NEW AVIAN MODEL OF EXPERIMENTAL GLOMERULONEPHRITIS CONSISTENT WITH MEDIATION BY CELLULAR-IMMUNITY - NONHUMORALLY MEDIATED GLOMERULONEPHRITIS IN CHICKENS
NEW AVIAN MODEL OF EXPERIMENTAL GLOMERULONEPHRITIS CONSISTENT WITH MEDIATION BY CELLULAR-IMMUNITY - NONHUMORALLY MEDIATED GLOMERULONEPHRITIS IN CHICKENS
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DOI：
10.1172/jci111328
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发表时间：
1984-01-01
影响因子：
15.9
通讯作者：
STURGILL, BC
中科院分区：
文献类型：
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作者：
BOLTON, WK;TUCKER, FL;STURGILL, BC
研究了细胞介导免疫（CMI）在体液介导免疫（HMI）缺陷鸡的实验性自身免疫性肾小球肾炎（EAG）发生中的作用。采用环磷酰胺法氏囊化（Bsx）和正常对照鸡。Bsx鸡仅在HMI严重抑制时才使用，法氏囊重量明显减少（0.89 .+-）。0.23 vs. 2.92。0.9 g)，血清IgG降低至0.01%。正常的10%，和完全缺乏HMI的羊红细胞免疫。用牛肾小球基底膜（GBM）在完全弗氏佐剂中免疫鸡制备EAG。CMI与PPD的差异无统计学意义，为3.89 +-。Bsx为0.45 mm，而Bsx为3.73 mm。0.75毫米的控制。68%的Bsx鸡未产生GBM循环抗体，抗体阳性的Bsx鸡抗GBM滴度< 1:12 12，而对照组为1:20 00。荧光显示，GBM中IgG沉积明显减少，为0.53 +-。0.16比2.19。对照组为0.32,64%的Bsx鸡不存在。Bsx鸡的增生性肾炎呈新月形，比对照组更严重，肾小球大小为20.8 +-。Bsx-GBM为0.6 U, 19.8 +-。对照gbm为1.2,14.9 .+-。Bsx为1.5,13.6 +-。正常鸡0.8。肾脏洗脱液在正常鸡中不产生疾病，而经放射自显像显示，将含有[H3]胸腺嘧啶的致敏细胞用于本地鸟类可增加系膜颗粒计数。在无HMI的情况下，CMI显然在鸡EAG发病机制中起主要作用。由此可见，CMI在其他类型肾小球肾炎的发展中也可能是至关重要的。
The role of cell-mediated immunity (CMI) in the production of experimental autoimmune glomerulonephritis (EAG) was studied in chickens deficient in humorally mediated immunity (HMI). Cyclophosphamide bursectomized (Bsx) and normal control chickens were used. Bsx chickens were used only if they had severe depression of HMI, which was evidenced by marked reduction in bursal weights (0.89 .+-. 0.23 vs. 2.92 .+-. 0.9 g), decreased serum IgG to .ltoreq. 10% of normal, and total lack of HMI to immunization with sheep red blood cells. EAG was produced by immunizing chickens with bovine glomerular basement membrane (GBM) in complete Freund''s adjuvant. CMI manifested by wattle thickness increments to PPD was not different, 3.89 .+-. 0.45 mm for Bsx compared with 3.73 .+-. 0.75 mm for controls. No circulating antibodies to GBM developed in 68% of Bsx chickens, and the anti-GBM titers were < 1:312 in those Bsx chickens positive for antibody compared with > 2,000 for controls. GBM deposits of IgG by fluorescence were much decreased, 0.53 .+-. 0.16 compared with 2.19 .+-. 0.32 for controls, and were absent in 64% of Bsx chickens. Proliferative nephritis with crescents was present and was even more severe in Bsx chickens than in controls, with glomerular sizes of 20.8 .+-. 0.6 U for Bsx-GBM, 19.8 .+-. 1.2 for control-GBM, 14.9 .+-. 1.5 for Bsx, and 13.6 .+-. 0.8 for normal chickens. Nephritic eluates did not produce disease in normal chickens, while administration of sensitized cells with [H3]thymidine to native birds was associated with increased mesangial grain counts by autoradiography. CMI apparently plays a major role in the pathogenesis of EAG in chickens in the absence of HMI. By implication, CMI may be crucial in the development of other types of glomerulonephritis as well.