Oksenberg J R
Dept of Neurology, UCSF School of Medicine 94143-0114.
West J Med. 1994 Sep;161(3):255-9.
Recent developments in molecular and cellular immunology have led to the formulation of refined models that describe how tolerance to self-antigens is broken and autoimmunity develops. This knowledge can now be used to develop alternative approaches to conventional immunosuppression for the treatment of autoimmune demyelinating disorders. The ideal therapy would reverse established disease or prevent further progression by selectively eliminating the aggressive effector molecules or cells while leaving the immune system virtually intact. Indeed, several groups are engaged in preliminary or advanced clinical studies of promising specific immunotherapies for multiple sclerosis and other autoimmune conditions. Current data suggest that the immune response that results in organ-specific autoimmunity is highly complex and redundant in humans. This suggests that antigen-specific approaches may be less successful than broader immunotherapeutic strategies for treating multiple sclerosis and related diseases.
分子与细胞免疫学的最新进展促使了一些精细模型的形成,这些模型描述了对自身抗原的耐受性是如何被打破以及自身免疫是如何发展的。现在,这一知识可用于开发替代传统免疫抑制的方法来治疗自身免疫性脱髓鞘疾病。理想的疗法将通过选择性地清除具有侵袭性的效应分子或细胞,同时使免疫系统基本保持完整,从而逆转已有的疾病或防止疾病进一步发展。事实上,有几个研究小组正在对针对多发性硬化症和其他自身免疫性疾病的有前景的特异性免疫疗法进行初步或高级临床研究。目前的数据表明,导致器官特异性自身免疫的免疫反应在人类中高度复杂且具有冗余性。这表明,对于治疗多发性硬化症及相关疾病,抗原特异性方法可能不如更广泛的免疫治疗策略成功。