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dc.contributor.authorMogga, S. J.en_US
dc.contributor.authorMustafa, Tehminaen_US
dc.contributor.authorSviland, Lisbeten_US
dc.contributor.authorNilsen, Runeen_US
dc.date.accessioned2007-01-09T14:02:24Z
dc.date.available2007-01-09T14:02:24Z
dc.date.issued2003-09eng
dc.PublishedScandinavian Journal of Immunology 2003 58(3): 327–334
dc.identifier.issn1365-3083
dc.identifier.issn0300-9475
dc.identifier.urihttps://hdl.handle.net/1956/2054
dc.description.abstractThe distribution and expression of CD40, its ligand CD40L (154) and related cytokines interleukin-12 (IL-12), tumour necrosis factor-α (TNF-α), interferon-γ (IFN-γ) and transforming growth factor-β1 (TGF-β1) were studied in the lungs of B6D2F1 hybrid mice during slowly progressive primary tuberculosis (TB) by immunohistochemistry. CD40 and CD40L are implicated in cell-mediated immunity (CMI) causing activation or apoptosis of infected cells. The phenomenon of apoptosis is associated with Mycobacterium tuberculosis survival. In this study, using frozen lung sections (n = 33), our results showed increased CD40, IL-12 and TGF-β1 expression in macrophages with progression of disease. High percentages of mycobacterial antigens (M.Ags), CD40L and IFN-γ expression were maintained throughout infection, and TNF-α-expressing cells were decreased. In lymphocytes, the percentage of IFN-γ-positive cells was increased, but CD40L and IL-12 were maintained with the progression of disease. M.Ags, CD40 and CD40L were expressed in the same areas of the lesions. We conclude that changes in the expression of CD40–CD40L and cytokines associated with M. tuberculosis infection favour the hypothesis that M. tuberculosis causes resistance of host cells to apoptosis causing perpetuation of infection.en_US
dc.format.extent1071705 byteseng
dc.format.mimetypeapplication/pdfeng
dc.language.isoengeng
dc.publisherBlackwell Publishing Ltd.eng
dc.titleIn Situ Expression of CD40, CD40L (CD154), IL-12, TNF-a, IFN-g and TGF-b1 in Murine Lungs during Slowly Progressive Primary Tuberculosisen_US
dc.typeJournal article
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2003 Blackwell Publishing Ltd.
dc.identifier.doihttps://doi.org/10.1046/j.1365-3083.2003.01304.x
dc.subject.nsiVDP::Medisinske Fag: 700::Helsefag: 800nob
dc.subject.nsiVDP::Medisinske Fag: 700::Basale medisinske, odontologiske og veterinærmedisinske fag: 710::Medisinsk immunologi: 716nob


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