Endotoxin-induced T lymphocyte proliferation.
Endotoxin-induced T lymphocyte proliferation.
复制标题
内毒素诱导 T 淋巴细胞增殖。
作者：
S. Vogel;M. Hilfiker;M. Caulfield
淋巴细胞对内毒素（LPS）的反应主要归因于该试剂作为B淋巴细胞的多克隆活化剂的作用。在这项研究中，我们发现，克隆的小鼠白细胞介素2依赖性细胞毒性T细胞系，CT 6，增殖响应LPS，从而提供了第一个证据，T细胞可以直接刺激LPS。该反应是剂量和时间依赖性的，并被多粘菌素B（一种LPS诱导的有丝分裂抑制剂）阻断。这是一个克隆的T细胞系，不含其他潜在污染的淋巴样细胞类型，这一事实排除了这种增殖是由于污染的B淋巴细胞或由巨噬细胞衍生产物如白细胞介素1介导的可能性。此外，高度纯化的脾T淋巴细胞群（通过阴性/阳性选择或通过严格的柱纯化程序纯化）含有响应于LPS增殖的T细胞的小亚群（约3%）。内毒素低反应C3 H/HeJ小鼠中缺少该群体。如在CT 6系中观察到的，脾T细胞响应于LPS的增殖被多粘菌素B抑制。此外，用抗T细胞抗体加补体处理LPS刺激的T细胞可阻断这些培养物对3 H-胸苷的摄取。外源性白细胞介素1未能刺激LPS刺激的T细胞培养物，因此不能解释观察到的刺激程度。这些发现支持并扩展了先前的发现，这些发现表明内毒素敏感性T细胞群体在诱导某些反应中的作用，例如LPS诱导的淋巴细胞依赖性LPS诱导巨噬细胞促凝血活性的佐剂性。
The lymphocyte response to endotoxin (LPS) has been attributed largely to the action of this agent as a polyclonal activator of B lymphocytes. In this study we found that a cloned murine interleukin 2-dependent cytotoxic T cell line, CT 6, proliferates in response to LPS, thus providing the first evidence that T cells can be stimulated directly by LPS. The response was dose and time dependent and was blocked by polymyxin B, an inhibitor of LPS-induced mitogenesis. The fact that this is a cloned T cell line, free of other potentially contaminating lymphoid cell types, precludes the possibility that this proliferation is due to contaminating B lymphocytes or is mediated by macrophage-derived products such as interleukin 1. Moreover, highly purified splenic T lymphocyte populations (purified by negative/positive selection or by a rigorous column purification procedure) contain a small subpopulation (approximately 3%) of T cells that proliferate in response to LPS. This population is missing in the endotoxin-hyporesponsive C3H/HeJ mouse. As was observed in the CT 6 line, proliferation of splenic T cells in response to LPS was inhibited by polymyxin B. Furthermore, treatment of LPS-stimulated T cells with anti-T cell antibodies plus complement blocks the uptake of 3H-thymidine by these cultures. Exogenous interleukin 1 failed to stimulate the T cell cultures comparably to LPS and therefore cannot account for the degree of stimulation observed. These findings support and extend previous findings that suggested a role for an endotoxin-sensitive T cell population in the induction of certain responses, such as LPS-induced adjuvanticity of the lymphocyte-dependent LPS induction of macrophage procoagulant activity.