Gerbal A, Ropars C
Rev Fr Transfus Immunohematol. 1976 Mar;19(1):127-44. doi: 10.1016/s0338-4535(76)80093-1.
Many cases of acquired B antigens, always observed in group A subjects have been so far reported. Most of them were found in patients with digestive tract disease, essentially colonic cancer. An investigation on 200 patients in a gastroenterology department showed that this B-like antigen was quite frequent (10,6%); it occurred only in A1 individuals and was related to infectious syndrome. Immunological and serological studies of many cases had shown that this B-like antigen differs from that of normal B cells. Groupe A1 cells transfused to patients acquired B activity; on the contrary group A2 and O cells remained unchanged. Likewise, only A1 cell became active when incubated in vitro with C. Tertium A., known to contain a deacetylase. In 1970, we postulated that a deacetylase enzyme could be responsible for this B-like antigen: this enzyme could transform the N-acetylgalactosamine (A specific sugar) into galactosamine, which could cross react with anti-B sera. The relationship between the acquired B antigen and a deacetylase was recently confirmed: A1 acquired B cells, chemically acetylated lost their B reactivity and enhanced their A1 activity. A polyagglutinability, different from that associated with T, Tn, Cad, Hempas has been always found in acquired B cells; nervertheless, because of its weakness, it could sometimes be unnoticed. Besides, it disappeared prior to B reactivity in case of recovery. Like acquired B activity, it decreased in low pH medium of after acetylation of the cells. Nevertheless, this polyagglutinability appears, contrarly to acquired B antigen, in vitro, on all the cells, irrespective of their ABO phenotypes. A deacetylation of N-acetyl-neruaminic acid could explain such a phenomenon.
迄今为止，已报道了许多在A型个体中观察到的获得性B抗原病例。其中大多数见于患有消化道疾病的患者，主要是结肠癌患者。对某消化内科的200例患者进行的一项调查显示，这种类B抗原相当常见（10.6%）；它仅出现在A1个体中，且与感染综合征有关。对许多病例的免疫学和血清学研究表明，这种类B抗原与正常B细胞的抗原不同。输给患者的A1型细胞获得了B活性；相反，A2型和O型细胞则保持不变。同样，当A1型细胞在体外与已知含有脱乙酰酶的第三梭状芽孢杆菌一起孵育时，只有A1型细胞会变得活跃。1970年，我们推测一种脱乙酰酶可能是这种类B抗原的成因：这种酶可以将N-乙酰半乳糖胺（A特异性糖）转化为半乳糖胺，后者可能与抗B血清发生交叉反应。获得性B抗原与脱乙酰酶之间的关系最近得到了证实：化学乙酰化的A1获得性B细胞失去了它们的B反应性，并增强了它们的A1活性。在获得性B细胞中一直发现有一种不同于与T、Tn、Cad、Hempas相关的多凝集性；然而，由于其较弱，有时可能未被注意到。此外，在恢复的情况下，它在B反应性之前消失。与获得性B活性一样，它在细胞乙酰化后的低pH介质中会降低。然而，与获得性B抗原相反，这种多凝集性在体外出现在所有细胞上，无论其ABO血型表型如何。N-乙酰神经氨酸的脱乙酰化可以解释这种现象。
