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      Mycobacterium Tuberculosis Infection and Inflammation: what is Beneficial for the Host and for the Bacterium?

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          Abstract

          Tuberculosis is still a major health problem in the world. Initial interactions between Mycobacterium tuberculosis and the host mark the pathway of infection and the subsequent host inflammatory response. This inflammatory response is tightly regulated by both the host and the bacterium during different stages of infection. As infection progresses, the initial intense pro-inflammatory response observed is regulated by suppressive mediators balancing inflammation. In this environment, M. tuberculosis battles to survive interfering with the host inflammatory response. In this review we discuss the major effector molecules involved in inflammation in relation to the different stages of M. tuberculosis infection.

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          Most cited references 216

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          The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors.

          The discovery of Toll-like receptors (TLRs) as components that recognize conserved structures in pathogens has greatly advanced understanding of how the body senses pathogen invasion, triggers innate immune responses and primes antigen-specific adaptive immunity. Although TLRs are critical for host defense, it has become apparent that loss of negative regulation of TLR signaling, as well as recognition of self molecules by TLRs, are strongly associated with the pathogenesis of inflammatory and autoimmune diseases. Furthermore, it is now clear that the interaction between TLRs and recently identified cytosolic innate immune sensors is crucial for mounting effective immune responses. Here we describe the recent advances that have been made by research into the role of TLR biology in host defense and disease.
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            Interleukin-10 and the interleukin-10 receptor.

            Interleukin-10 (IL-10), first recognized for its ability to inhibit activation and effector function of T cells, monocytes, and macrophages, is a multifunctional cytokine with diverse effects on most hemopoietic cell types. The principal routine function of IL-10 appears to be to limit and ultimately terminate inflammatory responses. In addition to these activities, IL-10 regulates growth and/or differentiation of B cells, NK cells, cytotoxic and helper T cells, mast cells, granulocytes, dendritic cells, keratinocytes, and endothelial cells. IL-10 plays a key role in differentiation and function of a newly appreciated type of T cell, the T regulatory cell, which may figure prominently in control of immune responses and tolerance in vivo. Uniquely among hemopoietic cytokines, IL-10 has closely related homologs in several virus genomes, which testify to its crucial role in regulating immune and inflammatory responses. This review highlights findings that have advanced our understanding of IL-10 and its receptor, as well as its in vivo function in health and disease.
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              Immunological and inflammatory functions of the interleukin-1 family.

              More than any other cytokine family, the interleukin (IL)-1 family is closely linked to the innate immune response. This linkage became evident upon the discovery that the cytoplasmic domain of the IL-1 receptor type I is highly homologous to the cytoplasmic domains of all Toll-like receptors (TLRs). Thus, fundamental inflammatory responses such as the induction of cyclooxygenase type 2, increased expression of adhesion molecules, or synthesis of nitric oxide are indistinguishable responses of both IL-1 and TLR ligands. Both families nonspecifically affect antigen recognition and lymphocyte function. IL-1beta is the most studied member of the IL-1 family because of its role in mediating autoinflammatory diseases. Although the TLR and IL-1 families evolved to assist in host defense against infection, unlike the TLR family, the IL-1 family also includes members that suppress inflammation, both specifically within the IL-1 family but also nonspecifically for TLR ligands and the innate immune response.
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                Author and article information

                Affiliations
                1simpleCenter for Microbial Interface Biology, Division of Infectious Diseases, Department of Internal Medicine, The Ohio State University Columbus, OH, USA
                Author notes

                Edited by: Amal Amer, The Ohio State University, USA

                Reviewed by: Jose A. Bengoechea, Fundacion Caubet-CIMERA Illes Balears, Spain; Andrey P. Anisimov, State Research Center for Applied Microbiology and Biotechnology, Russia

                *Correspondence: Jordi B. Torrelles, Center for Microbial Interface Biology, Division of Infectious Diseases, Department of Medicine, The Ohio State University, 460 West 12th Avenue, Biomedical Research Tower, Room 1016, Columbus, OH 43210, USA. e-mail: jordi.torrelles@ 123456osumc.edu

                This article was submitted to Frontiers in Cellular and Infection Microbiology, a specialty of Frontiers in Microbiology.

                Journal
                Front Microbiol
                Front. Microbio.
                Frontiers in Microbiology
                Frontiers Research Foundation
                1664-302X
                28 December 2010
                26 January 2011
                2011
                : 2
                3109289
                21687401
                10.3389/fmicb.2011.00002
                Copyright © 2011 Sasindran and Torrelles.

                This is an open-access article subject to an exclusive license agreement between the authors and Frontiers Media SA, which permits unrestricted use, distribution, and reproduction in any medium, provided the original authors and source are credited.

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                Figures: 2, Tables: 0, Equations: 0, References: 217, Pages: 16, Words: 17886
                Categories
                Microbiology
                Review Article

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