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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.

Exosomes function in antigen presentation during an in vivo Mycobacterium tuberculosis infection