Autoantibodies in lupus: Culprits or passive bystanders?

作者：Rekvig Ole P; Putterman Chaim; Casu Cinzia; Gao Hua Xin; Ghirardello Anna; Mortensen Elin S; Tincani Angela; Doria Andrea^*

来源：Autoimmunity Reviews, 2012, 11(8): 596-603.

DOI：10.1016/j.autrev.2011.10.021

• Systemic lupus erythematosus
• Autoantibodies
• Pathogenesis
• Lupus nephritis
• Neuropsychiatric SLE

Several autoantibodies are culprits in the pathogenesis of organ damage in systemic lupus erythematosus, by means of established or postulated mechanisms, whereby inducing a perturbation of cell structure and function, with consequent tissue-organ impairment. %26lt;br%26gt;Common autoantibody-mediated mechanisms of damage include cell surface binding with or without cytolysis, immune complex-mediated damage, penetration into living cells, binding to cross-reactive extracellular molecules. %26lt;br%26gt;Experimental data from both murine models and humans have recently clarified the key role of autoantibodies in severe organ involvements, including nephritis, neuropsychiatric (NP) dysfunction, and cerebrovascular disease (CVD). %26lt;br%26gt;In lupus nephritis early and late phases are distinguishable and mediated by different processes in which anti-chromatin antibodies are both inducing and perpetuating agents, by immune-complex formation and massive deposition in mesangial matrix at first, and in glomerular basement membrane at end-stage. %26lt;br%26gt;Also NP abnormalities occur very early, much earlier than other systemic manifestations, and exacerbate with the increase in autoantibody titers. Among the autoantibodies mainly implicated in neurolupus, anti-beta 2 glycoprotein I (beta 2GPI) antibodies are preferentially involved in focal NP events which are a consequence of noninflammatory microangiopathy; otherwise, anti-ribosomal P protein antibodies and N-methyl-D-aspartate receptor (NMDAR) antibodies cause diffuse NP events through a direct cytotoxic effect on neuronal cells at specific brain zones.

• 出版日期2012-6
• 单位河北医科大学