These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Anti-idiotypes against autoantibodies in normal immunoglobulins: evidence for network regulation of human autoimmune responses.
    Author: Rossi F, Dietrich G, Kazatchkine MD.
    Journal: Immunol Rev; 1989 Aug; 110():135-49. PubMed ID: 2676846.
    Abstract:
    This manuscript summarizes observations indicating that anti-idiotypes against human autoantibodies may be found in sera from patients recovered from autoimmune disease and in pooled normal polyspecific immunoglobulins (IVIg). The evidence that IVIg contain anti-idiotypes against autoantibodies includes: 1) inhibition by F(ab)2 from IVIg of the binding of F(ab)2 autoantibodies to their autoantigens; 2) specific retention of autoantibodies upon affinity chromatography of F(ab)2 fragments containing autoantibody activity on Sepharose-bound F(ab)2 from IVIg; 3) lack of detection of anti-allotypes and lack of significant anti-Fc activity in IVIg; 4) specific competitive displacement by polyclonal heterologous F(ab)2 anti-idiotypes of the binding of IVIg to affinity-purified F(ab)2 autoantibodies. The high number of donors contributing to IVIg endows the preparations with anti-idiotypic specificities that may not necessarily be detectable in plasma from single healthy individuals. Our observations of the presence in IVIg of anti-idiotypes against pathogenic autoantibodies and against IgG and IgM autoantibodies found in low amounts in normal sera supports the concept of a functional network regulating expression of autoimmunity in humans. We suggest that IVIg may be efficient in selected autoimmune diseases by providing a source of anti-idiotypes with a wide range of specificities brought as interconnected antibody species that may conpensate for altered connectivity of the immune network of patients with autoimmune diseases.
    [Abstract] [Full Text] [Related] [New Search]