Chan W L, Ziltener H J, Liew F Y
Department of Microbiology, UMDS, Medical School, Guy's Hospital, London, U.K.
Immunology. 1990 Nov;71(3):358-63.
Evidence presented here from kinetic studies of interleukin-3 (IL-3) production by spleen cells from adult mice infected subcutaneously with HSV-1 and stimulated with virus antigen in vitro shows that high levels of IL-3 were produced at the onset of the animal's recovery from the disease state. Injections of anti-IL-3 antibody into HSV-1-infected mice resulted in exacerbation of the disease. Primary mouse embryonic head cells grown in the presence of murine IL-3, when infected with HSV-1, showed a 1000-fold decrease in virus titre compared with untreated control cells. This inhibiting effect was reversed by anti-IL-3 and anti-IFN-alpha, beta and gamma antibodies. These data suggest that IL-3 plays a host-protective role against HSV infection and it does so probably by inducing brain cells to produce interferons which then inhibit virus replication.
此处呈现的证据来自对成年小鼠皮下感染单纯疱疹病毒1型（HSV-1）后脾脏细胞产生白细胞介素-3（IL-3）的动力学研究，这些脾脏细胞在体外经病毒抗原刺激后发现，在动物从疾病状态恢复开始时会产生高水平的IL-3。向感染HSV-1的小鼠注射抗IL-3抗体导致疾病加重。在鼠IL-3存在下生长的原代小鼠胚胎头部细胞，感染HSV-1后，与未处理的对照细胞相比，病毒滴度降低了1000倍。抗IL-3以及抗干扰素-α、β和γ抗体可逆转这种抑制作用。这些数据表明，IL-3在抗HSV感染中发挥宿主保护作用，其可能是通过诱导脑细胞产生干扰素，进而抑制病毒复制来实现的。
