Tryptophan aspartate-containing coat protein (CORO1A) suppresses Toll-like receptor signalling in Mycobacterium leprae infection

Clinical and Experimental Immunology - Tập 156 Số 3 - Trang 495-501 - 2009
Kazunari Tanigawa1, Koichi Suzuki1, Hiroaki Kimura2, Fumihiko Takeshita3, Huhehasi Wu1, Takao Akama1, Akira Kawashima1, Norihisa Ishii1
1Department of Bioregulation, Leprosy Research Center, National Institute of Infectious Diseases, Higashimurayama, Tokyo, Japan
2Department of Pathology, The Johns Hopkins School of Medicine, Baltimore, Md. USA
3Department of Molecular Biodefense Research, Yokohama City University School of Medicine, Kanazawa-ku, Yokohama, Japan

Tóm tắt

Summary Mycobacterium leprae is an intracellular pathogen that survives within the phagosome of host macrophages. Several host factors are involved in producing tolerance, while others are responsible for killing the mycobacterium. Tryptophan aspartate-containing coat protein (TACO; also known as CORO1A or coronin-1) inhibits the phagosome maturation that allows intracellular parasitization. In addition, the Toll-like receptor (TLR) activates the innate immune response. Both CORO1A and TLR-2 co-localize on the phagosomal membrane in the dermal lesions of patients with lepromatous leprosy. Therefore, we hypothesized that CORO1A and TLR-2 might interact functionally. This hypothesis was tested by investigating the effect of CORO1A in TLR-2-mediated signalling and, inversely, the effect of TLR-2-mediated signalling on CORO1A expression. We found that CORO1A suppresses TLR-mediated signal activation in human macrophages, and that TLR2-mediated activation of the innate immune response resulted in suppression of CORO1A expression. However, M. leprae infection inhibited the TLR-2-mediated CORO1A suppression and nuclear factor-κB activation. These results suggest that the balance between TLR-2-mediated signalling and CORO1A expression will be key in determining the fate of M. leprae following infection.

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Clinical and Experimental Immunology

Tập 156 Số 3

495-501

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