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Curr Opin Immunol. 2014 Dec;31:87-96. doi: 10.1016/j.coi.2014.10.004. Epub 2014 Oct 25.

Genetics of systemic lupus erythematosus: immune responses and end organ resistance to damage.

Author information

1
Division of Rheumatology, Center of Inflammation, Immunity and Regenerative Medicine, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA 22908, United States.
2
Division of Rheumatology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, United States.
3
Department of Public Health Sciences, Center for Public Health Genomics, University of Virginia, Charlottesville, VA 22908, United States.
4
Department of Psychiatry and Neurobehavioral Sciences, University of Virginia School of Medicine, Charlottesville, VA 22908, United States.
5
Division of Rheumatology, Department of Medicine, University of California, Los Angeles, Los Angeles, CA 90095, United States. Electronic address: BTsao@mednet.ucla.edu.
6
Division of Rheumatology, Center of Inflammation, Immunity and Regenerative Medicine, Department of Medicine, University of Virginia School of Medicine, Charlottesville, VA 22908, United States. Electronic address: sf2e@virginia.edu.

Abstract

Systemic lupus erythematosus (SLE) is a prototypic systemic autoimmune disorder. Considerable progress has been made to delineate the genetic control of this complex disorder. In this review, selected aspects of human and mouse genetics related to SLE are reviewed with emphasis on genes that contribute to both innate and adaptive immunity and to genes that contribute directly to susceptibility to end organ damage. It is concluded that the interactions among these two major pathways will provide further insight into the pathogenesis of SLE. An interactive model of the two major pathways is proposed without emphasis on the importance of breaking tolerance to autoantigens.

PMID:
25458999
PMCID:
PMC4274270
DOI:
10.1016/j.coi.2014.10.004
[Indexed for MEDLINE]
Free PMC Article

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