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Infection and Immunity, September 2002, p. 5167-5176, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.5167-5176.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Mycobacterium leprae Infection in Monocyte-Derived Dendritic Cells and Its Influence on Antigen-Presenting Function

Ken Hashimoto,1 Yumi Maeda,1 Hiroaki Kimura,1 Koichi Suzuki,1 Akihiro Masuda,2 Masanori Matsuoka,3 and Masahiko Makino1*

Department of Microbiology,1 Department of Bioregulation, Leprosy Research Center, National Institute of Infectious Diseases, Higashimurayama,3 Department of Pathology, Tokyo Women's Medical University, Shinjuku, Tokyo, Japan2

Received 20 February 2002/ Returned for modification 8 April 2002/ Accepted 31 May 2002

Host defense against Mycobacterium leprae infection is chiefly mediated by gamma interferon (IFN-{gamma})-secreting cytotoxic T cells. Since which antigen-presenting cell populations act to stimulate these T cells is not fully understood, we addressed the role of monocyte-derived dendritic cells (DCs). The DCs phagocytosed M. leprae and expressed bacterially derived antigens (Ags), such as phenolic glycolipid 1 (PGL-1), in the cytoplasm, as well as on the cell surface. The expression of HLA-ABC and -DR Ags on DCs was down-regulated by M. leprae infection, and that of CD86 was up-regulated, but not as fully as by Mycobacterium bovis BCG infection. Induction of CD83 expression required a large number of M. leprae cells. When a multiplicity of infection of >40 was used, the DCs induced a significant proliferative and IFN-{gamma}-producing response in autologous T cells. However, these responses were significantly lower than those induced by BCG- or Mycobacterium avium-infected DCs. A CD40-mediated signaling in M. leprae-infected DCs up-regulated the expression of HLA Ags, CD86, and CD83 but did not enhance T-cell-stimulating ability. Therefore, M. leprae-infected DCs are less efficient at inducing T-cell responses. However, when the surface PGL-1 on M. leprae-infected DCs was masked by a monoclonal antibody, the DCs induced enhanced responses in both CD4+- and CD8+-T-cell subsets. M. leprae is a unique pathogen which remains resistant to DC-mediated T-cell immunity, at least in the early stages of infection.

* Corresponding author. Mailing address: Department of Microbiology, Leprosy Research Center, National Institute of Infectious Diseases, 4-2-1 Aobacho, Higashimurayama, Tokyo 189-0002, Japan. Phone: 81-42-391-8059. Fax: 81-42-391-8212. E-mail: mmaki{at}nih.go.jp.

Editor: S. H. E. Kaufmann

Infection and Immunity, September 2002, p. 5167-5176, Vol. 70, No. 9
0019-9567/02/$04.00+0     DOI: 10.1128/IAI.70.9.5167-5176.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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