Murad Y M, Szabó Z, Ludányi K, Glant T T
Section of Molecular Medicine, Department of Biochemistry, Rush University Medical Center, Chicago, IL 60612, USA.
Clin Exp Immunol. 2005 Nov;142(2):303-11. doi: 10.1111/j.1365-2249.2005.02921.x.
Systemic immunization of BALB/c mice with human cartilage proteoglycan (PG) aggrecan induces progressive polyarthritis. The G1 domain of the PG aggrecan molecule contains most of the T cell epitopes, including three immunodominant ('arthritogenic') and at least six subdominant T cell epitopes. The three dominant T cell epitopes (P49, P70 and P155) were deleted individually or in combination by site directed mutagenesis, and the recombinant human G1 (rhG1) domain (wild type and mutated) proteins were used for immunization. Close to 100% of BALB/c mice immunized with the wild-type (nonmutated) rhG1 domain developed severe arthritis, which was 75% in the absence of P70 (5/4E8) epitope, and very low (< 10% incidence) when all three dominant T cell epitopes were deleted. The onset was delayed and the severity of arthritis reduced in animals when dominant T cell epitopes were missing from the immunizing rhG1 domain. The lack of T cell response to the deleted epitope(s) was specific, but the overall immune response against the wild-type rhG1 domain of human PG was not significantly affected. This study helped us to understand the dynamics and immune-regulatory mechanisms of arthritis, and supported the hypothesis that the development of autoimmune arthritis requires a concerted T cell response to multiple epitopes, rather than the immune response to a single arthritogenic structure.
用人软骨蛋白聚糖(PG)聚集蛋白聚糖对BALB/c小鼠进行全身免疫会诱发进行性多关节炎。PG聚集蛋白聚糖分子的G1结构域包含大部分T细胞表位,包括三个免疫显性(“致关节炎性”)和至少六个亚显性T细胞表位。通过定点诱变分别或联合缺失三个显性T细胞表位(P49、P70和P155),并使用重组人G1(rhG1)结构域(野生型和突变型)蛋白进行免疫。用野生型(未突变)rhG1结构域免疫的BALB/c小鼠近100%发生严重关节炎,在缺失P70(5/4E8)表位时为75%,当所有三个显性T细胞表位均缺失时发病率非常低(<10%)。当免疫的rhG1结构域缺失显性T细胞表位时,动物关节炎的发病延迟且严重程度降低。对缺失表位的T细胞反应缺失具有特异性,但针对人PG野生型rhG1结构域的总体免疫反应未受到显著影响。这项研究有助于我们了解关节炎的动态变化和免疫调节机制,并支持自身免疫性关节炎的发生需要T细胞对多个表位协同反应而非对单个致关节炎结构产生免疫反应这一假说。