CD11c+ CD103+ cells of Mycobacterium tuberculosis‐infected C57BL/6 but not of BALB/c mice induce a high frequency of interferon‐γ‐ or interleukin‐17‐producing CD4+ cells
The magnitude of the cellular adaptive immune response is critical for the control of Mycobacterium tuberculosis infection in the chronic phase. In addition, the genetic background is equally important for resistance or susceptibility to tuberculosis. In this study, we addressed whether lung populations of dendritic cells, obtained from genetically different hosts, would play a role in the magnitude and function of CD 4 + populations generated after M. tuberculosis infection. Thirty days post‐infection, C57 BL /6 mice, which generate a stronger interferon‐ γ ( IFN ‐ γ )‐mediated immune response than BALB /c mice, exhibited a higher number and frequency of lung CD 11c + CD 11b − CD 103 + cells compared with BALB /c mice, which exhibited a high frequency of lung CD 11c + CD 11b + CD 103 − cells. CD 11c + CD 11b − CD 103 + cells, purified from lungs of infected C57 BL /6 mice, but not from infected BALB /c mice, induced a higher frequency of IFN ‐ γ ‐producing or interleukin‐17 ( IL ‐17)‐producing CD 4 + cells. Moreover, CD 4 + cells also arrive at the lung of C57 BL /6 mice faster than in BALB /c mice. This pattern of immune response seems to be associated with higher gene expression for CCL 4, CCL 19, CCL 20 and CCR 5 in the lungs of infected C57 BL /6 mice compared with infected BALB /c mice. The results described here show that the magnitude of IFN ‐ γ ‐producing or IL ‐17‐producing CD 4 + cells is dependent on CD 11c + CD 11b − CD 103 + cells, and this pattern of immune response is directly associated with the host genetic background. Therefore, differences in the genetic background contribute to the identification of immunological biomarkers that can be used to design human assays to predict progression of M. tuberculosis infection..
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2015 |
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| Erschienen: |
2015 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:144 |
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| Enthalten in: |
Immunology - 144(2015), 4, Seite 574-586 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Sérgio, Cássia A [VerfasserIn] |
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| Links: |
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| RVK: |
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| doi: |
10.1111/imm.12411 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| 245 | 1 | 0 | |a CD11c+ CD103+ cells of Mycobacterium tuberculosis‐infected C57BL/6 but not of BALB/c mice induce a high frequency of interferon‐γ‐ or interleukin‐17‐producing CD4+ cells |
| 264 | 1 | |c 2015 | |
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| 520 | |a The magnitude of the cellular adaptive immune response is critical for the control of Mycobacterium tuberculosis infection in the chronic phase. In addition, the genetic background is equally important for resistance or susceptibility to tuberculosis. In this study, we addressed whether lung populations of dendritic cells, obtained from genetically different hosts, would play a role in the magnitude and function of CD 4 + populations generated after M. tuberculosis infection. Thirty days post‐infection, C57 BL /6 mice, which generate a stronger interferon‐ γ ( IFN ‐ γ )‐mediated immune response than BALB /c mice, exhibited a higher number and frequency of lung CD 11c + CD 11b − CD 103 + cells compared with BALB /c mice, which exhibited a high frequency of lung CD 11c + CD 11b + CD 103 − cells. CD 11c + CD 11b − CD 103 + cells, purified from lungs of infected C57 BL /6 mice, but not from infected BALB /c mice, induced a higher frequency of IFN ‐ γ ‐producing or interleukin‐17 ( IL ‐17)‐producing CD 4 + cells. Moreover, CD 4 + cells also arrive at the lung of C57 BL /6 mice faster than in BALB /c mice. This pattern of immune response seems to be associated with higher gene expression for CCL 4, CCL 19, CCL 20 and CCR 5 in the lungs of infected C57 BL /6 mice compared with infected BALB /c mice. The results described here show that the magnitude of IFN ‐ γ ‐producing or IL ‐17‐producing CD 4 + cells is dependent on CD 11c + CD 11b − CD 103 + cells, and this pattern of immune response is directly associated with the host genetic background. Therefore, differences in the genetic background contribute to the identification of immunological biomarkers that can be used to design human assays to predict progression of M. tuberculosis infection. | ||
| 540 | |a Nutzungsrecht: © 2014 John Wiley & Sons Ltd | ||
| 540 | |a © 2014 John Wiley & Sons Ltd. | ||
| 650 | 4 | |a helper type 1 cells | |
| 650 | 4 | |a tuberculosis | |
| 650 | 4 | |a dendritic cells | |
| 650 | 4 | |a genetic background | |
| 650 | 4 | |a helper type 17 cells | |
| 650 | 4 | |a Tuberculosis, Pulmonary - genetics | |
| 650 | 4 | |a Integrin alpha Chains - immunology | |
| 650 | 4 | |a CD8-Positive T-Lymphocytes - microbiology | |
| 650 | 4 | |a Th17 Cells - metabolism | |
| 650 | 4 | |a CD8-Positive T-Lymphocytes - metabolism | |
| 650 | 4 | |a Mycobacterium tuberculosis - immunology | |
| 650 | 4 | |a Dendritic Cells - metabolism | |
| 650 | 4 | |a Antigens, CD11b - metabolism | |
| 650 | 4 | |a Antigens, CD11c - immunology | |
| 650 | 4 | |a Dendritic Cells - immunology | |
| 650 | 4 | |a Tuberculosis, Pulmonary - immunology | |
| 650 | 4 | |a Lung - metabolism | |
| 650 | 4 | |a Dendritic Cells - microbiology | |
| 650 | 4 | |a Antigens, CD11b - immunology | |
| 650 | 4 | |a Integrin alpha Chains - metabolism | |
| 650 | 4 | |a Mycobacterium tuberculosis - pathogenicity | |
| 650 | 4 | |a Antigens, CD11c - metabolism | |
| 650 | 4 | |a CD8-Positive T-Lymphocytes - immunology | |
| 650 | 4 | |a Th17 Cells - immunology | |
| 650 | 4 | |a Interferon-gamma - immunology | |
| 650 | 4 | |a Tuberculosis, Pulmonary - metabolism | |
| 650 | 4 | |a Lung - immunology | |
| 650 | 4 | |a Interferon-gamma - metabolism | |
| 650 | 4 | |a Interleukin-17 - immunology | |
| 650 | 4 | |a Antigens, CD - immunology | |
| 650 | 4 | |a Interleukin-17 - metabolism | |
| 650 | 4 | |a Antigens, CD - metabolism | |
| 650 | 4 | |a Th17 Cells - microbiology | |
| 650 | 4 | |a Lung - microbiology | |
| 650 | 4 | |a Tuberculosis, Pulmonary - microbiology | |
| 700 | 1 | |a Bertolini, Thais B |4 oth | |
| 700 | 1 | |a Gembre, Ana Flávia |4 oth | |
| 700 | 1 | |a Prado, Rafael Q |4 oth | |
| 700 | 1 | |a Bonato, Vânia L. D |4 oth | |
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| 856 | 4 | 1 | |u http://dx.doi.org/10.1111/imm.12411 |3 Volltext |
| 856 | 4 | 2 | |u http://onlinelibrary.wiley.com/doi/10.1111/imm.12411/abstract |
| 856 | 4 | 2 | |u http://www.ncbi.nlm.nih.gov/pubmed/25322675 |
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