Abstract
An efficient immune response against the intracellular pathogen Mycobacterium tuberculosis is critically dependent on rapid detection of the invader by the innate immune response and the activation of the adaptive immune response. Toll-like receptors (TLRs) contribute to innate immunity by the detection of Mycobacteria-associated molecular patterns and mediating the secretion of antibacterial effector molecules. TLRs influence the adaptive immune response by upregulation of immunomodulatory molecules supporting the development of a Th1-biased T cell response. In this manner, activation of TLRs contributes to defense against microbial infection.
MeSH terms
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Animals
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Antigen Presentation
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Antigens, Bacterial / metabolism
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Apoptosis
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Dendritic Cells / immunology
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Drosophila Proteins*
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Humans
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Membrane Glycoproteins / genetics
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Membrane Glycoproteins / physiology*
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Mice
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Mice, Knockout
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Models, Immunological
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Mutation
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Mycobacterium tuberculosis / immunology
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Mycobacterium tuberculosis / pathogenicity
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Reactive Nitrogen Species / metabolism
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Receptors, Cell Surface / genetics
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Receptors, Cell Surface / physiology*
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Th1 Cells / immunology
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Toll-Like Receptors
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Tuberculosis / genetics
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Tuberculosis / immunology*
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Tuberculosis / pathology
Substances
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Antigens, Bacterial
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Drosophila Proteins
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Membrane Glycoproteins
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Reactive Nitrogen Species
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Receptors, Cell Surface
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Toll-Like Receptors