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Behavioral changes in systemic lupus erythematosus are of an autoimmune nature

Nature Clinical Practice Rheumatology volume 3, pages 592–593 (2007)Cite this article

Neuropsychiatric manifestations are present in approximately 70% of patients with systemic lupus erythematosus (SLE). Some patients also demonstrate signs of central nervous system (CNS) involvement, identified by neuroimaging and post-mortem.1 Approximately 20 different manifestations of behavioral disorders have been described in SLE. Although the precise nature and pathophysiology of these neuropsychiatric manifestations remain unknown, they might be associated with SLE disease-specific features and medication, as well as primary neurological and psychiatric disorders. Since many of the signs and symptoms of SLE can be attributed to the large number of identified autoantibodies, it would be reasonable to expect the same in neuropsychiatric SLE (NPSLE).1 Thus, increasing evidence suggests a role for autoimmune factors in contributing to neuropsychiatric expressions via direct and indirect autoantibody-induced neuronal damage.

Our group has recently identified a number of autoantibodies reported to be associated with, or specific to, NPSLE.2 Overall, 20 autoantibodies have been identified, but no specific neuropsychiatric manifestation has been associated with the full autoantibody list. Various autoantibody subtypes have been identified that target brain-specific antigens, including neuronal, N-methyl-D-aspartate (NMDA) receptor and lymphocytotoxic subtypes. Systemic antigens consist of subtypes specific to nuclear, cytoplasmic, phospholipid, and endothelial cell substrates. The most common behavioral expressions associated with these autoantibodies are cognitive impairment, psychosis, and depression (see supplementary online information). Specifically, psychosis has been associated with 8 autoantibodies. Although there does not seem to be any specificity among autoantibodies for any single behavioral manifestation, detection of autoantibodies could be helpful for the diagnosis of NPSLE.

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References

  1. Shoenfeld Y (2007) To smell autoimmunity: anti-P-ribosomal autoantibodies, depression, and the olfactory system. J Autoimmun 28: 165–169

    Article  CAS  Google Scholar 

  2. Zandman-Goddard G et al. (2007) Autoantibodies involved in neuropsychiatric SLE and antiphospholipid syndrome. Semin Arthritis Rheum 36: 297–315

    Article  CAS  Google Scholar 

  3. Scolding NJ and Joseph FG (2002) The neuropathology and pathogenesis of systemic lupus erythematosus. Neuropathol Appl Neurobiol 28: 173–189

    Article  CAS  Google Scholar 

  4. Elkon KB et al. (1985) Lupus autoantibodies target ribosomal P proteins. J Exp Med 162: 459–471

    Article  CAS  Google Scholar 

  5. Eber T et al. (2005) Anti-ribosomal P-protein and its role in psychiatric manifestations of systemic lupus erythematosus: myth or reality? Lupus 14: 571–575

    Article  CAS  Google Scholar 

  6. Katzav A et al. (2007) Induction of autoimmune depression in mice by anti-ribosomal P antibodies via the limbic system. Arthritis Rheum 56: 938–948

    Article  CAS  Google Scholar 

  7. Song C and Leonard BE (2005) The olfactory bulbectomised rat as a model of depression. Neurosci Biobehav Rev 29: 627–647

    Article  Google Scholar 

  8. Strous RD and Shoenfeld Y (2006) To smell the immune system: olfaction, autoimmunity and brain involvement. Autoimmun Rev 6: 54–60

    Article  CAS  Google Scholar 

  9. Emmer BJ et al. (2006) Selective involvement of the amygdala in systemic lupus erythematosus. PLoS Med 3: e499

    Article  Google Scholar 

  10. Weismann M et al. (2001) Functional magnetic resonance imaging of human olfaction. Neuroimaging Clin N Am 11: 237–250

    CAS  PubMed  Google Scholar 

Download references

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Authors and Affiliations

  1. RD Strous is Director of the Inpatient Unit at the Beer Yaakov Mental Health Center and Senior Lecturer in Psychiatry at the Sackler School of Medicine, Tel Aviv University.,

    Rael D Strous

  2. Y Shoenfeld is Director of the Department of Medicine 'B' and the Center for Autoimmune Diseases at the Tel Hashomer “Sheba” Medical Center, Tel Aviv, and incumbent of the Laura Schwarz-Kipp Chair for Research of Autoimmune Diseases, at the Sackler School of Medicine, Tel Aviv University, Israel.,

    Yehuda Shoenfeld

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  1. Rael D Strous
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  2. Yehuda Shoenfeld
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Correspondence to Yehuda Shoenfeld.

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The authors declare no competing financial interests.

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Strous, R., Shoenfeld, Y. Behavioral changes in systemic lupus erythematosus are of an autoimmune nature. Nat Rev Rheumatol 3, 592–593 (2007). https://doi.org/10.1038/ncprheum0622

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