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      New findings of Toll-like receptors involved in Mycobacterium tuberculosis infection

      Author(s): 1 , 2
      Publication date Created:
      Publication date (Electronic):
      Journal: Pathogens and Global Health
      Publisher: Informa UK Limited

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          Abstract

          Tuberculosis (TB), an important issue in the present age, affects millions of people each year. The infectious agent of TB, Mycobacterium tuberculosis (Mtb), interacts with the immune system which prevents the development of this bacterium as much as possible. In fact, the receptors on the surface of immune cells identify the bacteria, one of which is Toll-like receptors (TLRs). Different TLRs including 2, 4, 9 and 8 play critical roles in tuberculosis infection. In this paper, we focused on the role of TLRs which interact with different components of Mtb and, consequently, prevent the entrance and influence of bacteria on the body.

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          IL-23 and IL-17 in the establishment of protective pulmonary CD4+ T cell responses after vaccination and during Mycobacterium tuberculosis challenge.

          Susan Swain, Andrea Cooper, Troy D. Randall … (2007)
          Interferon-gamma is key in limiting Mycobacterium tuberculosis infection. Here we show that vaccination triggered an accelerated interferon-gamma response by CD4(+) T cells in the lung during subsequent M. tuberculosis infection. Interleukin 23 (IL-23) was essential for the accelerated response, for early cessation of bacterial growth and for establishment of an IL-17-producing CD4(+) T cell population in the lung. The recall response of the IL-17-producing CD4(+) T cell population occurred concurrently with expression of the chemokines CXCL9, CXCL10 and CXCL11. Depletion of IL-17 during challenge reduced the chemokine expression and accumulation of CD4(+) T cells producing interferon-gamma in the lung. We propose that vaccination induces IL-17-producing CD4(+) T cells that populate the lung and, after challenge, trigger the production of chemokines that recruit CD4(+) T cells producing interferon-gamma, which ultimately restrict bacterial growth.
          Article 0 comments Cited 433 times – based on 0 reviews     Review now
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            Host defense mechanisms triggered by microbial lipoproteins through toll-like receptors.

            H. D. Brightbill, D H Libraty, S. Krutzik … (1999)
            The generation of cell-mediated immunity against many infectious pathogens involves the production of interleukin-12 (IL-12), a key signal of the innate immune system. Yet, for many pathogens, the molecules that induce IL-12 production by macrophages and the mechanisms by which they do so remain undefined. Here it is shown that microbial lipoproteins are potent stimulators of IL-12 production by human macrophages, and that induction is mediated by Toll-like receptors (TLRs). Several lipoproteins stimulated TLR-dependent transcription of inducible nitric oxide synthase and the production of nitric oxide, a powerful microbicidal pathway. Activation of TLRs by microbial lipoproteins may initiate innate defense mechanisms against infectious pathogens.
            Article 0 comments Cited 263 times – based on 0 reviews     Review now
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              Regulation of antigen presentation by Mycobacterium tuberculosis: a role for Toll-like receptors.

              W. Boom, Scott V Harding (2010)
              Mycobacterium tuberculosis survives in antigen-presenting cells (APCs) such as macrophages and dendritic cells. APCs present antigens in association with major histocompatibility complex (MHC) class II molecules to stimulate CD4(+) T cells, and this process is essential to contain M. tuberculosis infection. Immune evasion allows M. tuberculosis to establish persistent or latent infection in macrophages and results in Toll-like receptor 2 (TLR2)-dependent inhibition of MHC class II transactivator expression, MHC class II molecule expression and antigen presentation. This reduction of antigen presentation might reflect a general mechanism of negative-feedback regulation that prevents excessive T cell-mediated inflammation and that M. tuberculosis has subverted to create a niche for survival in infected macrophages and evasion of recognition by CD4(+) T cells.
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                Author and article information

                Journal
                Title: Pathogens and Global Health
                Abbreviated Title: Pathogens and Global Health
                Publisher: Informa UK Limited
                ISSN (Print): 2047-7724
                ISSN (Electronic): 2047-7732
                Publication date Created: July 02 2017
                Publication date Created: July 04 2017
                Publication date (Electronic): July 17 2017
                Publication date (Print): July 04 2017
                Volume: 111
                Issue: 5
                Pages: 256-264
                Affiliations
                [1 ] Molecular Biology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
                [2 ] Nephrology and Urology Research Center, Baqiyatallah University of Medical Sciences, Tehran, Iran
                Article
                DOI: 10.1080/20477724.2017.1351080
                PMC ID: 5560203
                PubMed ID: 28715935
                SO-VID: 8c4339ad-ad05-46d1-8e00-5f87dac36040
                Copyright © © 2017
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