Experimental autoimmune myositis in SJL/J mice.
Experimental autoimmune myositis in SJL/J mice.
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DOI：
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发表时间：
1987-03
影响因子：
4.6
通讯作者：
N. L. Rosenberg;S. Ringel;B. Kotzin
中科院分区：
文献类型：
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作者：
N. L. Rosenberg;S. Ringel;B. Kotzin
通过注射由粗同质肌肉匀浆和完全弗氏佐剂（CFA）组成的乳剂，在SJL/J小鼠中产生实验性自身免疫性肌炎（EAM）。几乎所有注射SJL/J的小鼠都显示坏死肌纤维和周围肌内膜结缔组织中浸润的单个核细胞。SJL/J小鼠的疾病局限于骨骼肌。另外8个不同主要组织相容性类型的小鼠品系，同样注射后，均未能产生EAM。直接免疫荧光染色显示在肌细胞膜、膜周和肌内膜结缔组织中有明显的IgG沉积。在SJL/J免疫小鼠的受累肌肉和其他免疫菌株的未损伤肌肉中均存在这种染色。间接免疫荧光染色法检测到正常肌肉的循环抗肌肉抗体在SJL/J小鼠和非敏感菌株中均存在。酶联免疫吸附试验（ELISA）也被用于检测血清抗肌肉抗体活性。包括SJL/J在内的三株小鼠在注射肌肉和CFA后，抗肌肉抗体活性没有显著升高，而其他六株没有表现出组织学肌炎的小鼠的抗肌肉抗体活性则升高了10至20倍。这些结果表明，免疫后产生抗肌肉抗体的能力并不能决定对组织学疾病的易感性。虽然EAM以前在其他物种中被诱导，但在小鼠中还没有这种实验性疾病的描述。该小鼠模型可能为人类炎性肌病的免疫发病机制提供新的认识。
Experimental autoimmune myositis (EAM), was produced in SJL/J mice by injection of an emulsion of crude syngeneic muscle homogenate and complete Freund's adjuvant (CFA). Nearly all injected SJL/J mice showed necrotic muscle fibres associated with infiltrating mononuclear cells, both within the necrotic fibres and in surrounding endomysial connective tissue. The disease in SJL/J mice was confined to skeletal muscle. Eight other mouse strains of different major histocompatibility types, similarly injected, failed to develop EAM. Direct immunofluorescence staining revealed prominent IgG deposition at the muscle cell membrane and in perimysial and endomysial connective tissue. This staining was present in both involved muscle of immunized SJL/J mice as well as in undamaged muscle from other immunized strains. Circulating anti-muscle antibodies as detected by indirect immunofluorescence staining of normal muscle were also present in both SJL/J mice and non-susceptible strains. An enzyme-linked immunosorbent assay (ELISA) was also developed for detection of serum anti-muscle antibody activity. Three strains of mice, including SJL/J, failed to develop significantly elevated anti-muscle antibody activity after injection of muscle and CFA, whereas six other strains that did not demonstrate histological myositis developed a 10- to 20-fold elevation of anti-muscle antibody activity. These results suggest that the ability to produce anti-muscle antibodies after immunization does not determine susceptibility to histological disease. Although EAM has been previously induced in other species, there have not been previous descriptions of this experimental disease in mice. This murine model may provide new insight into the immunopathogenesis of human inflammatory myopathies.