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

Seung Jun Lee, Jong Hwa Jang, Gun Young Yoon, Da Rae Kang, Hee Jo Park, Sung Jae Shin, Hee Dong Han, Tae Heung Kang, Won Sun Park, Young Kyung Yoon, Byoung Yul Soh, In Duk Jung, Yeong Min Park

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)554-559
Number of pages6
JournalBMB Reports
Volume49
Issue number10
DOIs
Publication statusPublished - 2016 Jan 1

Keywords

  • Dendritic cells
  • MAB1843
  • MAPK
  • Mycobacterium abscessus
  • Th1 polarization

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

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  • Cite this

    Lee, S. J., Jang, J. H., Yoon, G. Y., Kang, D. R., Park, H. J., Shin, S. J., Han, H. D., Kang, T. H., Park, W. S., Yoon, Y. K., Soh, B. Y., Jung, I. D., & Park, Y. M. (2016). Mycobacterium abscessus D-alanyl-D-alanine dipeptidase induces the maturation of dendritic cells and promotes Th1-biased immunity. BMB Reports, 49(10), 554-559. https://doi.org/10.5483/BMBRep.2016.49.10.080