Kofler R, Dixon F J, Theofilopoulos A N
Department of Immunology, Scripps Clinic and Research Foundation, La Jolla, CA 92037, USA; Institute for General and Experimental Pathology, University of Innsbruck, Austria.
Department of Immunology, Scripps Clinic and Research Foundation, La Jolla, CA 92037, USA.
Immunol Today. 1987;8(12):374-80. doi: 10.1016/0167-5699(87)90213-1.
Autoimmune disease appears to be a consequence of the generation of self-reactive antibodies. The relationship between these autoantibodies and antibodies directed against exogenous antigens has fostered much recent work, especially on the murine models of systemic lupus erythematosus and rheumatoid arthritis, as Reinhard Kofler and his colleagues review here. While the complexities surrounding the origin of self-specific antibodies are still to be completely unravelled, it appears that lupus autoantibody expression may not result from defects in lg germline genes nor in mechanisms generating antibody repertoires (variable region gene selection, rearrangement, somatic mutation) but follows the same general principles governing responses to foreign antigens.
自身免疫性疾病似乎是自身反应性抗体产生的结果。这些自身抗体与针对外源抗原的抗体之间的关系推动了近期的许多研究工作，尤其是在系统性红斑狼疮和类风湿关节炎的小鼠模型方面，正如莱因哈德·科夫勒及其同事在此处综述的那样。虽然围绕自身特异性抗体起源的复杂性仍有待完全阐明，但狼疮自身抗体的表达似乎并非源于免疫球蛋白种系基因的缺陷，也不是源于产生抗体库的机制（可变区基因选择、重排、体细胞突变），而是遵循与对外源抗原反应相同的一般原则。
