Coutelier J P, Coulie P G, Wauters P, Heremans H, van der Logt J T
Unit of Experimental Medicine, Université Catholique de Louvain, Brussels, Belgium.
J Virol. 1990 Nov;64(11):5383-8. doi: 10.1128/JVI.64.11.5383-5388.1990.
Viruses such as lactate dehydrogenase-elevating virus and adenovirus induce in vivo a polyclonal activation of murine B lymphocytes, followed by a marked increase in the production of immunoglobulin G2a (IgG2a). The role of T lymphocytes in this phenomenon was studied by injection of an anti-CD4 monoclonal antibody able to inhibit the T-helper function. This treatment profoundly depressed the production of IgG2a, whereas it had no effect on the proliferation of B cells. Activated B cells obtained from such infected and treated mice remained able to produce various immunoglobulin isotypes after exposure to an appropriate stimulus. In particular, gamma interferon, which is known to be secreted after viral infection, induced the production of IgG2a. These observations support the hypothesis that the influence of viruses on the switch of immunoglobulins is mediated by T-helper lymphocytes.
诸如乳酸脱氢酶升高病毒和腺病毒之类的病毒在体内可诱导小鼠B淋巴细胞发生多克隆激活,随后免疫球蛋白G2a(IgG2a)的产生显著增加。通过注射能够抑制T辅助功能的抗CD4单克隆抗体来研究T淋巴细胞在此现象中的作用。这种处理显著抑制了IgG2a的产生,而对B细胞的增殖没有影响。从这种感染并经过处理的小鼠获得的活化B细胞在受到适当刺激后仍能够产生各种免疫球蛋白同种型。特别是,已知在病毒感染后分泌的γ干扰素可诱导IgG2a的产生。这些观察结果支持了以下假设:病毒对免疫球蛋白转换的影响是由T辅助淋巴细胞介导的。