Kobayashi M, Kobayashi H, Mori K, Pollard R, Suzuki F
Department of Internal Medicine, University of Texas Medical Branch, Galveston 77555-0835, USA.
Immunol Cell Biol. 1998 Jun;76(3):209-16. doi: 10.1046/j.1440-1711.1998.00736.x.
In the accompanying paper, the resistance to infections with HSV type 1 (HSV-1) and Candida albicans was improved in thermally injured mice treated with benzoylmesaconine (BEN), an aconitine-hydrolysate isolated from heated Aconiti tuber, or inoculated with splenic CD4+ T cells from BEN-treated mice (BEN T cells). In this paper, therefore, the antiviral mechanism of BEN T cells (or BEN) on the improved resistance of burned mice to the HSV-1 infection was studied. Burn-associated CD + CD11b+ TCRgamma/delta+ type-2 T cells have been shown to be a key on the increased susceptibility of thermally injured mice to infection with HSV-1 or C. albicans. The susceptibility of T6S-mice, mice inoculated with 1 x 10(6) cells/mouse of T6S cells (a clone of burn-associated type-2 T cells), to HSV-1 infection was similar to that of thermally injured mice. The adoptive transfer of BEN T cells to T6S-mice restores their impaired resistance to HSV-1 infection. The type-2 cytokine levels in sera of T6S-mice were decreased after inoculation of BEN T cells. BEN T cells inhibited the type-2 cytokine production by T6S cells when they were cocultured in vitro. BEN T cells, characterized as CD4+ CD28+ TCRalpha/beta+ Vicia villosa (VV) lectin-adherent T cells, showed non-specific ability to inhibit the cytokine production by various type-2 T cells. From the results of the cytokine-producing profile, BEN T cells were shown to be a different subset of CD4+ T cells from Th1 and Th2 cells, although these three CD4+ T cells had similar properties phenotypically. BEN T cells were induced in normal mice 1-4 days after the oral treatment of BEN (1 microg/kg or more). These results suggest that, through the induction of antagonistic CD4+ T cells against burn-associated type-2 T cells, BEN may improve the resistance of T6S-mice (or thermally injured mice) to the infection of HSV-1.
在随附论文中，用苯甲酰新乌头碱（BEN，一种从制川乌中分离得到的乌头碱水解产物）处理的热损伤小鼠，或接种来自经BEN处理小鼠的脾CD4⁺ T细胞（BEN T细胞）后，对1型单纯疱疹病毒（HSV - 1）和白色念珠菌感染的抵抗力有所提高。因此，在本文中，研究了BEN T细胞（或BEN）对烧伤小鼠抗HSV - 1感染抵抗力提高的抗病毒机制。烧伤相关的CD⁺ CD11b⁺ TCRγ/δ⁺ 2型T细胞已被证明是热损伤小鼠对HSV - 1或白色念珠菌感染易感性增加的关键因素。T6S小鼠（接种1×10⁶ 个细胞/只T6S细胞（一种烧伤相关2型T细胞克隆）的小鼠）对HSV - 1感染的易感性与热损伤小鼠相似。将BEN T细胞过继转移到T6S小鼠可恢复其受损的抗HSV - 1感染抵抗力。接种BEN T细胞后，T6S小鼠血清中的2型细胞因子水平降低。当BEN T细胞与T6S细胞在体外共培养时，BEN T细胞可抑制T6S细胞产生2型细胞因子。BEN T细胞的特征为CD4⁺ CD28⁺ TCRα/β⁺ 野豌豆（VV）凝集素黏附性T细胞，显示出抑制各种2型T细胞产生细胞因子的非特异性能力。从细胞因子产生谱的结果来看，BEN T细胞显示为CD4⁺ T细胞中不同于Th1和Th2细胞的一个亚群，尽管这三种CD4⁺ T细胞在表型上具有相似的特性。在正常小鼠口服BEN（1微克/千克或更高剂量）后1 - 4天可诱导产生BEN T细胞。这些结果表明，通过诱导针对烧伤相关2型T细胞的拮抗性CD4⁺ T细胞，BEN可能提高T6S小鼠（或热损伤小鼠）对HSV - 1感染的抵抗力。
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