Peres A, Seemayer T A, Lapp W S
Clin Immunol Immunopathol. 1986 Apr;39(1):102-11. doi: 10.1016/0090-1229(86)90209-6.
The effects of polyinosinic: polycytidylic acid (pI:C) on the graft-versus-host (GVH) reaction were studied. The drug pI:C rapidly and markedly induces interferon and augments natural killer (NK) cell activity. GVH reactions were induced by injecting parental lymphoid cells intravenously into F1 hybrid mice. The development of a GVH reaction was monitored by measuring the plaque-forming cell (PFC) response to sheep red blood cells (SRBC) and by histological examination. When 30 X 10(6) B6 lymphoid cells were injected into B6AF1 mice, the recipients developed profound immunosuppression by 10-12 days post-GVH induction. In addition, pathological changes indicative of GVH reactions were seen in the spleen, lymph nodes, thymus, liver, lung, pancreas, and salivary gland of these mice. However, the treatment of B6AF1 recipients with pI:C prior to parental cell transfer markedly reduced the degree of suppression of the immune response, as measured by the PFC response to SRBC. Also, such mice failed to demonstrate the histological lesions of GVH disease. Treatment of donor mice with pI:C had no effect in preventing either GVH-induced immunosuppression or pathological changes. This study suggests that a pI:C-induced mechanism, possibly involving NK cells, is capable of regulating the GVH reaction.
聚胞苷酸(pI:C)对移植物抗宿主(GVH)反应的影响。药物pI:C能快速且显著地诱导干扰素并增强自然杀伤(NK)细胞活性。通过将亲代淋巴细胞静脉注射到F1杂种小鼠体内诱导GVH反应。通过测量对绵羊红细胞(SRBC)的空斑形成细胞(PFC)反应以及组织学检查来监测GVH反应的发展。当将30×10⁶个B6淋巴细胞注射到B6AF1小鼠体内时,受体在GVH诱导后10 - 12天出现严重的免疫抑制。此外,在这些小鼠的脾脏、淋巴结、胸腺、肝脏、肺、胰腺和唾液腺中可见指示GVH反应的病理变化。然而,在亲代细胞转移前用pI:C处理B6AF1受体,通过对SRBC的PFC反应测量,显著降低了免疫反应的抑制程度。而且,这类小鼠未表现出GVH病的组织学损伤。用pI:C处理供体小鼠对预防GVH诱导的免疫抑制或病理变化均无作用。这项研究表明,一种可能涉及NK细胞的pI:C诱导机制能够调节GVH反应。