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In vitro studies on allotype suppression. III. compounds of antiallyotype serum active in release from allotype suppression

机译:异型抑制的体外研究。三,具有抑制异型释放的活性的抗异型血清化合物

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摘要

Spleen cells of b4b6 rabbits, shown to be deficient in their ability to produce b4Ig due to prenatal exposure to anti-b4, formed anti-T2 antibodies marked with the b4 determinant in response to solubilized T2 phage (S-T2) only when cultured in the presence of antibodies specific for the nonsuppressed type (b6), thus confirming and extending the previously reported observation of release from b4 suppression in cultured cells of b4-suppressed b4b5 rabbits treated with anti-b5 serum. Only antiallotype sera made in b4 rabbits were active in reversing b4 suppression. Anti-b5 or anti-b6 sera from rabbits of allotypes b6 or b5, respectively, when used in concentrations which completely or partially inhibited the formation of anti-T2 antibodies marked with the corresponding nonsuppressed allotype of the spleen donor, proved to be almost completely ineffective in causing release of suppression. Exceptions were noted when spleen cells of rabbits advanced in spontaneous escape from suppression were tested with such sera. The addition of normal b4 serum to non-b4 antiallotypic sera rendered them as effective in releasing b4 suppression in vitro as were antisera from b4 rabbits. Furthermore, the capacity of a b4 antiallotype serum to cause reversal of b4 suppression could be potentiated by the addition of normal b4 serum, indicating that nonantibody b4 Ig is a limiting factor in such a serum. Thus, the release from allotype suppression observed in cultures of spleen cells from b4-suppressed heterozygous rabbits is dependent upon the presence of two components: antibodies directed against the nonsuppressed allotype of the donor and normal b4Ig. These findings are interpreted in terms of alternate hypotheses involving (a) a mechanism of b4 derepression and (b) inactivation of a suppressor cell with recognition for a b4-labeled target.
机译:b4b6兔的脾细胞由于产前暴露于抗b4而显示出产生b4Ig的能力不足,仅当在特异性针对非抑制型(b6)的抗体的存在,从而证实并扩展了先前报道的用抗b5血清处理过的经b4抑制的b4b5兔的培养细胞从b4抑制释放的观察。在b4兔中仅产生抗异型血清能有效逆转b4抑制。当分别以完全或部分抑制以相应的非抑制性脾供体同种异型标记的抗T2抗体的浓度使用时,分别来自同种异型b6或b5兔的抗b5或抗b6血清被证明几乎完全导致抑制释放无效。当用这种血清测试自抑制性自发逃逸中进展的家兔的脾细胞时,有例外。向非b4抗allottypic血清中添加正常的b4血清使它们像从b4兔获得的抗血清一样,在体外释放b4抑制方面有效。此外,可以通过添加正常的b4血清来增强b4抗异型血清引起b4抑制作用逆转的能力,这表明非抗体b4Ig是这种血清中的限制因子。因此,在b4抑制的杂合兔的脾细胞培养物中观察到的异型抑制的释放取决于两种组分的存在:针对非抑制的供体同种型的抗体和正常的b4Ig。这些发现是根据其他假设进行解释的,这些假设涉及(a)b4抑制的机制和(b)抑制性细胞的失活并识别b4标记的靶标。

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