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Antibody
Institutes of Microbiology (F.N.) and Internal Medicine, Infectious Diseases, and Immunopathology (P.M.), University of Milan, Milan; and the Institutes of Internal Medicine, Endocrinology, and Metabolism (F.N., M.L.), Microbiology (P.Z., R.D.M.), and Anatomo-Pathology (G.M., S.G.), University of Catania, Catania, Italy; and Human Genome Sciences (G.G.), Rockville, Maryland 20850
Address all correspondence and requests for reprints to: Ferdinando Nicoletti, M.D., Via Luigi Sturzo n.3, 95021 Cannizzaro, Catania, Italy.
The role of endogenous interferon-
(IFN) in the development
of insulin-dependent diabetes mellitus (IDDM) in diabetes-prone BB rats
was evaluated. Several groups of these animals were treated under
different experimental conditions with a purified polyclonal antibody
(Ab), antirat IFN. The results show that when administered at doses
of 100 or 200 µg/week from the 30/33th until the 105th day of age,
the anti-IFN Ab reversibly reduced the incidence of IDDM compared to
that in control rats treated with either irrelevant rabbit IgG or PBS.
Moreover, when given up to the 105th day of age, these doses of
anti-IFN Abs exerted comparable preventive effects regardless of
whether application started as early as within 24 h after birth or
at the end of the prediabetic period (e.g. 70/75 days).
In contrast, under none of the above experimental conditions did larger
doses of anti-IFN Ab (500 µg or 1 mg/week) exert antidiabetogenic
effects in the BB rats. Apparently, this was due to the exuberant
production of neutralizing Abs elicited by the large amount of the
xenogeneic Ab injected. At histoimmunological analyses, the BB rats
treated with 200 µg/week anti-IFN Abs from 30–80 days of age
exhibited a milder insulitic process along with diminished spleen
frequency of activated lymphoid cells (MHC class II and interleukin-2
receptor positive). Taken together, these results provide further
in vivo evidence for the central pathogenic role of
IFN in BB rat IDDM and anticipate the usefulness of specific IFN
inhibitors in the prevention of the disease in the clinical setting.
Defining novel and less immunogenic forms of specific IFN inhibitors
than xenogeneic Abs is important for improving the efficiency of
anti-IFN-oriented approaches.
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