The role of antibody in recovery from experimental rabies. I. Effect of depletion of B and T cells.
The role of antibody in recovery from experimental rabies. I. Effect of depletion of B and T cells.
复制标题
抗体在实验性狂犬病恢复中的作用。
作者：
Aaron W. Miller;Herbert C. Morse;Jerry A. Winkelstein;Neal Nathanson
在脑内接种的成年小鼠中，无毒的高卵传代（HEP）毒株产生仅限于中枢神经系统（CNS）的隐性感染。重链同型（抗mu抗血清）免疫抑制增强了感染，死亡率约为60%，脑内病毒滴度升高。抗mu处理的小鼠不能提高对狂犬病毒的抗体反应，尽管它们的T细胞功能在脾淋巴细胞的刀豆蛋白A反应中是正常的。这表明B细胞反应在清除狂犬病毒的神经实质中起重要作用。与同型抑制相比，环磷酰胺治疗或成人胸腺切除术、x射线照射和骨髓重建在更大程度上增强了HEP感染。由于这些抑制技术损害T和B淋巴细胞反应，数据表明细胞免疫机制也可能有助于宿主防御中枢神经系统（CNS）病毒感染。
The avirulent high egg passage (HEP) strain of rabies virus produces an inapparent infection limited to the central nervous system (CNS) in intracerebrally inoculated adult mice. Heavy chain isotype (anti-mu antiserum) immunosuppression potentiates the infection, with a mortality of about 60% and with elevated virus titers in the brain. Anti-mu-treated mice fail to raise antibody responses to rabies virus although their T cell function is normal when measured by the concanavalin A response of splenic lymphocytes. This indicates that the B cell response plays an important role in clearance of rabies virus from the neuroparenchyma. Treatment with cyclophosphamide or by adult thymectomy, x-irradiation, and bone marrow reconstitution potentiates HEP infection to a greater extent than does isotype suppression. Since these suppressive techniques impair both T and B lymphocyte responses, the data suggest that cellular immune mechanisms may also contribute to host defenses against this central nervous system (CNS) virus infection.