Atsaldi G, Astaldi G C, Topuz U, Guarina L
Haematologia (Budap). 1975;9(1-2):21-33.
Investigation of the cell S--Ig in acute lymphocytic leukaemia (ALL), at the onset of relapse of the disease, shows quite marked differences from patient to patient according to the extent of the immunofluorescent-positive cells. They may vary from 0.5 to 25% or more. When these Ig-positive cells are treated with trypsin and then incubated "in vitro" for six hours, many of them are no longer Ig-positive, i.e. they do not synthesize Ig. It might be possible, that the membrane-Ig observed before trypsinization does not represent true Ig-determinants of mature B-cells (antibodies attached to leukaemia-specific determinants?). The extent of these features decrease in remission until their disappearance. Relationship between the cell immunological patterns and the treatment response in ALL could exist. In a group of ALL-patients under the same treatment, that is, vincristine and prednisone, the correlation between the course of the disease after the above-mentioned therapy showed quick and complete remission in patients with low percentage of Ig-positive cells (below 10%) and poor improvement (often without complete remission) in patients with higher percentage of Ig-positive cells. Among the most important B-lymphocyte abnormalities in chronic lymphocytic leukaemia (CLL) are the following: (a) fluorescence intensity may vary not only from patient to patient, but also from cell to cell in the same patient; (b) the Fc-receptor can be lacking; (c) the C3b-receptor is not always present, or it is from 2 to 20-folds less frequent than the C3d-receptor, whereas normal human lymphocytes do not show any outstanding differences between the number of EAC rosette-forming cells either when tested with mouse complement (C3d-receptor) or with human complement C3b-receptor); (d) the traffic capacity of peripheral-blood B-lymphocytes in CLL is quite defective. Results of the observations on lymphocytes in CLL, taken as a whole, suggest that CLL is in general given by the expansion of an abnormal clone of cells of B origin, arrested in their maturative development, non-responsive to the mitogen stimulation, accumulating in the peripheral-blood for a traffic deficiency. On the contrary, the T-cells class is apparently normal, and the T-cell extent in CLL-peripheral blood can be even greater than normal when taken as absolute value.
对急性淋巴细胞白血病(ALL)患者疾病复发时细胞表面免疫球蛋白(S--Ig)的研究表明,根据免疫荧光阳性细胞的比例,患者之间存在相当明显的差异。其比例可能在0.5%至25%或更高之间变化。当这些Ig阳性细胞用胰蛋白酶处理,然后在“体外”孵育6小时后,许多细胞不再呈Ig阳性,即它们不再合成Ig。有可能在胰蛋白酶处理前观察到的膜Ig并不代表成熟B细胞的真正Ig决定簇(附着于白血病特异性决定簇的抗体?)。这些特征在缓解期会逐渐减少直至消失。ALL中细胞免疫模式与治疗反应之间可能存在关联。在一组接受相同治疗(即长春新碱和泼尼松)的ALL患者中,上述治疗后疾病进程的相关性显示,Ig阳性细胞比例低(低于10%)的患者迅速完全缓解,而Ig阳性细胞比例高的患者改善不佳(通常无完全缓解)。慢性淋巴细胞白血病(CLL)中最重要的B淋巴细胞异常包括以下几点:(a)荧光强度不仅在患者之间存在差异,而且在同一患者的细胞之间也存在差异;(b)可能缺乏Fc受体;(c)C3b受体并非总是存在,或者其频率比C3d受体低2至20倍,而正常人淋巴细胞在用小鼠补体(C3d受体)或人补体C3b受体检测时,EAC花环形成细胞数量没有明显差异;(d)CLL患者外周血B淋巴细胞的迁移能力相当缺陷。总体而言,对CLL淋巴细胞的观察结果表明,CLL通常是由起源于B的异常细胞克隆扩增引起的,这些细胞在成熟发育中停滞,对有丝分裂原刺激无反应,因迁移缺陷而在外周血中积聚。相反,T细胞类显然正常,CLL外周血中的T细胞比例以绝对值计算甚至可能高于正常。