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Neutrophil Extracellular Traps That Are Not Degraded in Systemic Lupus Erythematosus Activate Complement Exacerbating the Disease

Jonatan Leffler, Myriam Martin, Birgitta Gullstrand, Helena Tydén, Christian Lood, Lennart Truedsson, Anders A. Bengtsson and Anna M. Blom
J Immunol February 17, 2012, 1102404; DOI: https://doi.org/10.4049/jimmunol.1102404
Jonatan Leffler
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Myriam Martin
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Birgitta Gullstrand
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Helena Tydén
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Christian Lood
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Lennart Truedsson
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Anders A. Bengtsson
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Anna M. Blom
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Abstract

Ongoing inflammation including activation of the complement system is a hallmark of systemic lupus erythematosus (SLE). Antimicrobial neutrophil extracellular traps (NETs) are composed of secreted chromatin that may act as a source of autoantigens typical for SLE. In this study, we investigated how complement interacts with NETs and how NET degradation is affected by complement in SLE patients. We found that sera from a subset of patients with active SLE had a reduced ability to degrade in vitro-generated NETs, which was mostly restored when these patients were in remission. Patients that failed to degrade NETs had a more active disease and they also displayed lower levels of complement proteins C4 and C3 in blood. We discovered that NETs activated complement in vitro and that deposited C1q inhibited NET degradation including a direct inhibition of DNase-I by C1q. Complement deposition on NETs may facilitate autoantibody production, and indeed, Abs against NETs and NET epitopes were more pronounced in patients with impaired ability to degrade NETs. NET-bound autoantibodies inhibited degradation but also further increased C1q deposition, potentially exacerbating the disease. Thus, NETs are a potent complement activator, and this interaction may play an important role in SLE. Targeting complement with inhibitors or by removing complement activators such as NETs could be beneficial for patients with SLE.

Footnotes

  • This work was supported by the Swedish Research Council (Grants K2009-68X-14928-06-3 and 2008-2201); the Swedish Foundation for Strategic Research; the Foundations of Österlund, Kock, Crafoord, King Gustav V's 80th Anniversary, the Swedish Rheumatism Association, the Swedish Society of Medicine, Knut and Alice Wallenberg, Inga-Britt and Arne Lundberg; and by grants for clinical research from the Foundation of the National Board of Health and Welfare and the Skåne University Hospital.

  • Received August 18, 2011.
  • Accepted January 18, 2012.
  • Copyright © 2012 by The American Association of Immunologists, Inc.
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The Journal of Immunology: 206 (5)
The Journal of Immunology
Vol. 206, Issue 5
1 Mar 2021
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Neutrophil Extracellular Traps That Are Not Degraded in Systemic Lupus Erythematosus Activate Complement Exacerbating the Disease
Jonatan Leffler, Myriam Martin, Birgitta Gullstrand, Helena Tydén, Christian Lood, Lennart Truedsson, Anders A. Bengtsson, Anna M. Blom
The Journal of Immunology February 17, 2012, 1102404; DOI: 10.4049/jimmunol.1102404

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Neutrophil Extracellular Traps That Are Not Degraded in Systemic Lupus Erythematosus Activate Complement Exacerbating the Disease
Jonatan Leffler, Myriam Martin, Birgitta Gullstrand, Helena Tydén, Christian Lood, Lennart Truedsson, Anders A. Bengtsson, Anna M. Blom
The Journal of Immunology February 17, 2012, 1102404; DOI: 10.4049/jimmunol.1102404
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Print ISSN 0022-1767        Online ISSN 1550-6606