Presentation is loading. Please wait.

Presentation is loading. Please wait.

Dendritic cells and alveolar macrophages mediate IL-13–induced airway inflammation and chemokine production  Margaret Crapster-Pregont, BS, Janice Yeo,

Published byΘεοφάνια Αναγνώστου Modified over 6 years ago

Similar presentations

Presentation on theme: "Dendritic cells and alveolar macrophages mediate IL-13–induced airway inflammation and chemokine production  Margaret Crapster-Pregont, BS, Janice Yeo,"— Presentation transcript:

1 Dendritic cells and alveolar macrophages mediate IL-13–induced airway inflammation and chemokine production  Margaret Crapster-Pregont, BS, Janice Yeo, BS, Raquel L. Sanchez, BS, Douglas A. Kuperman, PhD  Journal of Allergy and Clinical Immunology  Volume 129, Issue 6, Pages e3 (June 2012) DOI: /j.jaci Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2 Fig 1 IFN-γ inhibits IL-13–induced airway inflammation and mucus metaplasia. A, Cell types and numbers retrieved in BAL fluid from PBS-treated (open bars), IL-13–treated (black bars), and IL-13/IFN-γ–treated mice (shaded bars). Eos, Eosinophils; Lymphs, lymphocytes; Macs, macrophages. B-D, Representative images of mucus metaplasia in PBS-treated (Fig 1, B), IL-13–treated (Fig 1, C), and IL-13/IFN-γ–treated (Fig 1, D) wild-type mice (n = 6 mice per group). ∗P ≤ .05 versus PBS. †P ≤ .05 versus IL-13. Journal of Allergy and Clinical Immunology  , e3DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3 Fig 2 IFN-γ inhibits a subset of IL-13–induced chemokines. Levels of CCL11 (A), CCL24 (B), CCL22 (C), CCL17 (D), CCL8 (E), and CCL2 (F) in BAL fluid from PBS-treated (open bars), IL-13–treated (black bars), and IL-13/IFN-γ–treated wild-type mice (shaded bars) are shown (n = 6 mice per group). ∗P ≤ .05 versus PBS. †P ≤ .05 versus IL-13. Journal of Allergy and Clinical Immunology  , e3DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4 Fig 3 Dendritic cells and alveolar macrophages coexpress IL-13R and IFN-γR subunits. Numbers of IL-4Rα+/IFN-γRα+ cells (A) and their proportions that express CD11b and CD11c (B) from the lungs of PBS-treated (open bars) and IL-13–treated (shaded bars) wild-type mice in MHC-II+ cell–depleted flow-through and MHC-II+ cell–enriched bound fractions are shown (n = 6 mice per group). ∗P ≤ .05 versus flow-through. Journal of Allergy and Clinical Immunology  , e3DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

5 Fig 4 Dendritic cell and alveolar macrophage targeting protects mice from IL-13-induced airway inflammation and chemokine production. A, Gene expression levels of DC-SIGN in whole lung. GAPDH, Glyceraldehyde-3-phosphate dehydrogenase. B-D, Numbers of alveolar macrophages (Macs; Fig 4, B); numbers of eosinophils (Eos), lymphocytes (Lymphs), and neutrophils (Neuts; Fig 4, C); and levels of chemokines (Fig 4, D) in BAL fluid from CD11c-DTR mice (n = 6 mice per group). ∗P ≤ .05 versus PBS. †P ≤ .05 versus IL-13. Journal of Allergy and Clinical Immunology  , e3DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

6 Fig 5 Dendritic cell targeting protects mice from IL-13–induced airway inflammation and a subset of IL-13–induced chemokines. A, Gene expression levels of DC-SIGN in whole lung. GAPDH, Glyceraldehyde-3-phosphate dehydrogenase. B-D, Numbers of alveolar macrophages (Macs; Fig 5, B); numbers of eosinophils (Eos), lymphocytes (Lymphs), and neutrophils (Neuts; Fig 5, C); and levels of chemokines (Fig 5, D) in BAL fluid from CD11b-DTR mice (n = 6 mice per group). ∗P ≤ .05 versus PBS/PBS. †P ≤ .05 versus PBS/IL-13. Journal of Allergy and Clinical Immunology  , e3DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

7 Fig E1 Effects of DT treatment on baseline levels of dendritic cells and macrophages in whole lung. A and B, Percentages of CD11b+/CD11c+ cells (Fig E1, A) and CD204+/(F4/80)+ cells (Fig E1, B) detected in whole lungs of CD11c-DTR mice. C and D, Percentages of CD11b+/CD11c+ cells (Fig E1, C) and CD204+/(F4/80)+ cells (Fig E1, D) detected in whole lungs of CD11b-DTR mice. Representative plots are shown from 4 mice per group. Journal of Allergy and Clinical Immunology  , e3DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

8 Fig E2 Dendritic cell and alveolar macrophage targeting does not protect mice from IL-13–induced AHR and mucus metaplasia. AHR to acetylcholine injection (A) and representative images showing mucus metaplasia (B) in the lungs of CD11c-DTR mice (n = 6 mice per group.) ∗P ≤ .05 versus PBS. Journal of Allergy and Clinical Immunology  , e3DOI: ( /j.jaci ) Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

Download ppt "Dendritic cells and alveolar macrophages mediate IL-13–induced airway inflammation and chemokine production  Margaret Crapster-Pregont, BS, Janice Yeo,"

Similar presentations

Doina M. Racila, MD, Joel N. Kline, MD, MSc 

Doina M. Racila, MD, Joel N. Kline, MD, MSc 
Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides  Rachael A. Mintz-Cole, PhD, Eric.

Surface availability of beta-glucans is critical determinant of host immune response to Cladosporium cladosporioides  Rachael A. Mintz-Cole, PhD, Eric.
Glucagon-like peptide 1 receptor signaling attenuates respiratory syncytial virus– induced type 2 responses and immunopathology  Melissa H. Bloodworth,

Glucagon-like peptide 1 receptor signaling attenuates respiratory syncytial virus– induced type 2 responses and immunopathology  Melissa H. Bloodworth,
Maternal immune response to helminth infection during pregnancy determines offspring susceptibility to allergic airway inflammation  Kathrin Straubinger,

Maternal immune response to helminth infection during pregnancy determines offspring susceptibility to allergic airway inflammation  Kathrin Straubinger,
IL-4 induces IL-13–independent allergic airway inflammation

IL-4 induces IL-13–independent allergic airway inflammation
Weiguo Chen, PhD, Umasundari Sivaprasad, PhD, Aaron M

Weiguo Chen, PhD, Umasundari Sivaprasad, PhD, Aaron M
Weiguo Chen, MD, PhD, Yasuhiro Tabata, MD, PhD, Aaron M

Weiguo Chen, MD, PhD, Yasuhiro Tabata, MD, PhD, Aaron M
Let-7 microRNA–mediated regulation of IL-13 and allergic airway inflammation  Manish Kumar, MSc, Tanveer Ahmad, MSc, Amit Sharma, PhD, Ulaganathan Mabalirajan,

Let-7 microRNA–mediated regulation of IL-13 and allergic airway inflammation  Manish Kumar, MSc, Tanveer Ahmad, MSc, Amit Sharma, PhD, Ulaganathan Mabalirajan,
Umasundari Sivaprasad, PhD, David J. Askew, PhD, Mark B

Umasundari Sivaprasad, PhD, David J. Askew, PhD, Mark B
The role of viruses in acute exacerbations of asthma

The role of viruses in acute exacerbations of asthma
Virus-specific IgE enhances airway responsiveness on reinfection with respiratory syncytial virus in newborn mice  Azzeddine Dakhama, PhD, Young-Mok Lee,

Virus-specific IgE enhances airway responsiveness on reinfection with respiratory syncytial virus in newborn mice  Azzeddine Dakhama, PhD, Young-Mok Lee,
Innate IL-13–producing nuocytes arise during allergic lung inflammation and contribute to airways hyperreactivity  Jillian L. Barlow, PhD, Agustin Bellosi,

Innate IL-13–producing nuocytes arise during allergic lung inflammation and contribute to airways hyperreactivity  Jillian L. Barlow, PhD, Agustin Bellosi,
Expression of IL-4 receptor α on smooth muscle cells is not necessary for development of experimental allergic asthma  Frank Kirstein, PhD, William G.C.

Expression of IL-4 receptor α on smooth muscle cells is not necessary for development of experimental allergic asthma  Frank Kirstein, PhD, William G.C.
Frank Kirstein, PhD, Natalie E

Frank Kirstein, PhD, Natalie E
Maternal house dust mite exposure during pregnancy enhances severity of house dust mite–induced asthma in murine offspring  Phoebe K. Richgels, MS, Amnah.

Maternal house dust mite exposure during pregnancy enhances severity of house dust mite–induced asthma in murine offspring  Phoebe K. Richgels, MS, Amnah.
Lack of autophagy induces steroid-resistant airway inflammation

Lack of autophagy induces steroid-resistant airway inflammation
Nazanin Farhadi, MSc, Laura Lambert, BA, Chiara Triulzi, PhD, Peter J

Nazanin Farhadi, MSc, Laura Lambert, BA, Chiara Triulzi, PhD, Peter J
Compartmentalized chemokine-dependent regulatory T-cell inhibition of allergic pulmonary inflammation  Roshi Afshar, PhD, James P. Strassner, BS, Edward.

Compartmentalized chemokine-dependent regulatory T-cell inhibition of allergic pulmonary inflammation  Roshi Afshar, PhD, James P. Strassner, BS, Edward.
IL-33 induces innate lymphoid cell–mediated airway inflammation by activating mammalian target of rapamycin  Robert J. Salmond, PhD, Ananda S. Mirchandani,

IL-33 induces innate lymphoid cell–mediated airway inflammation by activating mammalian target of rapamycin  Robert J. Salmond, PhD, Ananda S. Mirchandani,
Antigen-specific effector CD8 T cells regulate allergic responses via IFN-γ and dendritic cell function  Yafang Tang, BSc, Shou Ping Guan, BSc, Benson.

Antigen-specific effector CD8 T cells regulate allergic responses via IFN-γ and dendritic cell function  Yafang Tang, BSc, Shou Ping Guan, BSc, Benson.

Similar presentations

Ads by Google