Pierce C W, Kapp J A, Solliday S M, Dorf M E, Benacerraf B
J Exp Med. 1974 Oct 1;140(4):921-38. doi: 10.1084/jem.140.4.921.
The effects of alloantisera against leukocyte alloantigens on plaque-forming cell (PFC) responses to sheep erythrocytes and the terpolymer of L-glutamic acid(60)-L-alanine(30)-L-tyrosine(10) (GAT) by mouse spleen cells in vitro have been investigated. Polyspecific antibodies against both H-2 and non-H-2 alloantigens on responding spleen cells suppressed both IgM and IgG PFC responses; antisera against alloantigens coded for by the K and I regions, but not the D region, of the H-2 complex also effectively suppressed PFC responses. The suppression was not due to cytotoxicity to the spleen cells or anti-immunoglobulin activity in the sera and was directly related to the amount of antiserum added to the cultures. The suppression was specific for spleen cells against which the alloantiserum was directed. The alloantisera suppressed responses most effectively when present during the first 24 h of incubation, and although not rendering lymphoid cells incapable of developing PFC responses after removal of noncell-bound antibody, did act by interfering with successful initiation of the PFC response. The alloantisera suppressed both IgM and IgG PFC responses when directed against alloantigens only on macrophages, but selectively suppressed IgG responses when directed against alloantigens only on lymphoid cells. The alloantisera did not interfere with the ability of macrophages to bind GAT or to support the viability of the lymphoid cells, but did interfere with the ability of macrophage-associated antigen to effectively stimulate antibody responses by the lymphoid cells. Possible mechanisms for the effects of alloantisera on macrophages and the selective suppression of IgG responses when the antisera are directed against alloantigens on lymphoid cells are discussed with reference to our current understanding of genetic restrictions governing cell interactions in the development of antibody responses in mice.
已研究了抗白细胞同种异体抗原的同种抗血清对小鼠脾细胞体外针对绵羊红细胞和L-谷氨酸（60）-L-丙氨酸（30）-L-酪氨酸（10）（GAT）三元共聚物形成空斑细胞（PFC）反应的影响。针对反应性脾细胞上的H-2和非H-2同种异体抗原的多特异性抗体抑制了IgM和IgG PFC反应；针对H-2复合体K区和I区而非D区编码的同种异体抗原的抗血清也有效抑制了PFC反应。这种抑制不是由于对脾细胞的细胞毒性或血清中的抗免疫球蛋白活性，并且与添加到培养物中的抗血清量直接相关。这种抑制对同种抗血清所针对的脾细胞具有特异性。当在孵育的最初24小时内存在时，同种抗血清最有效地抑制反应，并且尽管在去除非细胞结合抗体后不会使淋巴细胞无法产生PFC反应，但确实通过干扰PFC反应的成功启动而起作用。当仅针对巨噬细胞上的同种异体抗原时，同种抗血清抑制IgM和IgG PFC反应，但当仅针对淋巴细胞上的同种异体抗原时，选择性地抑制IgG反应。同种抗血清不干扰巨噬细胞结合GAT或维持淋巴细胞活力的能力，但确实干扰巨噬细胞相关抗原有效刺激淋巴细胞抗体反应的能力。参考我们目前对小鼠抗体反应发展中细胞相互作用的遗传限制的理解，讨论了同种抗血清对巨噬细胞的作用以及当抗血清针对淋巴细胞上的同种异体抗原时对IgG反应的选择性抑制的可能机制。
