无毒单磷酰脂质A对抑制性T细胞活性的灭活作用。
Inactivation of suppressor T-cell activity by nontoxic monophosphoryl lipid A.
作者信息
Baker P J, Hiernaux J R, Fauntleroy M B, Prescott B, Cantrell J L, Rudbach J A
机构信息
Laboratory of Microbial Immunity, National Institute of Allergy and Infectious Diseases, Bethesda, Maryland 20892.
出版信息
Infect Immun. 1988 May;56(5):1076-83. doi: 10.1128/iai.56.5.1076-1083.1988.
Abstract
Treatment with nontoxic monophosphoryl lipid A (MPL), which was derived from a polysaccharide-deficient, heptoseless Re mutant of Salmonella typhimurium, was found to inactivate suppressor T-cell activity, as evidenced by a decrease in the degree of low-dose immunological paralysis expressed and an increase in the magnitude of the antibody response to type III pneumococcal polysaccharide. The effects produced, which could not be attributed to the polyclonal activation of immune B cells by MPL, were dependent upon the dose of MPL used, as well as the time when MPL was given relative to low-dose priming or immunization with type III pneumococcal polysaccharide. Neither amplifier nor helper T-cell activity was decreased by treatment with the same, or larger, doses of MPL. The significance of these findings to the use of MPL as an immunological adjuvant or an immunomodulating agent is discussed.
摘要
用无毒的单磷酰脂质A（MPL）进行治疗，该物质源自鼠伤寒沙门氏菌的多糖缺陷型、无庚糖Re突变体，结果发现它能使抑制性T细胞活性失活，这可通过低剂量免疫麻痹程度的降低以及对III型肺炎球菌多糖抗体反应强度的增加得到证明。所产生的效果并非由MPL对免疫B细胞的多克隆激活所致，而是取决于所用MPL的剂量，以及MPL相对于低剂量启动或用III型肺炎球菌多糖免疫的给药时间。用相同或更大剂量的MPL处理并不会降低放大性T细胞或辅助性T细胞的活性。文中讨论了这些发现对于将MPL用作免疫佐剂或免疫调节剂的意义。
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