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BMB Rep. 2016 Oct;49(10):554-559.

Mycobacterium abscessus D-alanyl-D-alanine dipeptidase induces the maturation of dendritic cells and promotes Th1-biased immunity.

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Department of Immunology, Laboratory of Dendritic Cell Differentiation and Regulation, School of Medicine, Konkuk University, Chungju 27478, Korea.
Department of Dental Hygiene, Hanseo University, Seosan 31962, Korea.
Department of Microbiology, Institute for Immunology and Immunological Diseases, Brain Korea 21 PLUS Project for Medical Science, Yonsei University College of Medicine, Seoul 03722, Korea.
Department of Physiology, School of Medicine, Kangwon National University, Chuncheon 24341, Korea.
Division of Infectious Diseases, Department of Internal Medicine, Korea University Anam Hospital, College of Medicine, Korea University, Seoul 02841, Korea.
Department of Biochemistry, College of Medicine, Seonam University, Namwon 55724, Korea.


Mycobacterium abscessus, a member of the group of non-tuberculous mycobacteria, has been identified as an emerging pulmonary pathogen in humans. However, little is known about the protective immune response of antigenpresenting cells, such as dendritic cells (DCs), which guard against M. abscessus infection. The M. abscessus gene MAB1843 encodes D-alanyl-D-alanine dipeptidase, which catalyzes the hydrolysis of D-alanyl-D-alanine dipeptide. We investigated whether MAB1843 is able to interact with DCs to enhance the effectiveness of the host's immune response. MAB1843 was found to induce DC maturation via toll-like receptor 4 and its downstream signaling pathways, such as the mitogen-activated protein kinase and nuclear factor kappa B pathways. In addition, MAB1843-treated DCs stimulated the proliferation of T cells and promoted Th1 polarization. Our results indicate that MAB1843 could potentially regulate the immune response to M. abscessus, making it important in the development of an effective vaccine against this mycobacterium. [BMB Reports 2016; 49(10): 554-559].

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