Anti-Human CD11A Recombinant Antibody (Efalizumab) (CAT#: TAB-024)

Figure 1 Inhibition of ex vivo anti-CD3-, anti-CD2, and anti-CD3/anti-CD28-induced activation of circulating T cells in efalizumab-treated psoriatic patients.

(a) CD69 levels (MFI) on T cells stimulated ex vivo with increasing concentrations of anti-CD3 antibody at different time points during (up to day 84) and after efalizumab treatment. (b) CD11a expression on unstimulated T cells to assess CD11a saturation throughout the treatment period (up to day 84) and upon efalizumab washout. (c) A set of representative dot plots illustrates that efalizumab treatment by week 2 inhibits T-cell activation (CD69 MFI) induced by all three cell-surface stimuli, although less so with anti-CD3/CD28 stimuli. (d) Mean percent change in CD69 MFI with various stimuli, in patients on efalizumab treatment compared with baseline. *Indicates P<0.05. (e) Mean change in CD69 MFI with PMA/ionomycin stimulation on days 0 and 14 of efalizumab treatment showing no difference in T-cell activation by this stimuli. (f) A representative CD69 histogram for PMA/ionomycin stimulation illustrates that efalizumab treatment (black line, day 14) has no effect on PMA/ionomycin-mediated upregulation of CD69, as compared with baseline (gray line, day 0). Dotted line corresponds to the baseline CD69 expression on unstimulated T cells.

Guttman-Yassky, E., Vugmeyster, Y., Lowes, M. A., Chamian, F., Kikuchi, T., Kagen, M.,... & Dummer, W. (2008). Blockade of CD11a by efalizumab in psoriasis patients induces a unique state of T-cell hyporesponsiveness. Journal of Investigative Dermatology, 128(5), 1182-1191.

Figure 2 Inhibition of ex vivo anti-CD3- and anti-CD2-induced IFN-γ production by T cells in efalizumab-treated psoriatic patients.

(a) T cells' ability to synthesize IFN-γ in response to anti-CD3 antibody after 2 weeks of efalizumab treatment is highly diminished (P<0.02). (b) Representative FACS data for three different T-cell activation stimuli, anti-CD3, anti-CD2, PMA/ionomycin, at baseline and week 2 treatment with efalizumab. Efalizumab affected T-cell ability to produce IFN-γ in response to CD3 ligation but not to PMA/ionomycin stimulation. (c) Percent change in IFN-γ+ T cells in all study patients. Black lines correspond to individual patients.

Guttman-Yassky, E., Vugmeyster, Y., Lowes, M. A., Chamian, F., Kikuchi, T., Kagen, M.,... & Dummer, W. (2008). Blockade of CD11a by efalizumab in psoriasis patients induces a unique state of T-cell hyporesponsiveness. Journal of Investigative Dermatology, 128(5), 1182-1191.