Masuda A, Burton G F, Fuchs B A, Bhogal B S, Rupper R, Szakal A K, Tew J G
Department of Microbiology and Immunology, Medical College of Virginia/Virginia Commonwealth University, Richmond 23298.
Immunology. 1994 Jan;81(1):41-6.
Infection of mice with LP-BM5 elicits an immunodeficiency state referred to as murine acquired immune deficiency syndrome (MAIDS). Shortly after infection, retrovirus particles become associated with follicular dendritic cells (FDC) and this study was undertaken to determine whether retroviruses alter FDC functions. The FDC functions examined included the ability to: (1) retain antigen (Ag) trapped prior to infection; (2) trap new Ag after infection; (3) maintain specific IgG responses; and (4) provide co-stimulatory signals to B cells. Mice were infected with LP-BM5 and the ability of their FDC to trap and retain 125I-Ag (HSA) was assessed. Serum anti-HSA levels were monitored and FDC co-stimulatory activity was indicated by increased B-cell proliferation. HSA trapped on FDC prior to infection began to disappear by 3 weeks and was practically gone by 6 weeks. Serum anti-HSA titres were maintained normally for about 3 weeks after infection and then declined precipitously. The ability of FDC to trap new Ag began to disappear around the second and third week of infection and was markedly depressed by the fourth week. However, FDC recovered from infected mice retained their ability to co-stimulate anti-mu- and interleukin-4 (IL-4)-activated B cells throughout a 5-week period. In short, the ability of FDC to trap and retain specific Ag and maintain specific antibody levels was markedly depressed after retrovirus infection. However, FDC from infected mice continued to provide co-stimulatory signals and these signals may contribute to the lymphadenopathy and splenomegaly characteristic of MAIDS.
用LP - BM5感染小鼠会引发一种免疫缺陷状态，称为小鼠获得性免疫缺陷综合征（MAIDS）。感染后不久，逆转录病毒颗粒与滤泡树突状细胞（FDC）相关联，本研究旨在确定逆转录病毒是否会改变FDC的功能。所检测的FDC功能包括：（1）保留感染前捕获的抗原（Ag）；（2）感染后捕获新的Ag；（3）维持特异性IgG反应；（4）向B细胞提供共刺激信号。用LP - BM5感染小鼠，并评估其FDC捕获和保留125I - Ag（HSA）的能力。监测血清抗HSA水平，B细胞增殖增加表明FDC的共刺激活性。感染前捕获在FDC上的HSA在3周时开始消失，到6周时几乎完全消失。感染后血清抗HSA滴度通常维持约3周，然后急剧下降。FDC捕获新Ag的能力在感染的第二和第三周左右开始消失，到第四周时明显降低。然而，从感染小鼠中恢复的FDC在5周内仍保留其共刺激抗μ和白细胞介素 - 4（IL - 4）激活的B细胞的能力。简而言之，逆转录病毒感染后，FDC捕获和保留特异性Ag以及维持特异性抗体水平的能力明显降低。然而，感染小鼠的FDC继续提供共刺激信号，这些信号可能导致MAIDS特有的淋巴结病和脾肿大。
