Appeal No. 1999-2330
Application No. 08/219,200
also found that anti-CD80 (B7-1) and anti-CD86 (B7-2) antibodies3 were partially
effective in CD4+-mediated GVHD and that the combination of anti-CD80 and anti-
CD86 antibodies were effective in preventing GVHD lethality in murine experimental
models. Thus, arguably, Blazar would also lend some support to appellants' position
that contacting CD28 positive T cells with a soluble B7 fusion protein homolog inhibits
some degree of T cell proliferation.
Perrin, cited by the examiner, suggests that anti-CD80 (B7-1) attenuated the first
clinical disease episode of experimental allergic myeloencephalitis but not the relapses
and that CTLA4-Ig treatment resulted in attenuated disease, chiefly affecting
subsequent relapses. Perrin, page 21, column 1. While noting a difference in anti-
CD80 (B7-1) and CTLA4-Ig activity, Perrin would also reasonably support appellants'
position that contacting CD28 positive T cells with a soluble B7 fusion protein homolog
inhibits some degree of T cell proliferation.
Similarly, Yi-qun, Figure 1, evidences that anti-B7-1 provides some level of T-cell
proliferation inhibition. Yi-qun describes that CTLA4-Ig or anti-CD28 Fab inhibits
antigen specific T cell activation to the same extent as a combination of anti-B7-1 and
anti-B7-2 mAbs (Figure 3).
3 CD80 (B7-1) and CD86 (B7-2) bind to CD28 and CTLA-4 counter-receptors
on T cells. Blazar, page 3250, column 2.
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