Gianani R, Sarvetnick N
Department of Neuropharmacology, Scripps Research Institute, La Jolla, California 92037, USA.
Proc Natl Acad Sci U S A. 1996 Mar 19;93(6):2257-9. doi: 10.1073/pnas.93.6.2257.
To explain the pathogenesis of autoimmunity, we hypothesize that following an infection the immune response spreads to tissue-specific autoantigens in genetically predisposed individuals eventually determining progression to disease. Molecular mimicry between viral and self antigens could, in some instances, initiate autoimmunity. Local elicitation of inflammatory cytokines following infection probably plays a pivotal role in determining loss of functional tolerance to self autoantigens and the destructive activation of autoreactive cells. We also describe the potential role of interleukin 10, a powerful B-cell activator, in increasing the efficiency of epitope recognition, that could well be crucial to the progression toward disease.
为了解释自身免疫的发病机制，我们推测在感染后，免疫反应会扩散到遗传易感性个体的组织特异性自身抗原，最终导致疾病进展。在某些情况下，病毒抗原与自身抗原之间的分子模拟可能引发自身免疫。感染后局部炎症细胞因子的诱导可能在决定对自身自身抗原功能耐受性的丧失以及自身反应性细胞的破坏性激活中起关键作用。我们还描述了白细胞介素10（一种强大的B细胞激活剂）在提高表位识别效率方面的潜在作用，这很可能对疾病进展至关重要。
