Lack of high avidity IgM anti-ssDNA antibodies in cells from autoimmune-prone and autoimmune mice

Angela Panoskaltsis, Nicholas R.Stc Sinclair

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6 Scopus citations


Non-autoimmune prone CBA mice were compared with autoimmune prone NZB, NZW, and (NZB × NZW)F1 mice for the ability of their splenic cells to produce anti-ssDNA-forming cells spontaneously in vitro, measured in the plaque forming cell assay. The number of antibody forming cells was measured and the relative avidity of antibody produced determined using a plaque inhibition assay. Splenic lymphocytes from young animals of a non-autoimmune strain (CBAIJ) were shown to be capable of generating anti-ssDNA IgM antibody-forming cells in culture which displayed a higher avidity for antigen than that from autoimmune-prone or frankly autoimmune mice. Since an increased switching from IgM to IgG autoantibody production and defects in Fc-mediated signalling by IgG antibody have been identified in autoimmunity, we suggest that the metabolic block, normally in force in non-autoimmune-prone animals, accounts for this elevated avidity of IgM autoantibody.

Original languageEnglish (US)
Pages (from-to)381-389
Number of pages9
JournalInternational Immunology
Issue number5
StatePublished - May 1990

Bibliographical note

Funding Information:
This work was supported by the Arthritis Society of Canada, and is currently funded by the Medical Research Council of Canada (Cell Physiology) and by the Raymond C Raymond Foundation, which provided a studentship to one of us (A.P.). We wish to acknowledge the expert technical assistance of Luan Chau, Nicki Panoskaltsis, Rahbar Rahimpour, and Colin Anderson.


  • End product feedback
  • Immunoregulation
  • Regulation by Fc signals
  • Regulation of antibody responses
  • Self-non-self discrimination


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