Griffiths M M, Eichwald E J, Martin J H, Smith C B, DeWitt C W
Arthritis Rheum. 1981 Jun;24(6):781-9. doi: 10.1002/art.1780240605.
Seven inbred rat strains were tested for susceptibility to experimental type II collagen-induced arthritis and for development of cellular immunity to type II collagen by delayed hypersensitivity skin testing. WF (RT1u), LEW (RT1l), and DA (RT1a) were the most susceptible of the strains tested with respect to incidence (greater than 95%) and severity of disease. LEW and DA were strongly skin test reactive to calf type II collagen. BUF (RT1b) developed moderate skin test responses to calf type II collagen and showed low susceptibility to collagen arthritis (1/8). MAXX (RT1n), LEW.B3 (RT1nvl), and AUG (RT1c) were not susceptible to collagen arthritis and showed negative to very weak skin test responses to type II collagen. Disease susceptibility was inherited as a dominant trait in the F1 progeny of (WF X LEW.B3) matings. These data suggest that clinical expression of experimental collagen-induced arthritis and immune responsiveness to type II collagen are controlled in part by genes within or closely linked to the rat major histocompatibility complex--RT1.
对7个近交系大鼠品系进行了实验性II型胶原诱导性关节炎易感性测试,并通过迟发型超敏皮肤试验检测了对II型胶原的细胞免疫反应。就发病率(大于95%)和疾病严重程度而言,WF(RT1u)、LEW(RT1l)和DA(RT1a)是受试品系中最易感的。LEW和DA对小牛II型胶原的皮肤试验反应强烈。BUF(RT1b)对小牛II型胶原产生中度皮肤试验反应,对胶原性关节炎的易感性较低(1/8)。MAXX(RT1n)、LEW.B3(RT1nvl)和AUG(RT1c)对胶原性关节炎不易感,对II型胶原的皮肤试验反应为阴性至非常弱。疾病易感性在(WF×LEW.B3)交配的F1后代中作为显性性状遗传。这些数据表明,实验性胶原诱导性关节炎的临床表达和对II型胶原的免疫反应性部分受大鼠主要组织相容性复合体RT1内或与其紧密连锁的基因控制。