Utsunomiya T, Kobayashi M, Herndon D N, Pollard R B, Suzuki F
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555, USA.
Immunol Lett. 1995 Jan;44(1):59-66. doi: 10.1016/0165-2478(94)00183-r.
The effect of glycyrrhizin (GR) on the resistance of thermally injured mice to opportunistic herpes simplex virus type 1 (HSV) infection was investigated. We have previously reported that the susceptibility of thermally injured mice or normal mice inoculated with T6S cells (a clone of burn-associated CD8+ CD11b+ TCR gamma/delta + type-2 suppressor T cells), to HSV infection was about 100 times greater than it was in normal mice. When thermally injured mice were treated i.p. with a 10 mg/kg dose of GR 2 and 4 days after infection of HSV, the resistance of these mice to HSV was improved to levels observed in normal mice. The adoptive transfer of splenic mononuclear cells (MNC) from normal mice treated with GR (GR-MNC) to thermally injured mice (recipients) resulted in the improved resistance of recipients to HSV infection. Normal mice inoculated with T6S cells and exposed to HSV had an 80% mortality rate, when given GR-MNC they had a 95% survival rate. The suppressor cell activity of T6S cells was clearly counteracted by GR-MNC in vitro in a mixed lymphocyte-tumor cell reaction. The type of cells responsible for anti-suppressor cells in GR-MNC was shown to be a CD4+ CD28+ TCR alpha/beta + Vicia villosa lectin-adherent T cell. These results suggest that GR may reverse the increased susceptibility of thermally injured mice to HSV infection through the induction of CD4+ contrasuppressor T cells.
研究了甘草酸（GR）对热损伤小鼠抵抗机会性单纯疱疹病毒1型（HSV）感染的影响。我们之前报道过，热损伤小鼠或接种T6S细胞（一种烧伤相关的CD8 + CD11b + TCRγ/δ + 2型抑制性T细胞克隆）的正常小鼠对HSV感染的易感性比正常小鼠高约100倍。当热损伤小鼠在感染HSV后第2天和第4天腹腔注射10 mg/kg剂量的GR时，这些小鼠对HSV的抵抗力提高到了正常小鼠的水平。将用GR处理的正常小鼠的脾单核细胞（MNC）（GR-MNC）过继转移到热损伤小鼠（受体）中，导致受体对HSV感染的抵抗力提高。接种T6S细胞并暴露于HSV的正常小鼠死亡率为80%，给予GR-MNC后存活率为95%。在混合淋巴细胞-肿瘤细胞反应中，GR-MNC在体外明显抵消了T6S细胞的抑制细胞活性。GR-MNC中负责抗抑制细胞的细胞类型显示为CD4 + CD28 + TCRα/β + 野豌豆凝集素粘附T细胞。这些结果表明，GR可能通过诱导CD4 + 抗抑制性T细胞来逆转热损伤小鼠对HSV感染增加的易感性。
