Role of gamma delta T cells in immunopathology of pulmonary Mycobacterium avium infection in mice

Several studies have shown that gamma delta T cells influence granuloma development after infection with intracellular pathogens. The role of gamma delta T cells in controlling the influx of inflammatory cells into the lung after Mycobacterium avium infection was therefore examined with gene-disrupt...

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Veröffentlicht in:Infection and immunity 1998-11, Vol.66 (11), p.5508-5514
Hauptverfasser: Saunders, B M, Frank, A A, Cooper, A M, Orme, I M
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container_issue 11
container_start_page 5508
container_title Infection and immunity
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creator Saunders, B M
Frank, A A
Cooper, A M
Orme, I M
description Several studies have shown that gamma delta T cells influence granuloma development after infection with intracellular pathogens. The role of gamma delta T cells in controlling the influx of inflammatory cells into the lung after Mycobacterium avium infection was therefore examined with gene-disrupted mice (K/O). The mice were infected with either M. avium 724, a progressively replicating highly virulent strain of M. avium, or with M. avium 2-151 SmT, a virulent strain that induces a chronic infection. gamma delta-K/O mice infected with M. avium 2-151 SmT showed early enhanced bacterial growth within the lung compared to the wild-type mice, although granuloma formation was similar in both strains. gamma delta-K/O mice infected with M. avium 724 showed identical bacterial growth within the lung compared to the wild-type mice, but they developed more-compact lymphocytic granulomas and did not show the extensive neutrophil influx and widespread tissue necrosis seen in wild-type mice. These data support the hypothesis that isolates of M. avium that induce protective T-cell-specific immunity are largely unaffected by the absence of gammadelta T cells. Whereas with bacterial strains that induce poor protective immunity, the absence of gamma delta T cells led to significant reductions in both the influx of neutrophils and tissue damage within the lungs of infected mice.
doi_str_mv 10.1128/IAI.66.11.5508-5514.1998
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The role of gamma delta T cells in controlling the influx of inflammatory cells into the lung after Mycobacterium avium infection was therefore examined with gene-disrupted mice (K/O). The mice were infected with either M. avium 724, a progressively replicating highly virulent strain of M. avium, or with M. avium 2-151 SmT, a virulent strain that induces a chronic infection. gamma delta-K/O mice infected with M. avium 2-151 SmT showed early enhanced bacterial growth within the lung compared to the wild-type mice, although granuloma formation was similar in both strains. gamma delta-K/O mice infected with M. avium 724 showed identical bacterial growth within the lung compared to the wild-type mice, but they developed more-compact lymphocytic granulomas and did not show the extensive neutrophil influx and widespread tissue necrosis seen in wild-type mice. These data support the hypothesis that isolates of M. avium that induce protective T-cell-specific immunity are largely unaffected by the absence of gammadelta T cells. 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The role of gamma delta T cells in controlling the influx of inflammatory cells into the lung after Mycobacterium avium infection was therefore examined with gene-disrupted mice (K/O). The mice were infected with either M. avium 724, a progressively replicating highly virulent strain of M. avium, or with M. avium 2-151 SmT, a virulent strain that induces a chronic infection. gamma delta-K/O mice infected with M. avium 2-151 SmT showed early enhanced bacterial growth within the lung compared to the wild-type mice, although granuloma formation was similar in both strains. gamma delta-K/O mice infected with M. avium 724 showed identical bacterial growth within the lung compared to the wild-type mice, but they developed more-compact lymphocytic granulomas and did not show the extensive neutrophil influx and widespread tissue necrosis seen in wild-type mice. These data support the hypothesis that isolates of M. avium that induce protective T-cell-specific immunity are largely unaffected by the absence of gammadelta T cells. 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These data support the hypothesis that isolates of M. avium that induce protective T-cell-specific immunity are largely unaffected by the absence of gammadelta T cells. Whereas with bacterial strains that induce poor protective immunity, the absence of gamma delta T cells led to significant reductions in both the influx of neutrophils and tissue damage within the lungs of infected mice.</abstract><cop>United States</cop><pmid>9784564</pmid><doi>10.1128/IAI.66.11.5508-5514.1998</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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source American Society for Microbiology; MEDLINE; EZB-FREE-00999 freely available EZB journals; PubMed Central
subjects Animals
Cell Movement - genetics
Cell Movement - immunology
Female
Male
Mice
Mice, Inbred C57BL
Mice, Knockout
Mycobacterium avium
Mycobacterium avium - growth & development
Mycobacterium avium - immunology
Mycobacterium avium - pathogenicity
Neutrophils - immunology
Neutrophils - pathology
Receptors, Antigen, T-Cell, gamma-delta - genetics
Receptors, Antigen, T-Cell, gamma-delta - immunology
T-Lymphocyte Subsets - immunology
Tuberculosis - genetics
Tuberculosis - immunology
Tuberculosis - pathology
title Role of gamma delta T cells in immunopathology of pulmonary Mycobacterium avium infection in mice
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