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Nat Rev Rheumatol. 2016 Nov 22;12(12):716-730. doi: 10.1038/nrrheum.2016.186.

New insights into the immunopathogenesis of systemic lupus erythematosus.

Author information

1
Division of Rheumatology, Beth Israel Deaconess Medical Center, Harvard Medical School, 110 Francis Street, Boston, Massachusetts 02215, USA.
2
Division of Immunology, Boston Children's Hospital, Harvard Medical School, 300 Longwood Avenue, Boston, Massachusetts 02115, USA.
3
Department of Pediatrics, Lisbon Medical School, Lisbon University, Santa Maria Hospital, Avenida Professor Egas Moniz, 1649-035 Lisbon, Portugal.
4
Division of Allergy and Immunology, The Children's Hospital of Philadelphia, The University of Pennsylvania Perelman School of Medicine, 3615 Civic Center Boulevard, Philadelphia, Pennsylvania 19104, USA.

Abstract

The aetiology of systemic lupus erythematosus (SLE) is multifactorial, and includes contributions from the environment, stochastic factors, and genetic susceptibility. Great gains have been made in understanding SLE through the use of genetic variant identification, mouse models, gene expression studies, and epigenetic analyses. Collectively, these studies support the concept that defective clearance of immune complexes and biological waste (such as apoptotic cells), neutrophil extracellular traps, nucleic acid sensing, lymphocyte signalling, and interferon production pathways are all central to loss of tolerance and tissue damage. Increased understanding of the pathogenesis of SLE is driving a renewed interest in targeted therapy, and researchers are now on the verge of developing targeted immunotherapy directed at treating either specific organ system involvement or specific subsets of patients with SLE. Accordingly, this Review places these insights within the context of our current understanding of the pathogenesis of SLE and highlights pathways that are ripe for therapeutic targeting.

PMID:
27872476
DOI:
10.1038/nrrheum.2016.186
[Indexed for MEDLINE]

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