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The role of the idiotypic network in the induction of experimental systemic lupus erythematosus
Author(s) -
Mozes Edna,
Brocke Stefan,
Shoenfeld Yehuda,
Mendlovic Shlomo
Publication year - 1989
Publication title -
journal of cellular biochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.028
H-Index - 165
eISSN - 1097-4644
pISSN - 0730-2312
DOI - 10.1002/jcb.240400206
Subject(s) - antibody , idiotype , immunology , mesangium , autoantibody , immune complex , monoclonal antibody , systemic lupus erythematosus , immune system , titer , leukopenia , immunization , medicine , serology , kidney , pathology , glomerulonephritis , disease , endocrinology , chemotherapy
Systemic lupus erythematosus (SLE) has been induced in C3H.SW mice by their immunization with a human monoclonal anti‐DNA antibody that bears a common idiotype‐16/6 Id. Following immunization, high levels of murine anti‐16/6 and anti‐anti‐16/6 antibodies were detected in the sera of the immunized mice. Elevated titers of autoantibodies reacting with ssDNA, dsDNA, poly(I), poly(G), RNP, Ro, and La were also observed. The serological findings were associated with significant proteinuria, leukopenia, and elevated erythrocyte sedimentation rate. Immune complex deposition in the glomerular mesangium and sclerosis of the glomeruli were demonstrated. To study whether or not anti‐idiotypic antibodies are involved in the induction of the disease, a murine monoclonal antibody against the 16/6 Id was prepared and injected into C3H.SW mice. The anti‐16/6 Id antibody induced experimental SLE similarly to the 16/6 Id with an accelerated kidney pathology. A study performed on different mouse strains indicated that the susceptibility to the induction of SLE by the 16/6 Id is strain dependent and directly correlates to their ability to produce anti‐16/6 Id specific antibodies.