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Granholm, N A; Cavallo, T (1994) Pathogenesis of early nephritis in lupus prone mice with a genetic accelerating (lpr) factor. Autoimmunity 17:195-202
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Granholm, N A; Cavallo, T (1992) Bacterial lipopolysaccharide causes variable deposits of diverse immunoglobulin isotypes in kidneys of lupus-prone mice. Lupus 1:255-61
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Cavallo, T; Granholm, N A (1991) Bacterial lipopolysaccharide induces long-lasting IgA deficiency concurrently with features of polyclonal B cell activation in normal and in lupus-prone mice. Clin Exp Immunol 84:134-8
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Cavallo, T; Granholm, N A (1990) Bacterial lipopolysaccharide transforms mesangial into proliferative lupus nephritis without interfering with processing of pathogenic immune complexes in NZB/W mice. Am J Pathol 137:971-8
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Cavallo, T; Granholm, N A (1990) Accelerated (proliferative) lupus nephritis. Am J Pathol 137:1549-51
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Granholm, N A; Cavallo, T (1990) Prolonged circulation of immune complexes due to various altered immune functions contributes to nephritis in MRL/lpr mice. Clin Exp Immunol 82:300-6
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Cavallo, T; Granholm, N A (1990) Lipopolysaccharide from gram-negative bacteria enhances polyclonal B cell activation and exacerbates nephritis in MRL/lpr mice. Clin Exp Immunol 82:515-21
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Cavallo, T; Granholm, N A (1990) Repeated exposure to bacterial lipopolysaccharide interferes with disposal of pathogenic immune complexes in mice. Clin Exp Immunol 79:253-9
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Granholm, N A; Cavallo, T (1990) Mechanism of localization of immune complexes in NZB/W mice with early nephritis. Autoimmunity 8:17-24
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Granholm, N A; Cavallo, T (1989) Defective disposal of immune complexes and polyclonal B cell activation persist long after exposure to bacterial lipopolysaccharide in mice. Lab Invest 61:504-8
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