Figure 3
Figure 3. Role of CCRL2 in OVA-induced airway inflammation. WT and CCRL2−/− mice were sensitized and challenged with OVA by aerosol. BAL was collected 24 hours after the last aerosol. (A) Differential cell counts in BAL. (B) Evaluation of T-cell subsets in BAL. (C) CCRL2 membrane expression by MHCII+ cells, eosinophils, and T lymphocytes by FACS analysis. Histograms represent CCRL2 mAb staining of cells from WT (filled curves) and CCRL2−/− mice (open curves). (D) Cytokine and chemokine levels in BAL. (E) Total and OVA-specific IgE in serum (left panel) and bronchial hyperreactivity (AHR) to methacholine (middle panel) and mucus production (right panel). Data are mean ± SEM of 5 (A) or 3 (B-E) representative experiments with 6-12 mice per group. * P < .05; ** P < .01.

Role of CCRL2 in OVA-induced airway inflammation. WT and CCRL2−/− mice were sensitized and challenged with OVA by aerosol. BAL was collected 24 hours after the last aerosol. (A) Differential cell counts in BAL. (B) Evaluation of T-cell subsets in BAL. (C) CCRL2 membrane expression by MHCII+ cells, eosinophils, and T lymphocytes by FACS analysis. Histograms represent CCRL2 mAb staining of cells from WT (filled curves) and CCRL2−/− mice (open curves). (D) Cytokine and chemokine levels in BAL. (E) Total and OVA-specific IgE in serum (left panel) and bronchial hyperreactivity (AHR) to methacholine (middle panel) and mucus production (right panel). Data are mean ± SEM of 5 (A) or 3 (B-E) representative experiments with 6-12 mice per group. * P < .05; ** P < .01.

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