Crabb J H, Finberg R, Onderdonk A B, Kasper D L
Channing Laboratory, Brigham and Women's Hospital, Boston, Massachusetts 02115.
Rev Infect Dis. 1990 Jan-Feb;12 Suppl 2:S178-84.
Intraabdominal abscesses (IAA) caused by Bacteroides fragilis are a major sequela to colonic spillage into the peritoneum. The development of an animal model that closely reproduces the disease observed in humans permitted careful inspection of the cellular and/or humoral contributions to the development and control of this disease. The results obtained thus far describe an immunoregulatory T cell circuit that governs both the development of and the immunity against these abscesses. T cells of CD4+8+ phenotype induce the development of IAA in response to B. fragilis. CD8+ T cells generated in response to immunization with the B. fragilis capsular polysaccharide confer protection against the development of IAA. These cells elaborate an antigen-specific factor that mediates the observed protection by these cells. Moreover, a third type of T cell, a CD8+ cell that is also present in nonimmune individuals, is required for the immune T cell or its factor to confer protection. Thus, in the specific disease process of IAA induced by the encapsulated microorganism B. fragilis, immunity proceeds by cellular and not humoral mechanisms.
由脆弱拟杆菌引起的腹腔内脓肿(IAA)是结肠内容物漏入腹膜后的主要后遗症。一种能密切再现人类所观察到疾病的动物模型的建立,使得能够仔细研究细胞和/或体液对这种疾病发生和控制的作用。迄今为止获得的结果描述了一种免疫调节性T细胞回路,它控制着这些脓肿的发生和针对这些脓肿的免疫。CD4+8+表型的T细胞在脆弱拟杆菌的刺激下诱导IAA的发生。对脆弱拟杆菌荚膜多糖进行免疫接种所产生的CD8+T细胞可提供针对IAA发生的保护作用。这些细胞产生一种抗原特异性因子,介导这些细胞所观察到的保护作用。此外,免疫T细胞或其因子发挥保护作用还需要第三种T细胞,即非免疫个体中也存在的一种CD8+细胞。因此,在由有荚膜微生物脆弱拟杆菌诱导的IAA的特定疾病过程中,免疫是通过细胞机制而非体液机制进行的。