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B淋巴细胞的个体发生。II. 带有表面免疫球蛋白和补体受体的淋巴细胞的相对出现率。

Ontogeny of B lymphocytes. II. Relative rates of appearance of lymphocytes bearing surface immunoglobulin and complement receptors.

作者信息

Gelfand M C, Elfenbein G J, Frank M M, Paul W E

出版信息

J Exp Med. 1974 May 1;139(5):1125-41. doi: 10.1084/jem.139.5.1125.

Abstract

Many bursa-equivalent (B) lymphocytes of adult mice bear surface Ig and receptors for C3. The frequency of Ig-bearing cells increases rapidly immediately after birth, but these cells lack complement (C) receptors. Lymphocytes bearing C receptors are not found in the spleens of BALB/c, DBA/2, and C57BL/6 mice until 2 wk of age and do not attain substantial numbers until 3-4 wk of age. In AKR mice, a lag between appearance of Ig-bearing and complement receptor lymphocytes (CRL) is also observed but it is of much shorter duration. AKR mice have a frequency of CRL at 2 wk of age of 28% in comparison to a frequency of 4.8% for DBA/2 mice. The difference in frequency between young and adult mice and between "low" and "high CRL" strains cannot be explained by a nonspecific inability to form rosettes as similar results are obtained with soluble antigen-antibody-complement complexes. Analysis of CRL frequency in (AKR x DBA/2)F(1) mice and F(1) x parental backcross progeny suggests that two independent genes control the rate of appearance of CRL. Furthermore, the genetic difference in the ontogeny of CRL is recapitulated in the repopulation of the B-lymphocyte line in adult-irradiated mice restored with syngeneic bone marrow. Thus, the "CRL genes" described here appear to control B-cell differentiation throughout life.

摘要

成年小鼠的许多类囊泡(B)淋巴细胞带有表面免疫球蛋白(Ig)和C3受体。出生后,带有免疫球蛋白的细胞频率迅速增加,但这些细胞缺乏补体(C)受体。在BALB/c、DBA/2和C57BL/6小鼠的脾脏中,直到2周龄才发现带有C受体的淋巴细胞,直到3 - 4周龄才达到可观数量。在AKR小鼠中,也观察到带有免疫球蛋白的淋巴细胞和补体受体淋巴细胞(CRL)出现之间的滞后,但持续时间短得多。与DBA/2小鼠4.8%的频率相比,AKR小鼠在2周龄时CRL的频率为28%。幼鼠与成年鼠之间以及“低CRL”和“高CRL”品系之间频率的差异不能用形成花环的非特异性无能来解释,因为用可溶性抗原 - 抗体 - 补体复合物可得到类似结果。对(AKR×DBA/2)F1小鼠和F1×亲本回交后代中CRL频率的分析表明,两个独立基因控制着CRL的出现速率。此外,在成年受辐照小鼠用同基因骨髓恢复的B淋巴细胞系的再增殖中,CRL个体发生的遗传差异得以重现。因此,这里描述的“CRL基因”似乎在整个生命过程中控制着B细胞的分化。

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