Appeal No. 2000-1783 Page 8
Application No. 08/817,719
a non-IgE related disorder.@ Brief, page 7. Further, appellant argues that A[t]here is no
evidence in the literature to suggest that antigen-specific IgE plays any role in either
triggering or perpetuating autoimmunity.@ Id., page 8. On this record, we agree with
appellant that A[t]he use of antibodies to block [antigen]-induced IgE production,
therefore, has no relevance whatsoever to the claimed method.@ Id.
Bansal describes elevated levels of sCD23 in patients with rheumatoid arthritis
(RA) and suggests that A[i]t is possible that features of autoantibody production, B cell
hyperactivity and hypergammaglobulinaemia (increased levels of circulating γ-globulins)
observed in RA are mediated by high levels of sCD23.@ Page 282.
Armant teaches that sCD23 has multiple IgE-independent biological activities
including costimulation of IL-2 or IL-12-induced IFN-γ production and direct triggering of
TNF-α, IL-1α, IL-1β, and IL-6 release by peripheral blood mononuclear cells. Page
1005. Armant suggests that AsCD23 is a proinflammatory cytokine that, in addition,
may play an important role in the control of the immune response via the enhancement
of IFN-γ production.@ Abstract.
The examiner concludes that A[o]ne with ordinary skill in the art would have been
motivated to treat arthritis by administering anti-CD23 antibodies because [Bansal
teaches] that soluble CD23 levels are elevated in rheumatoid arthritis and that
hypergammaglobulinaemia . . . may be mediated by high levels of soluble CD23 with
the expectation that the administration of anti-CD23 would downregulate the
hypergammaglobulinaemia . . . in rheumatoid arthritis patients and downregulate the
inflammatory process in autoimmune diseases by inhibiting the sCD23 induced release
of mediators of the inflammatory process as taught by Armant.@ Answer, page 7.
However, appellant cites Bansal as evidence that the nature of the relationship
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