Chevalier S, Lacroix H, Soulillou J P
Laboratoire d'Immunologie Clinique, INSERM U211, Nantes.
Nephrologie. 1987;8(3):155-8.
We previously demonstrated in the (Lew.1W----Lew.1A) congeneic strain combination differing only at the RT1 Region that blood transfusion sharing RT1.B with the heart donor lead to longterm graft function. In the present paper, using the same genetic combination and limiting dilution analysis we studied the frequency of recipient splenocytes (Lew.1A) able to produce IL2 upon donor peritoneal macrophages challenge. We found that splenocytes of Lew.1A rats, previously transfused with Lew.1W blood and grafted with Lew.1W heart, contained suppressor cells which inhibited the capacity of autologous lymphocytes to produce IL2 upon Lew.1W challenge. When a Lew.1A recipient received either a Lew.1W heart without previous transfusion or a Lew.1W blood transfusion without heart graft there is no evidence of generation of suppressor cells. This suggests that both blood transfusion and allograft are required for IL2 suppression and that this suppression may be related to the heart tolerance.
我们之前在仅在RT1区域存在差异的(Lew.1W----Lew.1A)同源基因品系组合中证明,与心脏供体共享RT1.B的输血可导致长期移植物功能。在本文中,我们使用相同的基因组合和有限稀释分析,研究了在供体腹膜巨噬细胞刺激下能够产生白细胞介素2(IL2)的受体脾细胞(Lew.1A)的频率。我们发现,先前输注了Lew.1W血液并移植了Lew.1W心脏的Lew.1A大鼠的脾细胞含有抑制细胞,这些抑制细胞在受到Lew.1W刺激时会抑制自体淋巴细胞产生IL2的能力。当Lew.1A受体接受未预先输血的Lew.1W心脏或未进行心脏移植的Lew.1W输血时,没有证据表明会产生抑制细胞。这表明,IL2抑制需要输血和同种异体移植两者,并且这种抑制可能与心脏耐受性有关。