Benaroch P, Bordenave G
Unité d'Immunophysiologie Moléculaire, Institut Pasteur, Paris, France.
Eur J Immunol. 1988 Jan;18(1):51-8. doi: 10.1002/eji.1830180109.
Several approaches have been used in our attempts to increase the "natural" ability of normal T splenocytes (Tn) from BALB/c or BC8 mice (both Igha) to induce, in F1 hybrids, a suppression of Igh-1b expression (IgG2a of b haplotype). These heterozygous F1 were produced by mating these Igha mice and their Ighb-congenic partners (CB20 and C57BL/6, respectively). The most powerful approaches were to sensitize the Igha mice by either autologous splenocytes coated with Igh-1b or B splenocytes from Ighb-congenic mice. In F1 having paternally inherited the b haplotype the sensitized T splenocytes (Ts) prepared from such mice are able to induce, like Tn, when injected at birth, a chronic suppression of Igh-1b expression. However, the suppression was established with a much higher efficiency: already at 6 weeks of age in 100% of the F1 treated with 1 x 10(7) Ts, vs. a final rate of 70% progressively reached only at 42 weeks of age in the F1 treated with 4 x 10(7) Tn. In F1 having maternally inherited Ighb the differences were even more pronounced than with 4 x 10(7) Tn, i.e. the suppression induction was almost totally ineffective, whereas with 2 x 10(7)-4 x 10(7) Ts, a rate of 100% treated F1 subjected to suppression was reached at 19 weeks of age. As the productions of IgM, IgD and IgA of the b haplotype were not affected by the suppression, the Ts are believed to act on the Igh-1b+ cells. Attempts were also made to induce allotypic suppression of other b allotypes by the use, as sensitizing cells, of myeloma cells carrying Igh-6b (IgM of b haplotype). We failed in revealing any sign of a T cell reactivity against Igh-6b similar to the reactivity against Igh-1b. The use of Igh-6b+ myeloma cells grown in an Ighb or in an Igha background allowed us to assume that the cells responsible for the sensitization are, in the Ighb B lymphocyte population, either the Igh-1b+ lymphocytes or the lymphocytes having passively adsorbed this allotype, or both.
我们尝试了多种方法来提高BALB/c或BC8小鼠（均为Igha）的正常T脾细胞（Tn）在F1杂种中诱导抑制Igh-1b表达（b单倍型的IgG2a）的“天然”能力。这些杂合F1是通过将这些Igha小鼠与其Ighb同基因伴侣（分别为CB20和C57BL/6）交配产生的。最有效的方法是用包被有Igh-1b的自体脾细胞或来自Ighb同基因小鼠的B脾细胞使Igha小鼠致敏。在父系遗传了b单倍型的F1中，从这些小鼠制备的致敏T脾细胞（Ts）在出生时注射，能够像Tn一样诱导Igh-1b表达的慢性抑制。然而，抑制的建立效率要高得多：在用1×10⁷ Ts处理的F1中，6周龄时100%出现抑制，而在用4×10⁷ Tn处理的F1中，直到42周龄才逐渐达到70%的最终抑制率。在母系遗传了Ighb的F1中，差异比用4×10⁷ Tn时更加明显，即抑制诱导几乎完全无效，而在用2×10⁷ - 4×10⁷ Ts处理时，19周龄时100%接受处理的F1达到了抑制状态。由于b单倍型的IgM、IgD和IgA的产生不受抑制影响，因此认为Ts作用于Igh-1b⁺细胞。我们还尝试通过使用携带Igh-6b（b单倍型的IgM）的骨髓瘤细胞作为致敏细胞来诱导对其他b同种异型的同种异型抑制。我们未能发现任何与针对Igh-1b的反应性相似的针对Igh-6b的T细胞反应性迹象。在Ighb或Igha背景中培养的Igh-6b⁺骨髓瘤细胞的使用使我们能够假设，在Ighb B淋巴细胞群体中，负责致敏的细胞要么是Igh-1b⁺淋巴细胞，要么是被动吸附了这种同种异型的淋巴细胞，或者两者皆是。
