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and Not Th1/Th2 Imbalance1
Departments of
*
Immunology and
Molecular & Experimental Medicine, The Scripps Research Institute, La Jolla, CA 92037; and
Department of Health and Environment, Molecular and Immunological Pathology, Linköping University, Linköping, Sweden
Imbalances of Th1- and Th2-type responses have been postulated to
be a predisposing factor for both humoral and cellular mediated
autoimmune diseases. To further define their roles in systemic
autoimmunity, IL-4 and IFN-
gene knockout mice were studied for
susceptibility to the prototypic Th2-mediated mercury-induced
autoimmunity. A predominant Th2-type response following
HgCl2 treatment of wild-type B10.S mice was confirmed
by the findings of a significant increase in splenic IL-4 and
hypergammaglobulinemia primarily of the IgG1 isotype, without an
increase in IFN- levels. Paradoxically, IL-4-deficient mice
developed the characteristic anti-nucleolar autoantibodies and
tissue deposition of immune complexes, while IFN--deficient mice had
very low autoantibody levels and essentially normal immunohistology.
Studies to define defects in Ab responses of IFN--deficient mice,
using the T-dependent Ag (4-hydroxy-3-nitrophenyl)acetyl, revealed an
attenuated IgG response to low and to a lesser extent high doses of
(4-hydroxy-3-nitrophenyl)acetyl-hemocyanin, but maintenance of affinity
maturation. These results indicate that Th1/Th2 imbalance does not
directly play a role in susceptibility to mercury-induced autoimmunity,
and suggest that the dependence on Th1-type responses in certain
autoimmune diseases is due to the requirement for IFN- for Ab
production to weakly antigenic self molecules.
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