Majlessi L, Benaroch P, Denoyelle C, Bordenave G
Unité d'Immunophysiologie Moléculaire, Institut Pasteur, Paris, France.
J Immunol. 1993 Aug 15;151(4):1859-67.
Transfer into F1 Igha/b mice of splenocytes from Igha mice sensitized once against B cells from an Ighb congenic strain induces total, chronic, and IgG2ab (IgG2a of the Ighb haplotype)-specific allotype suppression in these recipients. We previously demonstrated that both the CD4+ and CD8+ T subsets were necessary for inducing suppression, but that CD8+, cells by themselves were sufficient for maintaining suppression. We have studied the suppression induction capacity of different mixtures of CD4+ and CD8+ subsets obtained by in vitro cytotoxic treatment of T splenocytes from normal or sensitized Igha mice, and we have established that suppression induction requires the cooperation between CD4+ and CD8+ populations, both of which have to be IgG2ab specific. In addition, Igha mice were sensitized in the absence of CD4+ or CD8+ cells by in vivo cytotoxic treatment performed before and after the sensitization in order to obtain an IgG2ab-specific CD4+ population that has arisen in the absence of CD8+ cells, and vice versa. We found that only IgG2ab-specific CD4+ cells from anti-CD8-treated mice (T'sens CD4+) had the ability to induce suppression in F1 Igha/b hosts. Nevertheless, the real effector cells in this suppression model display the CD8+ phenotype, as in vivo cytotoxic anti-CD8 treatment of Igha/b recipients of T'sens CD4+ abrogates the suppression induction capacity. Taken together, these results show that T'sens CD4+ have an important capacity to recruit CD8+ anti-IgG2ab effector cells from precursors that have been transferred with them into Igha/b hosts. These precursors are actually derived from the T'sens CD4+ cell preparation, because we have recently demonstrated that suppression is maintained by donor T cells throughout the recipient's life. CD4+ cells can have their anti-IgG2ab activity amplified only by means of target cells (i.e., B cells from Ighb congenic mice), whereas, in the absence of CD4+ cells, and despite the presence of target cells, CD8+ cells seem unable to acquire this amplified activity.
将曾对来自Ighb同基因品系的B细胞致敏一次的Igha小鼠的脾细胞转移到F1 Igha/b小鼠中，可在这些受体中诱导完全、慢性且IgG2ab（Ighb单倍型的IgG2a）特异性同种异型抑制。我们之前证明，CD4⁺和CD8⁺ T细胞亚群对于诱导抑制都是必需的，但CD8⁺细胞自身就足以维持抑制。我们研究了通过对正常或致敏的Igha小鼠的脾T细胞进行体外细胞毒性处理获得的不同CD4⁺和CD8⁺亚群混合物的抑制诱导能力，并且我们确定抑制诱导需要CD4⁺和CD8⁺群体之间的合作，二者都必须是IgG2ab特异性的。此外，为了获得在没有CD8⁺细胞的情况下产生的IgG2ab特异性CD4⁺群体，反之亦然，在致敏之前和之后通过体内细胞毒性处理使Igha小鼠在没有CD4⁺或CD8⁺细胞的情况下致敏。我们发现，只有来自抗CD8处理小鼠的IgG2ab特异性CD4⁺细胞（T'sens CD4⁺）有能力在F1 Igha/b宿主中诱导抑制。然而，在这个抑制模型中真正的效应细胞表现出CD8⁺表型，因为对T'sens CD4⁺的Igha/b受体进行体内细胞毒性抗CD8处理会消除抑制诱导能力。综上所述，这些结果表明，T'sens CD4⁺具有重要能力，可从与其一起转移到Igha/b宿主中的前体中募集CD8⁺抗IgG2ab效应细胞。这些前体实际上源自T'sens CD4⁺细胞制剂，因为我们最近证明，供体T细胞在受体的整个生命过程中维持抑制。CD4⁺细胞只能通过靶细胞（即来自Ighb同基因小鼠的B细胞）来增强其抗IgG2ab活性，而在没有CD4⁺细胞的情况下，尽管存在靶细胞，CD8⁺细胞似乎无法获得这种增强的活性。
