Woodruff J J, Woodruff J F
J Immunol. 1976 Sep;117(3):852-8.
The effect of influenza virus A/Japan 305 (H2N2) on the path of migration of recirculating lymphocytes has been studied. 51Cr-labeled rat thoracic duct lymphocytes (TDL) were incubated with virus at 37 degrees C for 1 hr and then infused i.v. into syngeneic recipients which were killed 1 hr later. Virus-treated TDL accumulated in the liver and their recovery in lymph nodes and spleen was severely reduced. Changes in lymphocytes induced by virus developed rapidly and were evident after incubation for only 15 min. UV-irradiated virus altered the pattern of lymphocyte localization but attachment of heat-inactivated virus to lymphocytes in vitro had no effect on their distribution in vivo. Evidence was obtained that some virus-treated TDL, initially sequestered in the liver, subsequently recovered their ability to circulate normally. Recovery was not complete and a population of cells failed to regain their ability to home into lymph nodes. Evidence is also presented demonstrating that influenza virus affected the homing properties of both T and B cells. It is suggested that aberrations in lymphocyte homing were mediated by the viral neuraminidase which induces changes in the cell membrane leading to their accumulation in the liver.
研究了甲型流感病毒A/日本305(H2N2)对再循环淋巴细胞迁移途径的影响。将51Cr标记的大鼠胸导管淋巴细胞(TDL)与病毒在37℃孵育1小时,然后静脉注射到同基因受体中,1小时后将受体处死。经病毒处理的TDL积聚在肝脏中,其在淋巴结和脾脏中的回收率严重降低。病毒诱导的淋巴细胞变化发展迅速,仅孵育15分钟后就很明显。紫外线照射的病毒改变了淋巴细胞定位模式,但热灭活病毒在体外与淋巴细胞的结合对其体内分布没有影响。有证据表明,一些经病毒处理的TDL最初被隔离在肝脏中,随后恢复了正常循环的能力。恢复并不完全,一群细胞未能重新获得归巢到淋巴结的能力。也有证据表明,流感病毒影响T细胞和B细胞的归巢特性。有人提出,淋巴细胞归巢异常是由病毒神经氨酸酶介导的,该酶诱导细胞膜变化,导致它们在肝脏中积聚。