title: Exosomes function in antigen presentation during an in vivo Mycobacterium tuberculosis infection.
abstract: Mycobacterium tuberculosis-infected macrophages and dendritic cells are limited in their ability to present antigen to CD4+ T cells suggesting that other mechanism of antigen presentation are driving the robust T cell response observed during an M. tuberculosis infection. These mechanisms could include antigens present in apoptotic bodies, necrotic debris, exosomes or even release of non-vesicular antigen from infected cells. However, there is limited data to support any of these mechanisms as important in driving T cell activation in vivo. In the present study we use Rab27a-deficient mice which show diminished trafficking of mycobacterial components to exosomes as well as M. tuberculosis strains that express recombinant proteins which traffic or fail to traffic to exosomes. We observed that exosomes released during a mouse M. tuberculosis infection contribute significantly to its T cell response. These finding imply that exosomes function to promote T cell immunity during a bacterial infection and are an important source of extracellular antigen.
authors.affiliation: Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana 46556, USA.
authors.forename: Victoria L
authors.initials: VL
authors.lastname: Smith
authors.affiliation: Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana 46556, USA.
authors.forename: Yong
authors.initials: Y
authors.lastname: Cheng
authors.affiliation: Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana 46556, USA.
authors.forename: Barry R
authors.initials: BR
authors.lastname: Bryant
authors.affiliation: Department of Biological Sciences, Eck Institute for Global Health, University of Notre Dame, Notre Dame, Indiana 46556, USA.
authors.forename: Jeffrey S
authors.initials: JS
authors.lastname: Schorey
mesh_terms: D000217:Acyltransferases / Q000235:genetics / Q000276:immunology; D000818:Animals; D017951:Antigen Presentation / Q000276:immunology*; D000942:Antigens, Bacterial / Q000235:genetics / Q000276:immunology*; D058491:Bacterial Load; D016207:Cytokines / Q000378:metabolism; D004195:Disease Models, Animal; D055354:Exosomes / Q000378:metabolism*; D015964:Gene Expression Regulation, Bacterial; D006801:Humans; D018836:Inflammation Mediators / Q000378:metabolism; D008213:Lymphocyte Activation / Q000276:immunology; D008264:Macrophages / Q000276:immunology / Q000378:metabolism / Q000382:microbiology; D051379:Mice; D018345:Mice, Knockout; D009163:Mycobacterium bovis / Q000276:immunology; D009169:Mycobacterium tuberculosis / Q000276:immunology*; D013601:T-Lymphocytes / Q000276:immunology / Q000378:metabolism; D014376:Tuberculosis / Q000276:immunology* / Q000378:metabolism* / Q000382:microbiology; D000075745:rab27 GTP-Binding Proteins / Q000172:deficiency / Q000378:metabolism
chemical_list: D000942:Antigens, Bacterial; D016207:Cytokines; D018836:Inflammation Mediators; D000075745:rab27 GTP-Binding Proteins; D000217:Acyltransferases; C112580:antigen 85A, Mycobacterium tuberculosis