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Receptor Deletion Prevents Autoantibody Production and Glomerulonephritis in Lupus-Prone (NZB x NZW)F1 Mice1
*
Institute of Anatomy of the University of Zürich, Zurich, Switzerland, and
Institute of Pathology of the University of Basel, Switzerland
(NZB x NZW)F1 female (BW) mice
spontaneously develop an autoimmune disease, characterized by the
production of autoantibodies (autoAbs) and glomerulonephritis, which
can be delayed by neutralizing IFN-
Abs and accelerated by IFN-
injections. To define the role of IFN- in the pathogenesis of
glomerulonephritis, we established a population of BW mice deficient in
IFN-R (BWR-/-) by repeated crossing; these mice were compared
with BWR+/+ and +/- littermates. Of the BWR+/+ and +/- mice,
50% showed immune complex glomerulonephritis with heavy proteinuria at
8 mo of age, while only 10% of the BWR-/- mice were affected at
14 mo. The serum concentration of anti-dsDNA and anti-histone
Abs was dramatically reduced in BWR-/- mice. The role of IFN-
in promoting class switch to IgG2a and IgG3 could not fully account for
the impaired production of anti-dsDNA in BWR-/- animals since,
IgM and IgG1 levels were also reduced. There was a high incidence of B
cell lymphoma in the BWR-/- mice, which might be related to the
suppression of autoAb production. Thus, the absence of
glomerulonephritis in BWR-/- mice is likely due to a dramatic yet
unexplained effect of the inactivation of IFN- signaling on autoAb
production.
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