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Autophagy in the fight against tuberculosis.



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Bento, Carla F 
Empadinhas, Nuno 
Mendes, Vítor 


Tuberculosis (TB), a chronic infectious disease mainly caused by the tubercle bacillus Mycobacterium tuberculosis, is one of the world's deadliest diseases that has afflicted humanity since ancient times. Although the number of people falling ill with TB each year is declining, its incidence in many developing countries is still a major cause of concern. Upon invading host cells by phagocytosis, M. tuberculosis can replicate within infected cells by arresting the maturation of the phagosome whose function is to target the pathogen for elimination. Host cells have mechanisms of controlling this evasion by inducing autophagy, an elaborate cellular process that targets bacteria for progressive elimination, decreasing bacterial loads within infected cells. In addition, autophagy activation also aids in the control of inflammation, contributing to a more efficient innate immune response against M. tuberculosis. Several innovative TB therapies have been envisaged based on autophagy manipulation, with some of them revealing high potential for future clinical trials and eventual implementation in healthcare systems. Thus, this review highlights the recent advances on the innate immune response regulation by autophagy upon M. tuberculosis infection and the promising new autophagy-based therapies for TB.



Animals, Antitubercular Agents, Autophagy, Drug Design, Humans, Immunity, Innate, Mycobacterium tuberculosis, Tuberculosis, Pulmonary

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DNA Cell Biol

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Mary Ann Liebert Inc
This work was funded by Bill & Melinda Gates Foundation (subcontract on the production of high quality chemical hit series with defined, tractable targets as drug leads for tuberculosis grant awarded to the Foundation for the National Institutes of Health) (OPP1024021), Fundação para a Ciência e a Tecnologia and EU-FEDER-COMPETE for funding (FCOMP-01-0124-FEDER-028359; PTDC/BIAMIC/2779/2012). VM would like to acknowledge Fundação para a Ciência e a Tecnologia for a postdoctoral fellowship (SFRH/BPD/79531/2011).