Boros D L
Ann N Y Acad Sci. 1986;465:313-23. doi: 10.1111/j.1749-6632.1986.tb18507.x.
Schistosomiasis mansoni is a chronic, T lymphocyte-mediated granulomatous disease that affects mainly the liver and intestines of the infected host. The chronic inflammatory process and subsequent fibrous repair are the major factors in the pathology of the disease. In the murine model of schistosomiasis at the onset of the chronic stage of the infection, the granulomatous response undergoes spontaneous modulation with concomitant alleviation of the pathologic disturbance. Analysis of the process of modulation revealed that it results from the interaction between inflammatory and regulatory subpopulations of T lymphocytes. At the acute phase of the infection, the granulomatous response is initiated and maintained by inflammatory TDH cells that release lymphokines which mobilize and recruit the macrophages, eosinophils, etc. for the generation of the lesion. Already at this stage, while the inflammatory influence prevails, a low number of suppressor T lymphocytes are present. With the progress of the infection, the overheated inflammatory response is curbed by regulatory processes. At least two, but perhaps more, T suppressor lymphocytes are involved in the maintenance of the modulation of the granulomatous response. Modulation is an active process that needs constant maintenance, probably by recruitment of fresh suppressor cells. Removal of the suppressor population causes an immediate elevation of the granulomatous response. During modulation, T suppressor lymphocytes either abrogate or greatly diminish inflammatory lymphokine production. This in turn may be the cause for decreased cell recruitment and diminution in newly formed granuloma size. Apparently a total abrogation of the granulomatous response is not desirable because released egg antigens can be harmful to liver parenchyma cells. This has been demonstrated both in thymus-deprived and in nude, infected mice. Thus, a smaller inflammatory response has the double advantage of not only being less destructive, but also shielding the underlying tissue from damage by parasite products. The various subpopulations of T lymphocytes communicate with one another by means of soluble suppressor factors that arise from the suppressor T cells. The factors may have different functions. One factor may regulate lymphokine production whereas another may recruit fresh suppressor cells from a pool of precursors. The factors act in an antigen-specific manner. Tentatively, one may assume that these factors are composed of two units: one is the I subregion membrane marker and the other is the specific recognition receptor. The nature of this receptor is still unclear, but it may be an anti-idiotypic determinant.(ABSTRACT TRUNCATED AT 400 WORDS)
曼氏血吸虫病是一种慢性的、由T淋巴细胞介导的肉芽肿性疾病，主要影响受感染宿主的肝脏和肠道。慢性炎症过程及随后的纤维修复是该疾病病理学的主要因素。在血吸虫病的小鼠模型中，感染进入慢性期时，肉芽肿反应会自发调节，同时病理紊乱也会减轻。对调节过程的分析表明，这是由T淋巴细胞的炎性亚群和调节亚群之间的相互作用导致的。在感染急性期，肉芽肿反应由炎性TDH细胞启动并维持，这些细胞释放淋巴因子，动员和招募巨噬细胞、嗜酸性粒细胞等以形成病变。在这个阶段，尽管炎性影响占主导，但已经存在少量抑制性T淋巴细胞。随着感染的进展，过度的炎性反应会受到调节过程的抑制。至少有两种，但可能更多的抑制性T淋巴细胞参与维持肉芽肿反应的调节。调节是一个需要持续维持的活跃过程，可能是通过招募新的抑制细胞来实现。去除抑制细胞群体会导致肉芽肿反应立即增强。在调节过程中，抑制性T淋巴细胞要么消除要么极大地减少炎性淋巴因子的产生。这反过来可能是细胞募集减少和新形成的肉芽肿大小减小的原因。显然，完全消除肉芽肿反应是不可取的，因为释放的虫卵抗原可能对肝实质细胞有害。这在无胸腺小鼠和裸感染小鼠中都得到了证实。因此，较小的炎性反应具有双重优势，不仅破坏性较小，而且能保护下层组织免受寄生虫产物的损害。T淋巴细胞的各种亚群通过抑制性T细胞产生的可溶性抑制因子相互通讯。这些因子可能具有不同的功能。一种因子可能调节淋巴因子的产生，而另一种可能从一群前体细胞中招募新的抑制细胞。这些因子以抗原特异性方式起作用。初步推测，这些因子可能由两个单元组成：一个是I亚区膜标记，另一个是特异性识别受体。该受体的性质仍不清楚，但可能是一种抗独特型决定簇。（摘要截选至400字）
