Skip to main content
Figure 2 | Respiratory Research

Figure 2

From: GITR signaling potentiates airway hyperresponsiveness by enhancing Th2 cell activity in a mouse model of asthma

Figure 2

GITR stimulation aggravates AHR and serum IgE responses in a mouse model of asthma. A. OVA-induced asthma model. Sensitization: i.p. injection of OVA/Alum (day 1, 7). Challenge: OVA inhalation (day 21, 24, 27). DTA-1 treatment: 1 hour before the first OVA challenge (day 21). AHR was measured before (day 18) and after (day 28) OVA challenges. BAL, blood and lungs were collected (day 28). One experiment is shown out of two independent experiments performed (giving similar results) with 6 mice per group in each experiment. B. Airway responsiveness to methacholine measured in OVA-sensitized mice before (O: control antibody; : DTA-1) and after (black circle: control antibody; black diamond: DTA-1) OVA challenges, expressed as enhanced pause (Penh). Bas: baseline Penh. *: P < 0.05 as compared to before OVA challenges and #: P < 0.05 as compared to control antibody treatment. C. ED50 values of the methacholine dose-response curves before (white bars) and after (black bars) OVA challenges. *: P < 0.05 as compared to before OVA challenges and #: P < 0.05 as compared to control antibody treatment. D. Numbers of leukocytes in the BAL after OVA inhalation in mice treated with control antibody (white bars) or DTA-1 (black bars). MNC: mononuclear cells; Eo: eosinophils; Neutro: neutrophils; Total: total cell counts. E. Serum levels of OVA-specific IgE in serum, before (white bars) and after (black bars) OVA challenges in DTA-1 or control antibody-treated mice. Results are expressed in experimental units (EU/ml). *: P < 0.05 as compared to before OVA challenges and #: P < 0.05 as compared to control antibody treatment.

Back to article page