MELLORS R C, ORTEGA L G, HOLMAN H R
J Exp Med. 1957 Aug 1;106(2):191-202. doi: 10.1084/jem.106.2.191.
Utilizing the fluorescent antibody method for the histologic demonstration of localized gamma-globulins, we have made the following observations (in contradistinction to the lack of such findings in a variety of normal and pathologic, control kidneys). In systemic lupus erythematosus (a) gamma-globulins were localized in the thickened capillary walls, the "wire-loop" lesions, and the so called "hyaline thrombi" in glomeruli; (b) these sites of localization of gamma-globulins were correlated to a considerable degree with the pattern of accentuated eosinophilia of the glomeruli, as seen in hematoxylin-eosin sections, or with the pattern of PAS-positive areas in the glomeruli in sections stained with the periodic acid-Schiff reaction; (c) and gamma-globulins were localized rarely in large cytoplasmic granules in tubular epithelium and occasionally in glomerular capsular crescents, tubular protein casts, and inflammatory cells, particularly in the cytoplasm of cells identified as immature and mature plasma cells. In nephrotic glomerulonephritis (a) gamma-globulins were localized in the glomerular basement membrane and appertaining structures in chronic membranous glomerulonephritis; (b) gamma-globulins were apparently localized in the altered mesangium in chronic lobular glomerulonephritis; and (c) in the tubular protein casts, presumably representing abnormal glomerular filtrates, gamma-globulins were present in a lesser concentration and other serum proteins in a greater concentration than found in the glomeruli. In positive lupus erythematosus preparations the nuclei of leukocytes, while undergoing transformation and subsequent phagocytosis to form lupus erythematosus cells, were the sites of localization of gamma-globulin (presumably the lupus erythematosus factor) whereas in control preparations no nuclear localization of gamma-globulin occurred. These observations are discussed in relation to the pathogenesis of renal lesions in systemic lupus erythematosus, chronic membranous glomerulonephritis, and amyloidosis.
利用荧光抗体法对局部γ球蛋白进行组织学显示，我们有以下观察结果（与多种正常和病理对照肾脏中缺乏此类发现形成对比）。在系统性红斑狼疮中：（a）γ球蛋白定位于肾小球中增厚的毛细血管壁、“线圈样”病变及所谓的“透明血栓”处；（b）γ球蛋白的这些定位部位在很大程度上与苏木精 - 伊红切片中所见的肾小球嗜酸性增强模式相关，或与经高碘酸 - 希夫反应染色的切片中肾小球的PAS阳性区域模式相关；（c）γ球蛋白很少定位于肾小管上皮细胞的大细胞质颗粒中，偶尔定位于肾小球囊新月体、肾小管蛋白管型及炎性细胞中，特别是定位于被鉴定为未成熟和成熟浆细胞的细胞质中。在肾病性肾小球肾炎中：（a）γ球蛋白定位于慢性膜性肾小球肾炎的肾小球基底膜及相关结构中；（b）γ球蛋白明显定位于慢性小叶性肾小球肾炎中改变的系膜中；（c）在可能代表异常肾小球滤过液的肾小管蛋白管型中，γ球蛋白的浓度低于肾小球，而其他血清蛋白的浓度高于肾小球。在阳性红斑狼疮制剂中，白细胞的细胞核在经历转化并随后被吞噬形成红斑狼疮细胞时，是γ球蛋白（可能是红斑狼疮因子）的定位部位，而在对照制剂中未发生γ球蛋白的核定位。这些观察结果结合系统性红斑狼疮、慢性膜性肾小球肾炎和淀粉样变性中肾脏病变的发病机制进行了讨论。
