Autoantibodies in lupus

Culprits or passive bystanders?

Ole P. Rekvig, Chaim Putterman, Cinzia Casu, Hua Xin Gao, Anna Ghirardello, Elin S. Mortensen, Angela Tincani, Andrea Doria

Research output: Contribution to journalArticle

72 Citations (Scopus)

Abstract

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. 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. 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).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. 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-β2 glycoprotein I (β2GPI) antibodies are preferentially involved in focal NP events which are a consequence of non-inflammatory 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.

Original languageEnglish (US)
Pages (from-to)596-603
Number of pages8
JournalAutoimmunity Reviews
Volume11
Issue number8
DOIs
StatePublished - Jun 2012

Fingerprint

Autoantibodies
Antigen-Antibody Complex
Antibodies
Cerebrovascular Disorders
Glomerular Basement Membrane
Lupus Nephritis
Nephritis
Ribosomal Proteins
Systemic Lupus Erythematosus
Chromatin
Anti-Idiotypic Antibodies
Glycoproteins
Brain

Keywords

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

ASJC Scopus subject areas

  • Immunology
  • Immunology and Allergy

Cite this

Rekvig, O. P., Putterman, C., Casu, C., Gao, H. X., Ghirardello, A., Mortensen, E. S., ... Doria, A. (2012). Autoantibodies in lupus: Culprits or passive bystanders? Autoimmunity Reviews, 11(8), 596-603. https://doi.org/10.1016/j.autrev.2011.10.021

Autoantibodies in lupus : Culprits or passive bystanders? / Rekvig, Ole P.; Putterman, Chaim; Casu, Cinzia; Gao, Hua Xin; Ghirardello, Anna; Mortensen, Elin S.; Tincani, Angela; Doria, Andrea.

In: Autoimmunity Reviews, Vol. 11, No. 8, 06.2012, p. 596-603.

Research output: Contribution to journalArticle

Rekvig, OP, Putterman, C, Casu, C, Gao, HX, Ghirardello, A, Mortensen, ES, Tincani, A & Doria, A 2012, 'Autoantibodies in lupus: Culprits or passive bystanders?', Autoimmunity Reviews, vol. 11, no. 8, pp. 596-603. https://doi.org/10.1016/j.autrev.2011.10.021
Rekvig OP, Putterman C, Casu C, Gao HX, Ghirardello A, Mortensen ES et al. Autoantibodies in lupus: Culprits or passive bystanders? Autoimmunity Reviews. 2012 Jun;11(8):596-603. https://doi.org/10.1016/j.autrev.2011.10.021
Rekvig, Ole P. ; Putterman, Chaim ; Casu, Cinzia ; Gao, Hua Xin ; Ghirardello, Anna ; Mortensen, Elin S. ; Tincani, Angela ; Doria, Andrea. / Autoantibodies in lupus : Culprits or passive bystanders?. In: Autoimmunity Reviews. 2012 ; Vol. 11, No. 8. pp. 596-603.
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