Figure 2.

Prevention of adoptively transferred EAE by treatment with anti-CD44 and antiintegrin α₄ mAbs and amelioration of clinical signs by treatment with antiintegrin α_M mAbs. MBP peptide Ac1-11-specific T cells (5 × 10⁶/mouse, n = 5–15 mice/group) were transferred into naive (PL × SJL)F₁ mice after in vitro activation with antigen for 3 days. Mice in each group were treated twice (a) or over a longer time period (b) with mAbs IM7.8.1 (open circles), MEL-14 (closed circles), or PBS as control (open squares). Each mAb (250 μg) was given on the indicated days (marked by i). Mice were scored daily, and the mean EAE scores (± SEM) at each day after transfer are shown. The figure shows representative results from at least three experiments. In a second series of experiments (c and d), mice were treated with 250 μg of mAbs R1-2 (open circles), MEL-14 (closed circles), or PBS as control (open squares) on days as indicated by i. Mice were scored daily, and the mean EAE scores (± SEM) at each day after transfer are shown. The figures shows representative results from at least three experiments. (c) Continuous injections of antiintegrin α₄ mAb R1-2 prevent clinical signs of EAE as long as antibodies are administered. (d) During a mild course of EAE, continuous injections of R1-2 fully prevent clinical signs of EAE for at least 24 days. In the last series of experiments (e and f), mice were treated with antiintegrin α_M mAb M1/70 (e, full circles), 5C6 (f, full circles), or PBS as control (open squares). Clinical effects of treatment with these mAbs were moderate.