The role of T cell — Macrophage interactions in tuberculosis
Identifieur interne : 003231 ( Main/Exploration ); précédent : 003230; suivant : 003232The role of T cell — Macrophage interactions in tuberculosis
Auteurs : Stefan H. E. Kaufmann [Allemagne] ; Inge E. A. Flesch [Allemagne]Source :
- Springer Seminars in Immunopathology [ 0344-4325 ] ; 1988-12-01.
Abstract
Abstract: Acquired resistance against tuberculosis paradigmatically depends on specific T lymphocytes and mononuclear phagocytes. The etiological agent,Mycobacterium tuberculosis is capable of replicating in mononuclear phagocytes which act both as habitat and as effectors of protection. Upon interaction with antigen-specific T lymphocytes infected mononuclear phagocytes acquire tuberculosis activities. Here, data from experimental tuberculosis studies in mice are summarized which show that: interleukins produced by cloned T cells and recombinant interferon-γ are capable of activating tuberculostatic capacities in macrophages; both CD4 and CD8 T cells, after adequate stimulation, produce interferon-γ; CD8 T cells lyse macrophages in an antigen-specific way; not only CD8 but also CD4 T cells possess an antigen-specific cytolytic potential; lysis of infected macrophages results in mycobacterial growth inhibition. Evidence is also presented that tuberculostatic activities of activated macrophages depend on phagosome-lysosome fusion and are independent of reactive oxygen metabolites and that some strains ofM. tuberculosis are resistant against interferon-γ activated macrophages. These findings suggest that both helper and cytolytic T cells participate in the immune response to tuberculosis and that similar T cell mechanisms contribute to resistance as well as pathogenesis. Protection against tuberculosis, therefore, depends on subtle coordination of the immune response.
Url:
DOI: 10.1007/BF02053845
Affiliations:
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E." last="Kaufmann">Stefan H. E. Kaufmann</name><affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Medical Microbiology and Immunology, University of Ulm, Oberer Eselsberg, D-7900, Ulm</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region><settlement type="city">Ulm</settlement></placeName><orgName type="university">Université d'Ulm</orgName></affiliation></author><author><name sortKey="Flesch, Inge E A" sort="Flesch, Inge E A" uniqKey="Flesch I" first="Inge E. A." last="Flesch">Inge E. A. Flesch</name><affiliation wicri:level="4"><country xml:lang="fr">Allemagne</country><wicri:regionArea>Department of Medical Microbiology and Immunology, University of Ulm, Oberer Eselsberg, D-7900, Ulm</wicri:regionArea><placeName><region type="land" nuts="1">Bade-Wurtemberg</region><region type="district" nuts="2">District de Tübingen</region><settlement type="city">Ulm</settlement></placeName><orgName type="university">Université d'Ulm</orgName></affiliation></author></analytic><monogr></monogr><series><title level="j">Springer Seminars in Immunopathology</title><title level="j" type="abbrev">Springer Semin Immunopathol</title><idno type="ISSN">0344-4325</idno><idno type="eISSN">1432-2196</idno><imprint><publisher>Springer-Verlag</publisher><pubPlace>New York</pubPlace><date type="published" when="1988-12-01">1988-12-01</date><biblScope unit="volume">10</biblScope><biblScope unit="issue">4</biblScope><biblScope unit="page" from="337">337</biblScope><biblScope unit="page" to="358">358</biblScope></imprint><idno type="ISSN">0344-4325</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0344-4325</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Abstract: Acquired resistance against tuberculosis paradigmatically depends on specific T lymphocytes and mononuclear phagocytes. The etiological agent,Mycobacterium tuberculosis is capable of replicating in mononuclear phagocytes which act both as habitat and as effectors of protection. Upon interaction with antigen-specific T lymphocytes infected mononuclear phagocytes acquire tuberculosis activities. Here, data from experimental tuberculosis studies in mice are summarized which show that: interleukins produced by cloned T cells and recombinant interferon-γ are capable of activating tuberculostatic capacities in macrophages; both CD4 and CD8 T cells, after adequate stimulation, produce interferon-γ; CD8 T cells lyse macrophages in an antigen-specific way; not only CD8 but also CD4 T cells possess an antigen-specific cytolytic potential; lysis of infected macrophages results in mycobacterial growth inhibition. Evidence is also presented that tuberculostatic activities of activated macrophages depend on phagosome-lysosome fusion and are independent of reactive oxygen metabolites and that some strains ofM. tuberculosis are resistant against interferon-γ activated macrophages. These findings suggest that both helper and cytolytic T cells participate in the immune response to tuberculosis and that similar T cell mechanisms contribute to resistance as well as pathogenesis. Protection against tuberculosis, therefore, depends on subtle coordination of the immune response.</div></front></TEI><affiliations><list><country><li>Allemagne</li></country><region><li>Bade-Wurtemberg</li><li>District de Tübingen</li></region><settlement><li>Ulm</li></settlement><orgName><li>Université d'Ulm</li></orgName></list><tree><country name="Allemagne"><region name="Bade-Wurtemberg"><name sortKey="Kaufmann, Stefan H E" sort="Kaufmann, Stefan H E" uniqKey="Kaufmann S" first="Stefan H. E." last="Kaufmann">Stefan H. E. Kaufmann</name></region><name sortKey="Flesch, Inge E A" sort="Flesch, Inge E A" uniqKey="Flesch I" first="Inge E. A." last="Flesch">Inge E. A. Flesch</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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