Abstract
There is a growing data base suggesting the existence of a primary B cell defect in New Zealand mice. To identify and characterize this possibility further, attention has been focused on developmental aspects of B lymphocyte clone formation in congenitally athymic (nude), hereditarily asplenic (Dh/+), conventionally housed, and germfree New Zealand Black (NZB) mice. Lipopolysaccharide-induced and background B lymphocyte cloning of fetal liver, spleen, lymph node, bone marrow, and thymus in semisolid agar was compared in NZB mice to age-matched NZW, BALB/c, C57BL/6, C3H/He, and DBA/2N mice. The number of splenic B cell colony-forming cells and the peak day for colony formation were similar for BALB/c, C57BL/6, C3H/He, and DBA/2N mice; adult values were reached by 14 to 30 days and were approximately 400/2.5 x 104 cells. A slightly higher value, with similar age kinetics, was observed in NZW mice. In contrast, NZB mice have statistically higher values compared to other strains from birth through 2 months of age; peak adult values were approximately 860/2.5 x 104 splenic cells. Moreover, with age, the number of splenic colony-forming cells rapidly diminished and was significantly reduced after 6 months. Similar data were obtained when B lymphocyte clones were compared by using bone marrow and lymph node. Further, the number of B lymphocyte clones of 17-day-old NZB fetal liver was significantly higher than in control mice. Finally, of particular interest, the number of B lymphocyte clones in NZB Dh/+ mice was similar to that +/+ mice and the number of B lymphocyte clones in NZB nude mice was similar to that in nude/+ littermates, suggesting that this B cell defect is thymus independent and unrelated to antigen-nonspecific suppressor function.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1260-1265 |
| Number of pages | 6 |
| Journal | Journal of Immunology |
| Volume | 123 |
| Issue number | 3 |
| State | Published - 1979 |
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ASJC Scopus subject areas
- Immunology
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Studies of congenitally immunologic mutant New Zealand mice. III. Growth of B lymphocyte clones in congenitally athymic (nude) and hereditarily asplenic (Dh/+) NZB mice : A primary B cell defect. / Ohsugi, Y.; Gershwin, M. Eric.
In: Journal of Immunology, Vol. 123, No. 3, 1979, p. 1260-1265.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Studies of congenitally immunologic mutant New Zealand mice. III. Growth of B lymphocyte clones in congenitally athymic (nude) and hereditarily asplenic (Dh/+) NZB mice
T2 - A primary B cell defect
AU - Ohsugi, Y.
AU - Gershwin, M. Eric
PY - 1979
Y1 - 1979
N2 - There is a growing data base suggesting the existence of a primary B cell defect in New Zealand mice. To identify and characterize this possibility further, attention has been focused on developmental aspects of B lymphocyte clone formation in congenitally athymic (nude), hereditarily asplenic (Dh/+), conventionally housed, and germfree New Zealand Black (NZB) mice. Lipopolysaccharide-induced and background B lymphocyte cloning of fetal liver, spleen, lymph node, bone marrow, and thymus in semisolid agar was compared in NZB mice to age-matched NZW, BALB/c, C57BL/6, C3H/He, and DBA/2N mice. The number of splenic B cell colony-forming cells and the peak day for colony formation were similar for BALB/c, C57BL/6, C3H/He, and DBA/2N mice; adult values were reached by 14 to 30 days and were approximately 400/2.5 x 104 cells. A slightly higher value, with similar age kinetics, was observed in NZW mice. In contrast, NZB mice have statistically higher values compared to other strains from birth through 2 months of age; peak adult values were approximately 860/2.5 x 104 splenic cells. Moreover, with age, the number of splenic colony-forming cells rapidly diminished and was significantly reduced after 6 months. Similar data were obtained when B lymphocyte clones were compared by using bone marrow and lymph node. Further, the number of B lymphocyte clones of 17-day-old NZB fetal liver was significantly higher than in control mice. Finally, of particular interest, the number of B lymphocyte clones in NZB Dh/+ mice was similar to that +/+ mice and the number of B lymphocyte clones in NZB nude mice was similar to that in nude/+ littermates, suggesting that this B cell defect is thymus independent and unrelated to antigen-nonspecific suppressor function.
AB - There is a growing data base suggesting the existence of a primary B cell defect in New Zealand mice. To identify and characterize this possibility further, attention has been focused on developmental aspects of B lymphocyte clone formation in congenitally athymic (nude), hereditarily asplenic (Dh/+), conventionally housed, and germfree New Zealand Black (NZB) mice. Lipopolysaccharide-induced and background B lymphocyte cloning of fetal liver, spleen, lymph node, bone marrow, and thymus in semisolid agar was compared in NZB mice to age-matched NZW, BALB/c, C57BL/6, C3H/He, and DBA/2N mice. The number of splenic B cell colony-forming cells and the peak day for colony formation were similar for BALB/c, C57BL/6, C3H/He, and DBA/2N mice; adult values were reached by 14 to 30 days and were approximately 400/2.5 x 104 cells. A slightly higher value, with similar age kinetics, was observed in NZW mice. In contrast, NZB mice have statistically higher values compared to other strains from birth through 2 months of age; peak adult values were approximately 860/2.5 x 104 splenic cells. Moreover, with age, the number of splenic colony-forming cells rapidly diminished and was significantly reduced after 6 months. Similar data were obtained when B lymphocyte clones were compared by using bone marrow and lymph node. Further, the number of B lymphocyte clones of 17-day-old NZB fetal liver was significantly higher than in control mice. Finally, of particular interest, the number of B lymphocyte clones in NZB Dh/+ mice was similar to that +/+ mice and the number of B lymphocyte clones in NZB nude mice was similar to that in nude/+ littermates, suggesting that this B cell defect is thymus independent and unrelated to antigen-nonspecific suppressor function.
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M3 - Article
VL - 123
SP - 1260
EP - 1265
JO - Journal of Immunology
JF - Journal of Immunology
SN - 0022-1767
IS - 3
ER -