Study of congenitally immunologic mutant New Zealand mice. cell function of NZB-X(id) mice

Y. Ohsugi, M. Eric Gershwin, A. Ahmed

Research output: Contribution to journalArticle

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Abstract

NZB mice bearing the CBA/N X chromosome linked defect were generated by repetitive backcrossing and selection of the X(id) gene. The male offspring resulting from the cross of NZB with CBA/N were selected as being X(id)Y on the basis of sera IgM and IgG3 levels and responsiveness to DNP-Lys-Ficoll. Following this inbreeding protocol, 6th generation backcross NZB X(id)Y mice compared to littermate controls with respect to B cell function. Sera immunoglobulin levels of IgG1, IgG(2a), IgG(2b) and IgA were similar in X(id)Y and XY mice. In contrast, levels of IgM and IgG3, from X(id)Y mice were approximately 15% and 50%, respectively of values found in littermates. Furthermore, X(id)Y mice failed to respond to DNP-Lys-Ficoll and had less than 3% splenic Lyb 5.1-bearing cells. Splenic immunoglobulin cell surface profiles, obtained by the fluorescent activated cell sorter, indicated a significant reduction in the frequency of X(id) bearing cells in X(ld) animals. Such profiles were similar to those obtained for spleen cells from reference control CBA/N mice. Finally, an elevated number of splenic, lymph node and bone marrow background and lipopolysaccharide-induced B cell clones in semi-solid phase agar was found in NZB but not C57BL/6, C3H, BALB/c and DBA/2 controls. In contrast, NZB X(id)Y mice had virtually no detectable B cell colonies. This data, obtained on significantly inbred X(id)Y NZB mice, suggests that the X(id) gene is dominant over several aspects of polyclonal B cell activation in NZB mice and indicates that seral observation of these mice will be valuable in understanding the interactions of genetic immunologic mutations and cellular function in autoimmunity.

Original languageEnglish (US)
Pages (from-to)129-137
Number of pages9
JournalJournal of Immunogenetics
Volume8
Issue number2
StatePublished - 1981

Fingerprint

New Zealand
Inbred NZB Mouse
Immunoglobulin G
B-Lymphocytes
Inbreeding
Immunoglobulin M
Dominant Genes
Inbred CBA Mouse
B-Cell Antigen Receptors
X Chromosome
Serum
Autoimmunity
Immunoglobulin A
Agar
Immunoglobulins
Spleen
Clone Cells
Lymph Nodes
Bone Marrow
Observation

ASJC Scopus subject areas

  • Immunology
  • Genetics

Cite this

Study of congenitally immunologic mutant New Zealand mice. cell function of NZB-X(id) mice. / Ohsugi, Y.; Gershwin, M. Eric; Ahmed, A.

In: Journal of Immunogenetics, Vol. 8, No. 2, 1981, p. 129-137.

Research output: Contribution to journalArticle

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abstract = "NZB mice bearing the CBA/N X chromosome linked defect were generated by repetitive backcrossing and selection of the X(id) gene. The male offspring resulting from the cross of NZB with CBA/N were selected as being X(id)Y on the basis of sera IgM and IgG3 levels and responsiveness to DNP-Lys-Ficoll. Following this inbreeding protocol, 6th generation backcross NZB X(id)Y mice compared to littermate controls with respect to B cell function. Sera immunoglobulin levels of IgG1, IgG(2a), IgG(2b) and IgA were similar in X(id)Y and XY mice. In contrast, levels of IgM and IgG3, from X(id)Y mice were approximately 15{\%} and 50{\%}, respectively of values found in littermates. Furthermore, X(id)Y mice failed to respond to DNP-Lys-Ficoll and had less than 3{\%} splenic Lyb 5.1-bearing cells. Splenic immunoglobulin cell surface profiles, obtained by the fluorescent activated cell sorter, indicated a significant reduction in the frequency of X(id) bearing cells in X(ld) animals. Such profiles were similar to those obtained for spleen cells from reference control CBA/N mice. Finally, an elevated number of splenic, lymph node and bone marrow background and lipopolysaccharide-induced B cell clones in semi-solid phase agar was found in NZB but not C57BL/6, C3H, BALB/c and DBA/2 controls. In contrast, NZB X(id)Y mice had virtually no detectable B cell colonies. This data, obtained on significantly inbred X(id)Y NZB mice, suggests that the X(id) gene is dominant over several aspects of polyclonal B cell activation in NZB mice and indicates that seral observation of these mice will be valuable in understanding the interactions of genetic immunologic mutations and cellular function in autoimmunity.",
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