Yakura H, Shen F W, Kaemmer M, Boyse E A
J Exp Med. 1981 Jan 1;153(1):129-35. doi: 10.1084/jem.153.1.129.
The Lyb-2 cell-surface alloantigens of the mouse are selectively and perhaps exclusively expressed in the B lymphocyte lineage, but not on antibody- forming cells. Thus if the Lyb-2 molecule is concerned in specific B cell function, it must participate in the generative phase of the antibody response. Accordingly, monoclonal Lyb-2 antibody was found to depress the plaque- forming cell (PFC) response to sheep erythrocytes in 5-d Mishell-Dutton assays when added within the first 3 d of culture, but not later. The rate of PFC generation was not affected, signifying an absolute reduction in the number of PFC generated. Because reduction of PFC counts by Lyb-2 antibody was not affected by exclusion of Lyt-2(+) T cells, it is unlikely that the reduction depends on augmented suppression by T cells. Augmented B cell- mediated suppression is also unlikely, because the PFC response of serial combinations of congenic Lyb-2.1 and Lyb-2.2 cells, in the presence of monoclonal Lyb-2.1 antibody, was reduced only in direct proportion to the number of Lyb-2.1 cells present. The PFC response of Lyb-2.1/Lyb-2.2 heterozygous cells was not reduced by Lyb-2.1 antibody, presumably because generation of PFC is impeded only if most Lyb-2 sites are blocked. Further evidence that the molecule identified by Lyb-2 plays a critical role in the generation of antibody-forming cells (AFC) in response to T-dependent antigen comes from the finding that Lyb-2 antibody does not reduce the PFC response to the T-independent antigens trinitrophenylated (TNP) Brucella abortus and TNP-FicolI, although elimination of Lyb-2(+) cells from the starting population by Lyb-2 antibody and complement reduces the PFC response to T- dependent and T-independent antigens alike.
小鼠的Lyb-2细胞表面同种异体抗原在B淋巴细胞系中选择性表达,甚至可能是特异性表达,但在抗体形成细胞上不表达。因此,如果Lyb-2分子参与特定的B细胞功能,它必定在抗体应答的产生阶段发挥作用。相应地,在5天的米舍尔-达顿试验中,发现单克隆Lyb-2抗体在培养的前3天内加入时会抑制对绵羊红细胞的空斑形成细胞(PFC)应答,但在之后加入则无此作用。PFC生成速率未受影响,这表明生成的PFC数量绝对减少。由于Lyb-2抗体导致的PFC数量减少不受Lyt-2(+) T细胞排除的影响,因此这种减少不太可能依赖于T细胞增强的抑制作用。B细胞介导的增强抑制作用也不太可能,因为在单克隆Lyb-2.1抗体存在的情况下,同基因Lyb-2.1和Lyb-2.2细胞的系列组合的PFC应答仅与存在的Lyb-2.1细胞数量成比例减少。Lyb-2.1/Lyb-2.2杂合细胞的PFC应答未被Lyb-2.1抗体降低,推测是因为只有当大多数Lyb-2位点被阻断时,PFC的生成才会受到阻碍。进一步证明由Lyb-2识别的分子在对T依赖性抗原的抗体形成细胞(AFC)生成中起关键作用的证据来自以下发现:Lyb-2抗体不会降低对T非依赖性抗原三硝基苯化(TNP)流产布鲁氏菌和TNP-菲可利的PFC应答,尽管用Lyb-2抗体和补体从起始群体中去除Lyb-2(+)细胞会同等程度地降低对T依赖性和T非依赖性抗原的PFC应答。