Gleichmann H, Gleichmann E, André-Schwartz J, Schwartz R S
J Exp Med. 1972 Mar 1;135(3):516-32. doi: 10.1084/jem.135.3.516.
The pathogenesis of glomerulonephritis in F(1) hybrid mice injected with parental spleen cells was investigated in several ways. Whenever glomerulonephritis developed, the lesion had the typical morphology produced by antigen-antibody complexes. Experiments employing backcross mice demonstrated that the antigen is supplied by the recipient and that it is specified by the H-2 gene complex, or by a locus closely linked to H-2. The source of the antibody was investigated by staining glomerular lesions with fluorescein isothiocyanate-tagged anti-immunoglobulin allotype sera. Only donor-type allotypes could be detected. The ability of the donor's immunocytes to respond to the recipient's histocompatibility antigens in such a way as to produce nephritogenic immune complexes varied from strain to strain, and seemed to be controlled by a gene unrelated to H-2. The results suggest that cell surface antigens, such as histocompatibility antigens, may be of importance in the pathogenesis of several kinds of glomerulonephritis.
通过多种方式研究了注射亲本脾细胞的F(1)杂种小鼠肾小球肾炎的发病机制。每当发生肾小球肾炎时，病变都具有抗原-抗体复合物产生的典型形态。采用回交小鼠的实验表明，抗原由受体提供，并且由H-2基因复合体或与H-2紧密连锁的基因座所指定。通过用异硫氰酸荧光素标记的抗免疫球蛋白同种异型血清对肾小球病变进行染色来研究抗体的来源。仅能检测到供体型同种异型。供体免疫细胞以产生致肾炎免疫复合物的方式对受体组织相容性抗原作出反应的能力因品系而异，并且似乎受与H-2无关的基因控制。结果表明，细胞表面抗原，如组织相容性抗原，可能在几种肾小球肾炎的发病机制中起重要作用。
