Malmström V, Bäcklund J, Jansson L, Kihlberg J, Holmdahl R
Section for Medical Inflammation Research, Lund University, Lund, Sweden.
Arthritis Res. 2000;2(4):315-26. doi: 10.1186/ar106. Epub 2000 Jun 5.
The immunodominant T-cell epitope that is involved in collagen-induced arthritis (CIA) is the glycosylated type II collagen (CII) peptide 256-270. In CII transgenic mice, which express the immunodominant CII 256-270 epitope in cartilage, the CII-specific T cells are characterized by a partially tolerant state with low proliferative activity in vitro, but with maintained effector functions, such as IFN-gamma secretion and ability to provide B cell help. These mice were still susceptible to CIA. The response was mainly directed to the glycosylated form of the CII 256-270 peptide, rather than to the nonglycosylated peptide. Tolerance induction was rapid; transferred T cells encountered CII within a few days. CII immunization several weeks after thymectomy of the mice did not change their susceptibility to arthritis or the induction of partial T-cell tolerance, excluding a role for recent thymic emigrants. Thus, partially tolerant CII autoreactive T cells are maintained and are crucial for the development of CIA.
参与胶原诱导性关节炎（CIA）的免疫显性T细胞表位是糖基化的II型胶原（CII）肽256 - 270。在软骨中表达免疫显性CII 256 - 270表位的CII转基因小鼠中，CII特异性T细胞的特征是处于部分耐受状态，体外增殖活性低，但效应功能得以维持，如分泌干扰素-γ以及为B细胞提供辅助的能力。这些小鼠仍易患CIA。反应主要针对CII 256 - 270肽的糖基化形式，而非非糖基化肽。耐受诱导迅速；转移的T细胞在几天内就接触到CII。小鼠胸腺切除术后数周进行CII免疫，并未改变它们对关节炎的易感性或部分T细胞耐受的诱导情况，排除了近期胸腺迁出细胞的作用。因此，部分耐受的CII自身反应性T细胞得以维持，并且对CIA的发展至关重要。
