Mellors R C
J Exp Med. 1966 Jun 1;123(6):1025-34. doi: 10.1084/jem.123.6.1025.
The transplantation of spleen cells from old NZB/Bl mice with renal disease induced both the structural and the functional changes of membranous glomerulonephritis in young NZB/Bl mice within a few weeks and well in advance of its usual spontaneous occurrence. The development of hypergammaglobulinemia and lymphoid cell hyperplasia in the young mice indicated that immunologically competent cells, derived from either the transplant or the recipient, proliferated during this process. These experiments, together with other findings, provide further support for the view that membranous glomerulonephritis in NZB/Bl mice is produced by immunological, and probably autoimmune, mechanisms and that the renal disease is apparently almost wholly unrelated to the hemolytic process.
将患有肾脏疾病的老年NZB/Bl小鼠的脾细胞移植到年轻的NZB/Bl小鼠体内，在几周内就诱发了膜性肾小球肾炎的结构和功能变化，且比该病通常自然发生的时间要早得多。年轻小鼠体内高丙种球蛋白血症和淋巴细胞增生的发展表明，在此过程中，来自移植细胞或受体的免疫活性细胞发生了增殖。这些实验以及其他研究结果进一步支持了以下观点：NZB/Bl小鼠的膜性肾小球肾炎是由免疫机制（可能是自身免疫机制）引起的，并且这种肾脏疾病显然几乎与溶血过程完全无关。
