Suppressor αβ T lymphocytes control innate resistance to endotoxic shock
Suppressor αβ T lymphocytes control innate resistance to endotoxic shock
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DOI：
10.1086/432727
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发表时间：
2005-09-15
影响因子：
6.4
通讯作者：
Vazquez-Torres, A
中科院分区：
文献类型：
--
作者：
Jones-Carson, J;Fantuzzi, G;Vazquez-Torres, A
大量的研究集中在阐明先天免疫系统细胞合成的细胞因子参与内毒素休克的危及生命的多器官衰竭的机制。我们在这里表明，抗体T细胞，这是适应性细胞免疫反应的原型，抑制在脂多糖（LPS）诱导的内毒素血症的早期阶段触发的促炎级联反应。缺乏ab T细胞导致LPS攻击小鼠的爆发性死亡，同时大量释放促炎细胞因子肿瘤坏死因子（TNF）-α和干扰素（IFN）-γ，以及免疫抑制细胞因子转化生长因子（TGF）-β的合成显著减少。LPS刺激后不久出现的细胞毒性T淋巴细胞抗原（CTLA）阳性α β T细胞似乎控制TGF-β的合成。TGF-β或CTLA 4的中和导致LPS攻击小鼠中IFN-γ和TNF-α血清浓度的相似增加。这些观察结果表明，抑制性ab T淋巴细胞保护免受内毒素血症的先天阶段释放的促炎级联反应。
A considerable amount of research has focused on elucidating the mechanisms by which cytokines synthesized by cells of the innate immune system participate in the life-threatening multiple-organ failure of endotoxic shock. We show here that ab T cells, which are archetypes of the adaptive cellular immune response, suppress the proinflammatory cascade triggered during the early stages of lipopolysaccharide (LPS)-induced endotoxemia. The absence of ab T cells led to the fulminant death of LPS-challenged mice, coinciding with a massive release of the proinflammatory cytokines tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma and a marked reduction in the synthesis of the immunosuppressive cytokine transforming growth factor (TGF)-beta. Cytotoxic T lymphocyte antigen (CTLA)-positive alpha beta T cells emerging shortly after LPS challenge appear to control TGF-beta synthesis. The neutralization of either TGF-beta or CTLA4 resulted in similar increases in IFN-gamma and TNF-alpha serum concentrations in LPS-challenged mice. These observations suggest that suppressor ab T lymphocytes protect against the proinflammatory cascade unleashed during the innate stages of endotoxemia.