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Regulation of allergic airway inflammation by class I–restricted allergen presentation and CD8 T-cell infiltration  James W. Wells, PhD, Christopher J.

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Presentation on theme: "Regulation of allergic airway inflammation by class I–restricted allergen presentation and CD8 T-cell infiltration  James W. Wells, PhD, Christopher J."— Presentation transcript:

1 Regulation of allergic airway inflammation by class I–restricted allergen presentation and CD8 T-cell infiltration  James W. Wells, PhD, Christopher J. Cowled, BS, Angela Giorgini, PhD, David M. Kemeny, PhD, Alistair Noble, PhD  Journal of Allergy and Clinical Immunology  Volume 119, Issue 1, Pages (January 2007) DOI: /j.jaci Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2 Fig 1 A, Class I/II presentation by lung/splenic DCs to OT-I CD8 or CD4 OT-II cells. B, CFSE dilution in gated Vα2+Vβ5+ CD4 or CD8 T cells from mediastinal lymph nodes after primary intranasal challenge. C, Percentage of Vα2+Vβ5+ CD4/CD8 OVA-specific cells in BAL fluid and lymph nodes after secondary challenge. ∗P < .05. Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3 Fig 2 OVA-specific TC1 cells are recruited to the lungs. OT-I CD8 cells were transferred to C57BL/6 mice, followed by intranasal OVA (days 1 and 4). A, OVA-specific CD8 cells in lung cell extracts determined by using H-2Kb/SIINFEKL pentamers. B, IFN-γ production in response to peptide determined by means of intracellular staining. C, BAL T-cell intracellular cytokine staining. Figures indicate percentages of the CD8+ cell population. Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4 Fig 3 IgE inhibition by intranasally primed OT-I CD8 cells. OT-I CD8 cells were transferred intravenously to C57BL/6 mice, followed by 2 intranasal administrations of PBS (squares) or OVA (circles) on days 1 and 4. Mice were immunized with OVA/alum on day 6 and subsequently bled every 4 to 7 days from the tail. Serum OVA-specific IgE levels were measured in arbitrary units by means of ELISA. ∗P < .05; ∗∗∗P < .001. Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

5 Fig 4 Respiratory DCs cross-present inhaled allergen and prime TC1 but not TH1 differentiation. A, Mice were challenged with OVA intranasally. Twenty-four hours later, DCs were purified from indicated tissues and cultured with OT-I CD8 cells, and proliferation was assessed. B, Lung/splenic DCs from naive mice were cultured with OT-I CD8/OT-II CD4 cells plus OVA for 6 days and restimulated for cytokines. ∗P < .05. Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

6 Fig 5 OVA-specific TC1 cells suppress allergic airway inflammation. OVA-sensitized mice were injected with unprimed OT-I CD8 cells or OT-II CD4 cells and challenged as shown in panel A. B, Percentage of OVA-specific CD8 cells and peptide-induced IFN-γ. C, IL-12/anti–IL-12 was administered alongside 6-day OVA challenge, and inflammatory cells in BAL fluid were measured. D, Effect of transferred OT-I/OT-II cells on BAL cytokines. ∗P < .05; ∗∗P < .005. Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci ) Copyright © 2007 American Academy of Allergy, Asthma & Immunology Terms and Conditions

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