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兔中的同种异型抑制。I. 携带父本同种异型免疫球蛋白的细胞的个体发生以及用抗同种异型抗血清处理后这些细胞的命运。

Allotype suppression in the rabbit. I. The ontogeny of cells bearing immunoglobulin of paternal allotype and the fate of these cells after treatment with antiallotype antisera.

作者信息

Harrison M R, Mage R G

出版信息

J Exp Med. 1973 Oct 1;138(4):764-74. doi: 10.1084/jem.138.4.764.

Abstract

The ability to distinguish immunoglobulin (Ig) of paternal allotype both on lymphocyte membranes and in the serum of neonatal b(4)b(5) heterozygous rabbits has allowed us to study the postnatal ontogeny of cells bearing endogenously synthesized Ig that could not have been derived from the mother. In normal b(4)b(5) rabbits, such endogenously synthesized Ig of paternal allotype is present on the membranes of bone marrow-derived (B) lymphocytes from birth, but does not appear as detectable circulating Ig until approximately 2 wk of age. In the neonate, cells bearing the paternal allotype are potential targets for the induction of chronic allotype suppression. Within 24 h of exposure to anti-allotype antisera in vivo, Ig of the suppressed paternal allotype is no longer detectable on the surface of neonatal lymphoid cells. Further, this lymphocyte membrane Ig is eliminated and not simply masked by the suppressing antibodies. Finally, cells bearing the suppressed allotype are deleted from all lymphoid organs for the duration of total allotype suppression, and reappear first in bone marrow and peripheral blood at the time of spontaneous escape from suppression.

摘要

在新生b(4)b(5)杂合兔的淋巴细胞膜和血清中鉴别父本同种异型免疫球蛋白(Ig)的能力,使我们能够研究携带内源性合成Ig的细胞的出生后个体发育情况,这些Ig不可能来自母体。在正常的b(4)b(5)兔中,这种父本同种异型的内源性合成Ig从出生起就存在于骨髓来源的(B)淋巴细胞膜上,但直到大约2周龄时才作为可检测到的循环Ig出现。在新生儿中,携带父本同种异型的细胞是诱导慢性同种异型抑制的潜在靶标。在体内接触抗同种异型抗血清后24小时内,被抑制的父本同种异型的Ig在新生儿淋巴细胞表面不再可检测到。此外,这种淋巴细胞膜Ig被消除,而不仅仅是被抑制性抗体掩盖。最后,在完全同种异型抑制期间,携带被抑制同种异型的细胞从所有淋巴器官中被清除,并在自发摆脱抑制时首先出现在骨髓和外周血中。

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