Merrill J T
Clinical Pharmacology Research Program, Oklahoma Medical Research Foundation, Oklahoma City 73104, USA.
Lupus. 2004;13(5):335-8. doi: 10.1191/0961203304lu1022oa.
A hallmark of systemic lupus erythematosus (SLE) and related autoimmune diseases such as the antiphospholipid syndrome (APL or Hughes syndrome) is an apparent breakdown in tolerance, the process by which the body distinguishes self from nonself in order to maintain a versatile immune defense while protecting itself from self-annihilation. To some extent, loss of tolerance is a desirable feature of host immunity, and is known to occur in healthy individuals. Optimal tolerance then is probably not an all or nothing phenomenon. Autoimmunity should be seen as a breakdown in homeostasis rather than a completely aberrant kind of immunity. This leads to special considerations in the assessment of potentially toleragenic therapies, in which an attempt is made to re-educate the immune system. LJP 1082 is designed as a polyvalent antigenic structure aimed at crosslinking specific surface immunoglobulin and tolerizing B cells to beta2-glycoprotein I. Issues of antigenic selection and multiplex forces influencing tolerance and immunity may have impact on its optimal development and use in patients.
系统性红斑狼疮（SLE）及相关自身免疫性疾病（如抗磷脂综合征，即APL或休斯综合征）的一个标志是耐受性明显破坏，耐受性是机体区分自身与非自身以维持多功能免疫防御并保护自身免于自我毁灭的过程。在一定程度上，耐受性丧失是宿主免疫的一个理想特征，且已知在健康个体中也会发生。因此，最佳耐受性可能并非全有或全无的现象。自身免疫应被视为体内稳态的破坏，而非一种完全异常的免疫类型。这在评估潜在的免疫耐受疗法时会引发特殊考量，这类疗法旨在对免疫系统进行重新教育。LJP 1082被设计为一种多价抗原结构，旨在交联特定的表面免疫球蛋白并使B细胞对β2糖蛋白I产生耐受性。抗原选择以及影响耐受性和免疫的多重因素问题可能会对其在患者中的最佳研发和应用产生影响。
