citationOliver, B. and Elliott, J. and Saphonn, V. and Vun, M. and French, M. and Price, P. 2010. Interferon-? and IL-5 production correlate directly in HIV patients Co-infected with mycobacterium tuberculosis with or without immune restoration disease. AIDS Research and Human Retroviruses. 26 (12): pp. 1287-1289.
dc.identifier.urihttp://hdl.handle.net/20.500.11937/3963
dc.identifier.doi10.1089/aid.2010.0004
dc.description.abstract

IL-5 and interferon-? responses were investigated in mitogen-stimulated whole-blood cultures from HIV patients with and without Mycobacterium tuberculosis disease, to determine whether an imbalance of Th1/Th2 cytokines contributes to susceptibility to M. tuberculosis disease or to immune restoration disease (IRD) associated with M. tuberculosis after starting antiretroviral therapy (ART). Interferon-? levels were constant on ART, whilst IL-5 levels generally rose over time. We suggest that increased IL-5 production reflects a recovery of CD4 + T cell function and that a Th1/Th2 imbalance is not associated with increased susceptibility to M. tuberculosis disease or IRD associated with M. tuberculosis upon starting ART. Copyright © 2010, Mary Ann Liebert, Inc.

dc.publisherMary Ann Liebert, Inc.
dc.titleInterferon-? and IL-5 production correlate directly in HIV patients Co-infected with mycobacterium tuberculosis with or without immune restoration disease
dc.typeJournal Article
dcterms.source.volume26
dcterms.source.number12
dcterms.source.startPage1287
dcterms.source.endPage1289
dcterms.source.issn0889-2229
dcterms.source.titleAIDS Research and Human Retroviruses
curtin.departmentSchool of Biomedical Sciences
curtin.accessStatusFulltext not available


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