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梅毒期间的细胞介导免疫。

Cell-mediated immunity during syphilis.

作者信息

Pavis C S, Folds J D, Baseman J B

出版信息

Br J Vener Dis. 1978 Jun;54(3):144-50. doi: 10.1136/sti.54.3.144.

Abstract

Evidence is presented which reinforces the complexity of the host-parasite interaction during the course of syphilis. Infection with Treponema pallidum evokes a complicated antibody response and an assortment of cell-mediated immune reactions in the host. It appears that humoral immunity plays a minor role towards the complete elimination of syphilitic infection while the cellular limb of the immune response may be an important host defence mechanism. Information now available indicates that a state of anergy, or immunosuppression, exists in the early stages of human and experimental rabbit syphilis based upon negative skin reactions to T. pallidum antigen(s), the abnormal histological appearance of lymphoid organs, and impaired in vitro lymphocyte reactivity. It is also evident that in the later stages of the disease cellular immunity becomes activated as delayed type skin reactions can normally be elicited in tertiary syphilitics and lymphocyte behaviour in cell culture appears normal. Several mechanisms have been invoked to explain the delay in an effective immune response against syphilitic infection and the duration of the disease: (1) a capsule-like substance on the outer surface of virulant T. pallidum may act as a barrier against treponemicidal antibody; (2) this material and other biological properties of virulent treponemes could enable spirochaetes to escape being engulfed by macrophages and other phagocytic cells; (3) antigenic competition among different treponemal antigens causing partial tolerance; (4) T. pallidum infection may bring about the elaboration of immunosuppressive substances of host or treponemal origin which inhibit the proper function of lymphocytes, macrophages, and other cell types.

摘要

现有证据强化了梅毒病程中宿主 - 寄生虫相互作用的复杂性。梅毒螺旋体感染可引发宿主复杂的抗体反应及一系列细胞介导的免疫反应。体液免疫在梅毒感染的完全清除中似乎作用较小,而免疫反应的细胞部分可能是重要的宿主防御机制。目前可得的信息表明,基于对梅毒螺旋体抗原的皮肤阴性反应、淋巴器官异常的组织学表现以及体外淋巴细胞反应受损,在人类和实验性兔梅毒的早期存在无反应或免疫抑制状态。同样明显的是,在疾病后期细胞免疫被激活,因为三期梅毒患者通常可引发迟发型皮肤反应,且细胞培养中的淋巴细胞行为看似正常。已提出多种机制来解释针对梅毒感染的有效免疫反应延迟及疾病持续时间:(1)毒力强的梅毒螺旋体外表面的一种类似荚膜的物质可能作为抗梅毒螺旋体抗体作用的屏障;(2)这种物质及毒力强的梅毒螺旋体的其他生物学特性可能使螺旋体逃避被巨噬细胞和其他吞噬细胞吞噬;(3)不同梅毒螺旋体抗原之间的抗原竞争导致部分耐受性;(4)梅毒螺旋体感染可能导致宿主或梅毒螺旋体来源的免疫抑制物质的产生,这些物质会抑制淋巴细胞、巨噬细胞和其他细胞类型的正常功能。

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