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 language | English (US) |
|---|---|
| Pages (from-to) | 129-137 |
| Number of pages | 9 |
| Journal | Journal of Immunogenetics |
| Volume | 8 |
| Issue number | 2 |
| State | Published - 1981 |
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ASJC Scopus subject areas
- Immunology
- Genetics
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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 journal › Article
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TY - JOUR
T1 - Study of congenitally immunologic mutant New Zealand mice. cell function of NZB-X(id) mice
AU - Ohsugi, Y.
AU - Gershwin, M. Eric
AU - Ahmed, A.
PY - 1981
Y1 - 1981
N2 - 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.
AB - 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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M3 - Article
C2 - 6971904
AN - SCOPUS:0019845931
VL - 8
SP - 129
EP - 137
JO - International Journal of Immunogenetics
JF - International Journal of Immunogenetics
SN - 1744-3121
IS - 2
ER -