Yoshino S, Yoshino J
Rheumatology Unit, Royal Adelaide Hospital, Australia.
Cell Immunol. 1994 Oct 15;158(2):305-13. doi: 10.1006/cimm.1994.1278.
To study a role for T cells in nonspecifically induced arthritis, rats were injected intraarticularly into ankle joints with mineral oils including 2,6,10,15,19,23-hexamethyltetracosane (squalene) and incomplete Freund's adjuvant. The results showed that moderate joint inflammation had developed by Day 6 after the nonspecific stimulation. This was then followed by induction of severe arthritis, reaching a peak on Day 21. Histologically, the early phase of arthritis was associated with edema of synovial tissues containing many polymorphs and monocytes/macrophages and the late phase of the joint inflammation with marked hyperplasia of synovial membrane with dense infiltration of CD5+ and alpha beta+ T cells. Depletion of alpha beta+ T cells by a monoclonal antibody against TCR alpha beta suppressed both induction and progression of the late phase of arthritis. Thus, pathogenic T cells appear to be recruited to joint tissues following nonspecific stimulation.
为研究T细胞在非特异性诱导性关节炎中的作用,将大鼠踝关节腔内注射包括2,6,10,15,19,23 - 六甲基二十四烷(角鲨烯)和不完全弗氏佐剂在内的矿物油。结果显示,非特异性刺激后第6天出现中度关节炎症,随后发展为严重关节炎,在第21天达到高峰。组织学上,关节炎早期与滑膜组织水肿有关,滑膜组织中有许多多形核细胞和单核细胞/巨噬细胞,而关节炎症后期则表现为滑膜膜明显增生,伴有CD5 +和αβ + T细胞的密集浸润。用抗TCRαβ单克隆抗体清除αβ + T细胞可抑制关节炎后期的诱导和进展。因此,致病性T细胞似乎在非特异性刺激后被募集到关节组织中。