Fig. 5: Effect of an anti-CD52 antibody on lung function and inflammation in mice.

a The experimental protocol for testing the effect of a mouse anti-CD52 (αCD52) antibody on pulmonary function and inflammation was designed to mimic the clinical protocol used to treat multiple sclerosis patients with a human αCD52 antibody (alemtuzumab). Female BALB/cByJ mice were immunized on day 1 with 100 µg of house dust mite (HDM) in 2 mg of aluminum hydroxide (alum) by intraperitoneal (i.p.) injection. On day 7, mice were intraperitoneally administered with 500 µg of either the αCD52 antibody (Group 1, red bars; n = 8) or isotype control antibody (Group 2, black bars; n = 9), or phosphate-buffered saline (PBS) (Group 3, white bars; n = 4). On days 8, 9 and 10, mice in Groups 1 and 2 were intravenously (i.v.) administered 250 µg of the αCD52 antibody or isotype control antibody, respectively, and simultaneously challenged intranasally (i.n.) with 50 µg HDM. Mice in Group 3 were only challenged with PBS i.n. on days 8, 9, and 10. On day 11, lung function was measured by invasive plethysmography and leukocyte counts were determined in bronchial alveolar lavage (BAL) by flow cytometry. Compared to HDM-exposed mice receiving the control isotype antibody, HDM-exposed mice administered the αCD52 antibody had significantly reduced lung resistance (b) and improved dynamic compliance (c). HDM-exposed mice receiving the αCD52 antibody also had significantly decreased numbers of total cells, eosinophils, T cells, and neutrophils in BAL (d) as well as decreased inflammation and thickness of the airway epithelium (e) compared to HDM-exposed mice injected with the isotype control antibody. Scale bars equal 50 μm. Data are shown as mean ± SE and derived from two independent experiments yielding similar results. Two-tailed unpaired Student’s t-tests were used to determine statistically significant differences between groups. *P < 0.05, **P < 0.005; ***P < 0.0005; ****P < 0.0001.