Effect of xid on autoimmune C3H-gld/gld mice

Michael F Seldin, J. Patton Reeves, Curtis L. Scribner, John B. Roths, Wendy F. Davidson, Herbert C. Morse, Alfred D. Steinberg

Research output: Contribution to journalArticlepeer-review

18 Scopus citations


The xid gene was introduced into C3H-gld/gld mice to determine its effects on the development of autoimmune disease. C3H-gld/gld.xid mice were compared with C3H-gld/gld mice for the development of lymphadenopathy, surface phenotype of lymph node (LN) cells, c-myb oncogene RNA production, serum immunoglobulin (Ig) levels, and autoantibody production. In addition, C3H-gld/gld and C3H-lpr/lpr mice were examined for serum Ig and autoantibody levels. The results showed that the xid gene had no effect on either the development of the severe lymphadenopathy characteristic of C3H-gld/gld mice or the phenotype of the Ly-2-, L3T4-, Ly-5(B220)+ T-cell subset that is expanded in the LN and spleens of these mice. Similarly, xid did not affect the high levels of c-myb oncogene RNA expression by C3H-gld/gld LN and spleen cells. By contrast, the xid gene caused a significant reduction in serum IgM but not IgA levels and almost completely ablated the generation of both IgM and IgG anti-ssDNA antibodies and anti-dsDNA antibodies. These data suggest that the xid gene can dramatically decrease the B-cell manifestations of autoimmunity in gld homozygotes without affecting their abnormal T-cell expansion. Comparisons of age-matched C3H-gld/gld and C3H-lpr/lpr mice showed that they had similarly elevated serum IgM and IgA levels and anti-ssDNA and anti-dsDNA antibody levels providing further evidence that gld and Ipr produce parallel defects in C3H mice.

Original languageEnglish (US)
Pages (from-to)249-255
Number of pages7
JournalCellular Immunology
Issue number1
StatePublished - 1987
Externally publishedYes

ASJC Scopus subject areas

  • Cell Biology
  • Immunology


Dive into the research topics of 'Effect of xid on autoimmune C3H-gld/gld mice'. Together they form a unique fingerprint.

Cite this