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Record Nr. |
UNINA9910437838803321 |
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Titolo |
The New paradigm of immunity to tuberculosis / / Maziar Divangahi, editor |
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Pubbl/distr/stampa |
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New York, : Springer, c2013 |
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ISBN |
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Edizione |
[1st ed. 2013.] |
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Descrizione fisica |
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1 online resource (294 p.) |
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Collana |
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Advances in experimental medicine and biology ; ; v.783 |
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Altri autori (Persone) |
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Disciplina |
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Soggetti |
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Tuberculosis - Immunological aspects |
Tuberculosis - Vaccination |
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Lingua di pubblicazione |
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Formato |
Materiale a stampa |
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Livello bibliografico |
Monografia |
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Note generali |
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Description based upon print version of record. |
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Nota di bibliografia |
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Includes bibliographical references and index. |
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Nota di contenuto |
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Epidemiology of tuberculosis immunology -- Host pathogen specificity in tuberculosis -- Genetic determinants of susceptibility to mycobacterial infections -- Evolution of mycobacterium tuberculosis -- Mycobacterium tuberculosis genes involved in regulation of host cell death -- Dying to live: how the death modality of the infected macrophage affects immunity to tuberculosis -- Cytokines in the balance of protection and pathology during mycobactyerial infections -- Antigen-specific CD8+ T cells and protective immunity to tuberculosis -- Foxp3+ regulatory T cells in tuberculosis -- CD1a, CD1b, and CD1c in immunity against mycobacteria -- CD1d and natural killer T cells in immunity to mycobacterium tuberculosis -- The role of B cells and humoral immunity in mycobacterium tuberculosis infection -- Looking within the zebrafish to understand the tuberculosis granuloma -- Immunization strategies against pulmonary tuberculosis: Considerations of T cell geography. |
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Sommario/riassunto |
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This book illustrates the intimate relationship between alveolar macrophages and Mycobacterium tuberculosis (M.tb.), and the former’s role in both innate and adaptive immunity against M.tb. It covers research done over the last decade. It also explores the role of macrophage death following infection with M.tb. in determining whether successful immunity is stimulated, or whether clinical disease develops; furthermore, the function of host lipid mediators in |
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