Gern J E, Vrtis R, Kelly E A, Dick E C, Busse W W
Department of Pediatrics, University of Wisconsin School of Medicine, Madison 53792, USA.
J Immunol. 1996 Aug 15;157(4):1605-12.
There is evidence that rhinovirus (RV) infections are frequent causes of increased asthmatic symptoms and can specifically enhance allergic inflammation in the airway. To further define effects of RV infection on cellular immunity, we have begun to develop in vitro models for study. When human PBMC were incubated with 35S-labeled RV16, specific binding via ICAM-1 on monocytes was observed. Incubation of PBMC with RV also led to a dose-related increase in the expression of the early activation marker CD69 on 30 to 70% of T cells. The RV16-induced increases in CD69 were blocked by anti-ICAM-1 mAb, and were not elicited by UV-inactivated (noninfectious) virus. The degree of CD69 enhancement correlated with the number of monocytes in mixtures of PBMC, did not occur in monocyte-depleted cultures, and was mediated by one or more soluble factor(s). RV also induced secretion of IFN-gamma from both peripheral blood T cells and NK cells, and IFN-gamma mRNA was greatest in T cells that were CD69+. Finally, supernatant from RV-activated CD3+CD69+ cells had biologic activity that promoted eosinophil survival in vitro; this RV16-associated activity was blocked when co-incubations were performed with IFN-gamma mAbs. These observations suggest that RV nonspecifically activates a large proportion of T cells through a monocyte-dependent mechanism. Such changes in vivo could enhance airway inflammation, and this may include effects on inflammatory cells in the airways of allergic individuals.
有证据表明，鼻病毒（RV）感染是哮喘症状加重的常见原因，并且能够特异性增强气道中的过敏性炎症。为了进一步明确RV感染对细胞免疫的影响，我们已开始建立体外研究模型。当人外周血单核细胞（PBMC）与35S标记的RV16一起孵育时，可观察到单核细胞通过细胞间黏附分子-1（ICAM-1）发生特异性结合。PBMC与RV一起孵育还导致30%至70%的T细胞上早期活化标志物CD69的表达呈剂量相关增加。RV16诱导的CD69增加被抗ICAM-1单克隆抗体阻断，且紫外线灭活（无感染性）病毒不会引发这种增加。CD69增强的程度与PBMC混合物中单核细胞的数量相关，在单核细胞耗竭的培养物中未出现，并且由一种或多种可溶性因子介导。RV还诱导外周血T细胞和自然杀伤（NK）细胞分泌γ干扰素（IFN-γ），且IFN-γ mRNA在CD69+的T细胞中含量最高。最后，RV激活的CD3+CD69+细胞的上清液具有促进嗜酸性粒细胞在体外存活的生物活性；当与IFN-γ单克隆抗体共同孵育时，这种与RV16相关的活性被阻断。这些观察结果表明，RV通过单核细胞依赖性机制非特异性激活大部分T细胞。体内的这种变化可能会增强气道炎症，这可能包括对过敏性个体气道中炎症细胞的影响。
