title: Inflammation in tuberculosis: interactions, imbalances and interventions.
abstract: Inflammation is critical for tuberculosis (TB) pathogenesis. The nonresolving aspect of inflammation in TB is caused by sophisticated intracellular survival strategies of tubercle bacilli. TB is a continuum comprising a spectrum of lesions as a consequence of complex regulation of inflammation. Proinflammatory cytokines, including interferons, tumor necrosis factor and interleukin 1 along with microRNAs and eicosanoids form an interactive network during TB. Cross-regulation between proinflammatory mediators strongly impacts on infected cell death patterns. These processes, in concert with local concentrations of proteases, such as cathepsins, serpins and matrix-metalloproteinases, affect tissue integrity, shape the architecture of granulomas and modulate tissue repair. With inflammation networks being uncovered in TB, the relevance of several pathways for novel interventions becomes clearer.
authors.affiliation: Max Planck Institute for Infection Biology, Department of Immunology, Berlin, Germany. Electronic address: kaufmann@mpiib-berlin.mpg.de.
authors.forename: Stefan H E
authors.initials: SH
authors.lastname: Kaufmann
authors.forename: Anca
authors.initials: A
authors.lastname: Dorhoi
mesh_terms: D000818:Animals; D016923:Cell Death; D006801:Humans; D007249:Inflammation / Q000276:immunology; D009169:Mycobacterium tuberculosis / Q000276:immunology; D014376:Tuberculosis / Q000276:immunology* / Q000473:pathology