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. 2014 Oct 21;44(11):1386–1398. doi: 10.1111/cea.12395

Figure 5.

Figure 5

Blockade of γδT cells during HDM-induced allergic airway disease promotes eosinophilic lung infiltration and airway remodelling. TH2 and γδT cells are increased in the BALF (a) and lung (b) following continuous challenge with 25 μg HDM. Following establishment of allergic airway disease, female BALB/c mice were administered 100 μL of 200 μg/mL anti-TCRδ blocking mAb (or hamster Ig control) i.v. (twice weekly) and disease parameters assessed at the end of week 5 (c). Lung tissue eosinophils from each group were quantified by differential counting of Wright-Gimsa-stained cytospins (d). Lung IL-4 (e), IL-5 (f), IL-13 (g) and serum total IgE (h) were measured by ELISA. Airway resistance in response to 30 mg/mL methacholine challenge (i). Detection of biologically active TGF-β activity was measured in lung tissue homogenate using a SEAP reporter bioassay (j). Quantitative analysis of Sirius Red-stained lung sections for subepithelial peribronchiolar collagen density (k). Peribronchiolar smooth muscle thickness (l). Values are expressed as mean ± SEM, n = 8–12 mice per group. *P < 0.05 in comparison with PBS controls, †P < 0.05 in comparison with HDM Ig controls (Mann–Whitney U-test).