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Immunology and genetics of induced systemic autoimmunity
Linköping University, Faculty of Health Sciences. Linköping University, Department of Molecular and Clinical Medicine, Molecular and Immunological Pathology. Östergötlands Läns Landsting, Centre for Laboratory Medicine, Department of Clinical Pathology and Clinical Genetics.
2005 (English)In: Autoimmunity Reviews, ISSN 1568-9972, Vol. 4, no 5, 282-288 p.Article in journal (Refereed) Published
Abstract [en]

Systemic lupus erythematosus is a multigenic disorder of unknown etiology. To investigate the role of specific genes in lupus, we have examined the effects of single gene deletions on mercury-induced autoimmunity. Deficiency of certain genes abrogated induction of autoimmunity, while absence of others had little effect. The most interesting observations were obtained with genes related to interferon-γ. Genes involved in upregulation of IFN-γ expression did not significantly influence autoimmunity whereas absence of IFN-γ or IFN-γ receptor led to greatly reduced autoantibody responses and immunopathology. Absence of IRF-1, a gene expressed in response to IFN-γ, resulted in selective retention of anti-chromatin autoantibodies demonstrating that specific defects in signaling pathways and gene expression subsequent to IFN-γ/IFN-γ receptor interaction influence specific disease parameters. These studies show that single gene deletions can have various outcomes ranging from no effect, suppression of one or more features of disease, to suppression of all features of disease, and that all three outcomes can be observed in the IFN-γ pathway. IFN-γ influences the expression and function of other lupus relevant genes such as IL-6 and β2microglobulin, therefore the effects of these gene deletions on disease expression may also reflect responses downstream of IFN-γ function. © 2005 Elsevier B.V. All rights reserved.

Place, publisher, year, edition, pages
2005. Vol. 4, no 5, 282-288 p.
National Category
Medical and Health Sciences
URN: urn:nbn:se:liu:diva-30156DOI: 10.1016/j.autrev.2004.12.005Local ID: 15642OAI: diva2:250977
Available from: 2009-10-09 Created: 2009-10-09 Last updated: 2011-01-12

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Hultman, Per
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