Appeal No. 2006-0624 Page 10
Application No. 10/096,127
inhibitor. See Abstract and claim 2. Ashkenazi also teaches that “[p]roduction of
[gamma IFN] at inappropriate levels has been implicated in the pathogenesis of
several autoimmune and inflammatory diseases and in graft rejection . . . and
has also been found to cause exacerbation of autoimmune diseases such as
multiple sclerosis and psoriasis.” Col. 5, lines 1-8. Finally, Levinson teaches that
Crohn’s disease and psoriasis are TH1 related disorders, Col. 49, lines 28-35,
and that TH1 cells are know to secrete gamma IFN, Col. 2, lines 53-54.
We thus find that given the teachings of Queen that antibodies to IFN
gamma may be used to treat autoimmune diseases, the teachings of Ashkenazi I
and Ashkenazi II that IFN-gamma exacerbates psoriasis and that another auto-
immune disease, Crohn’s disease may be treated with antibodies to IFN gamma,
the references as combined would suggest to the ordinary artisan that psoriasis,
known to be an autoimmune disease, may be treated with antibodies to IFN
gamma. Levinson provides further motivation to combine the references by
teaching that Crohn’s disease and psoriasis are TH1 related disorders, and thus
the ordinary artisan would have been motivated to use the same therapy in each
disease. Thus we find, when the references are read for all they teach, they
suggest or teach to the ordinary artisan the treatment of the autoimmune disease
psoriasis with antibodies to IFN gamma. Moreover, we find that the ordinary
artisan would have been motivated to PEGylate the antibodies to IFN gamma
because Tomassi teaches the advantages of PEGylating antibodies, such as low
binding capacity for cell surface Fc receptors, reduced immunogenicity, good
storage stability, and non-toxicity. The ordinary artisan would have been
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