Appeal No. 1999-2330
Application No. 08/219,200
Blazar is cited by the examiner for the proposition that the relevant art is
unpredictable and that any conclusion regarding efficacy of the CD28/B7 blockade on
altering the in vivo immune response should be interpreted in light of the type of
reagent infused.2 Answer, page 3. Blazar discloses that antiCD80 (B7-1) or anti-
CD86 (B7-2) antibodies were ineffective in preventing T cell CD8-mediated GVHD
lethality. The claimed invention, however, is directed to inhibiting T cell proliferation
comprising contacting CD28 positive T cells with a soluble B7 fusion protein so as to
bind CD28 on the CD28 positive T cells with the soluble B7 protein and thereby
inhibiting T cell proliferation. The examiner has not explained the relevance of Blazar's
prevention of T cell CD8-mediated GVHD lethality to the claimed inhibition of T cell
proliferation by binding CD28 on the CD28 positive T cells with the soluble B7 fusion
protein, in support of the position of lack of enablement of the claimed invention.
The appellants argue that the in vivo data in Lenschow describing CTLA4Ig, a
molecule homologous to CD28 and which binds to both human and murine B7,
supports enablement of the claimed invention. This would appear to be the same
CTLA4Ig which was described in Blazar as reducing the GVHD capacity of donor T
cells infused into fully allogenic recipients in vivo (Blazar, page 3250, column 2). Blazar
2 Appellants' invention relates to B7 (now referred to in the art as B7-1) fusion
protein.
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