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A peptide derived from a polyreactive monoclonal anti‐DNA natural antibody can modulate lupus development in (NZB×NZW)F 1 mice
Author(s) -
C Jouanne,
Stratis Avraméas,
Béatrice Payelle-Brogard
Publication year - 1999
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1999.00721.x
Subject(s) - antibody , idiotype , biology , monoclonal antibody , autoantibody , systemic lupus erythematosus , microbiology and biotechnology , immunology , population , monoclonal , medicine , disease , environmental health
In lupus‐prone (NZB×NZW)F 1 (B/W) mice, elevated levels of polyreactive autoantibodies bearing the D23 idiotype (Id), characteristic of natural antibodies, were detected before and after the appearance of pathological anti‐DNA antibodies. While these D23 Id + antibodies were able to regulate anti‐DNA antibodies in the early stage of the disease, we found that during disease evolution they had lost their normal ability to regulate anti‐DNA antibodies and furthermore could participate in the lupus‐like syndrome. To explore further the role of the D23 Id + antibodies, we injected young B/W mice with a peptide corresponding to the V H CDR3 region of the D23 monoclonal natural antibody (mNAb). High levels of monospecific antipeptide, as well as polyreactive antibodies, were induced. Among them, the most markedly enhanced antibody population was DNA‐reactive immunoglobulin G1 (IgG1). Compared with controls, these immunized mice had a delayed 50% survival rate and proteinuria developed later. Furthermore, IgG1 able to react with IgG2a anti‐DNA monoclonal antibodies derived from B/W mice were also produced after peptide immunization. Thus, a peptide corresponding to the CDR3 of the D23 mNAb antibody might play a role in the regulation of murine lupus.