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  • 1.
    Jacobsen, Marc
    et al.
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Repsilber, Dirk
    Institute for Medical Biometry and Statistics, University at Lübeck, Lübeck, Germany; Institute for Biochemistry and Biology, University Potsdam, Potsdam-Golm, Germany.
    Gutschmidt, Andrea
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Neher, Albert
    Asklepios Center for Respiratory Medicine and Thoracic Surgery, Munich-Gauting, Germany .
    Feldmann, Knut
    Asklepios Center for Respiratory Medicine and Thoracic Surgery, Munich-Gauting, Germany .
    Mollenkopf, Hans J
    Microarray Core Facilities, Max Planck Institute for Infection Biology, Berlin, Germany.
    Ziegler, Andreas
    Kaufmann, Stefan H E
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Candidate biomarkers for discrimination between infection and disease caused by Mycobacterium tuberculosis2007Ingår i: Journal of Molecular Medicine, ISSN 0946-2716, E-ISSN 1432-1440, Vol. 85, nr 6, s. 613-21Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    Infection with Mycobacterium tuberculosis is controlled by an efficacious immune response in about 90% of infected individuals who do not develop disease. Although essential mediators of protection, e.g., interferon-gamma, have been identified, these factors are insufficient to predict the outcome of M. tuberculosis infection. As a first step to determine additional biomarkers, we compared gene expression profiles of peripheral blood mononuclear cells from tuberculosis patients and M. tuberculosis-infected healthy donors by microarray analysis. Differentially expressed candidate genes were predominantly derived from monocytes and comprised molecules involved in the antimicrobial defense, inflammation, chemotaxis, and intracellular trafficking. We verified differential expression for alpha-defensin 1, alpha-defensin 4, lactoferrin, Fcgamma receptor 1A (cluster of differentiation 64 [CD64]), bactericidal permeability-increasing protein, and formyl peptide receptor 1 by quantitative polymerase chain reaction analysis. Moreover, we identified increased protein expression of CD64 on monocytes from tuberculosis patients. Candidate biomarkers were then assessed for optimal study group discrimination. Using a linear discriminant analysis, a minimal group of genes comprising lactoferrin, CD64, and the Ras-associated GTPase 33A was sufficient for classification of (1) tuberculosis patients, (2) M. tuberculosis-infected healthy donors, and (3) noninfected healthy donors.

  • 2. Olofsson, P. S.
    et al.
    Söderström, L. Å.
    Jern, C.
    Sirsjö, Allan
    Örebro universitet, Hälsoakademin.
    Ria, M.
    Sundler, E.
    De Faire, U.
    Wiklund, P. G.
    Öhrvik, J.
    Hedin, U.
    Paulsson-Berne, G.
    Hamsten, A.
    Eriksson, P.
    Hansson, G. K.
    Genetic variants of TNFSF4 and risk for carotid artery disease and stroke2009Ingår i: Journal of Molecular Medicine, ISSN 0946-2716, E-ISSN 1432-1440, Vol. 87, nr 4, s. 337-346Artikel i tidskrift (Refereegranskat)
    Abstract [en]

    In two independent human cohorts, the minor allele of SNP rs3850641 in TNFSF4 was significantly more frequent in individuals with myocardial infarction than in controls. In mice, Tnfsf4 expression is associated with increased atherosclerosis. The expression of TNFSF4 in human atherosclerosis and the association between genotype and cerebrovascular disease have not yet been investigated. TNFSF4 messenger RNA (mRNA) levels were significantly higher in human atherosclerotic lesions compared with controls (730∈±∈30 vs 330∈±∈65 arbitrary units, p∈<∈0.01). TNFSF4 was mainly expressed by macrophages in atherosclerotic lesions. In cell culture, endothelial cells upregulated TNFSF4 in response to tumor necrosis factor alpha (TNF-α; 460∈±∈110 vs 133∈±∈8 arbitrary units, p∈<∈0.001 after 6 h of stimulation). We analyzed the TNFSF4 gene in 239 patients who had undergone carotid endarterectomy and 138 matching controls from The Biobank of Karolinska Carotid Endarterectomies and Stockholm Heart Epidemiology Program cohorts and 929 patients and 1,382 matching controls from the Sahlgrenska Academy Study on Ischemic Stroke and Case Control Study of Stroke cohorts, limiting inclusion to patients with ischemic stroke. Participants were genotyped for the rs3850641 SNP in TNFSF4. Genotype associations were neither found with TNFSF4 mRNA levels nor with atherosclerosis associated systemic factors or risk for stroke. This study shows that TNFSF4 is expressed on antigen-presenting cells in human carotid atherosclerotic lesions but provides no evidence for an association of TNFSF4 gene variation with the risk for ischemic stroke.

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