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The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus

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Standard

The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus. / Troldborg, Anne; Thiel, Steffen; Trendelenburg, Marten et al.
I: Journal of Rheumatology, Bind 45, Nr. 8, 01.08.2018, s. 1136-1144.

Publikation: Bidrag til tidsskrift/Konferencebidrag i tidsskrift /Bidrag til avis › Tidsskriftartikel › Forskning › peer review

Harvard

Troldborg, A, Thiel, S, Trendelenburg, M, Friebus-Kardash, J, Nehring, J, Steffensen, R, Hansen, SWK, Laska, MJ, Deleuran, B, Jensenius, JC, Voss, A & Stengaard-Pedersen, K 2018, 'The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus', Journal of Rheumatology, bind 45, nr. 8, s. 1136-1144. https://doi.org/10.3899/jrheum.171033

APA

Troldborg, A., Thiel, S., Trendelenburg, M., Friebus-Kardash, J., Nehring, J., Steffensen, R., Hansen, S. W. K., Laska, M. J., Deleuran, B., Jensenius, J. C., Voss, A., & Stengaard-Pedersen, K. (2018). The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus. Journal of Rheumatology, 45(8), 1136-1144. https://doi.org/10.3899/jrheum.171033

CBE

Troldborg A, Thiel S, Trendelenburg M, Friebus-Kardash J, Nehring J, Steffensen R, Hansen SWK, Laska MJ, Deleuran B, Jensenius JC, et al. 2018. The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus. Journal of Rheumatology. 45(8):1136-1144. https://doi.org/10.3899/jrheum.171033

MLA

Troldborg, Anne et al. "The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus". Journal of Rheumatology. 2018, 45(8). 1136-1144. https://doi.org/10.3899/jrheum.171033

Vancouver

Troldborg A, Thiel S, Trendelenburg M, Friebus-Kardash J, Nehring J, Steffensen R et al. The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus. Journal of Rheumatology. 2018 aug. 1;45(8):1136-1144. doi: 10.3899/jrheum.171033

Author

Troldborg, Anne ; Thiel, Steffen ; Trendelenburg, Marten et al. / The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus. I: Journal of Rheumatology. 2018 ; Bind 45, Nr. 8. s. 1136-1144.

Bibtex

@article{602ff7f5959d44c694626ec3f0c1265c,
title = "The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus",
abstract = "OBJECTIVE: The pathogenesis of systemic lupus erythematosus (SLE) involves complement activation. Activation of complement through the classical pathway (CP) is well established. However, complement activation through pattern recognition not only happens through the CP, but also through the lectin pathway (LP). We investigated the hypothesis that the LP is activated in SLE and involved in the pathogenesis of the disease.METHODS: Using immunoassays developed in-house, we measured concentrations of LP proteins in a cohort of 372 patients with SLE and 170 controls. We estimated complement activation measuring total C3, and investigated whether LP protein concentrations were associated with complement activation and disease activity. Protein changes and disease activity over time were assessed in a cohort of 52 patients with SLE followed with repeated samples over a 5-year period.RESULTS: Concentrations of LP proteins in SLE were altered compared with controls. The differences observed in LP proteins associated with complement activation were reflected by a decrease in total C3. The pattern recognition molecules (M-ficolin, CL-L1, and CL-K1), the serine protease (MASP-3), and the associated protein (MAp19) displayed a negative correlation with disease activity. Changes in MASP-2 concentrations over time correlated significantly with increased disease activity. Association between active proteinuria and serum concentration was observed for MASP-3 and MAp19.CONCLUSION: In patients with SLE, we measured specific changes in LP proteins that are associated with complement activation and disease activity, indicating that the LP is activated in patients with SLE. These novel findings substantiate the involvement of the LP in SLE.",
keywords = "Complement activation, Complement system, Innate immunity, Lectin pathway, Systemic lupus erythematosus",
author = "Anne Troldborg and Steffen Thiel and Marten Trendelenburg and Justa Friebus-Kardash and Josephine Nehring and Rudi Steffensen and Hansen, {S{\o}ren Werner Karlskov} and Laska, {Magdalena Janina} and Bent Deleuran and Jensenius, {Jens Christian} and Anne Voss and Kristian Stengaard-Pedersen",
note = "doi: 10.3899/jrheum.171033.",
year = "2018",
month = aug,
day = "1",
doi = "10.3899/jrheum.171033",
language = "English",
volume = "45",
pages = "1136--1144",
journal = "Journal of Rheumatology",
issn = "0315-162X",
publisher = "Journal of Rheumatology Publishing Co. Ltd.",
number = "8",

}

RIS

TY - JOUR

T1 - The Lectin Pathway of Complement Activation in Patients with Systemic Lupus Erythematosus

AU - Troldborg, Anne

AU - Thiel, Steffen

AU - Trendelenburg, Marten

AU - Friebus-Kardash, Justa

AU - Nehring, Josephine

AU - Steffensen, Rudi

AU - Hansen, Søren Werner Karlskov

AU - Laska, Magdalena Janina

AU - Deleuran, Bent

AU - Jensenius, Jens Christian

AU - Voss, Anne

AU - Stengaard-Pedersen, Kristian

N1 - doi: 10.3899/jrheum.171033.

PY - 2018/8/1

Y1 - 2018/8/1

N2 - OBJECTIVE: The pathogenesis of systemic lupus erythematosus (SLE) involves complement activation. Activation of complement through the classical pathway (CP) is well established. However, complement activation through pattern recognition not only happens through the CP, but also through the lectin pathway (LP). We investigated the hypothesis that the LP is activated in SLE and involved in the pathogenesis of the disease.METHODS: Using immunoassays developed in-house, we measured concentrations of LP proteins in a cohort of 372 patients with SLE and 170 controls. We estimated complement activation measuring total C3, and investigated whether LP protein concentrations were associated with complement activation and disease activity. Protein changes and disease activity over time were assessed in a cohort of 52 patients with SLE followed with repeated samples over a 5-year period.RESULTS: Concentrations of LP proteins in SLE were altered compared with controls. The differences observed in LP proteins associated with complement activation were reflected by a decrease in total C3. The pattern recognition molecules (M-ficolin, CL-L1, and CL-K1), the serine protease (MASP-3), and the associated protein (MAp19) displayed a negative correlation with disease activity. Changes in MASP-2 concentrations over time correlated significantly with increased disease activity. Association between active proteinuria and serum concentration was observed for MASP-3 and MAp19.CONCLUSION: In patients with SLE, we measured specific changes in LP proteins that are associated with complement activation and disease activity, indicating that the LP is activated in patients with SLE. These novel findings substantiate the involvement of the LP in SLE.

AB - OBJECTIVE: The pathogenesis of systemic lupus erythematosus (SLE) involves complement activation. Activation of complement through the classical pathway (CP) is well established. However, complement activation through pattern recognition not only happens through the CP, but also through the lectin pathway (LP). We investigated the hypothesis that the LP is activated in SLE and involved in the pathogenesis of the disease.METHODS: Using immunoassays developed in-house, we measured concentrations of LP proteins in a cohort of 372 patients with SLE and 170 controls. We estimated complement activation measuring total C3, and investigated whether LP protein concentrations were associated with complement activation and disease activity. Protein changes and disease activity over time were assessed in a cohort of 52 patients with SLE followed with repeated samples over a 5-year period.RESULTS: Concentrations of LP proteins in SLE were altered compared with controls. The differences observed in LP proteins associated with complement activation were reflected by a decrease in total C3. The pattern recognition molecules (M-ficolin, CL-L1, and CL-K1), the serine protease (MASP-3), and the associated protein (MAp19) displayed a negative correlation with disease activity. Changes in MASP-2 concentrations over time correlated significantly with increased disease activity. Association between active proteinuria and serum concentration was observed for MASP-3 and MAp19.CONCLUSION: In patients with SLE, we measured specific changes in LP proteins that are associated with complement activation and disease activity, indicating that the LP is activated in patients with SLE. These novel findings substantiate the involvement of the LP in SLE.

KW - Complement activation

KW - Complement system

KW - Innate immunity

KW - Lectin pathway

KW - Systemic lupus erythematosus

U2 - 10.3899/jrheum.171033

DO - 10.3899/jrheum.171033

M3 - Journal article

C2 - 29907670

VL - 45

SP - 1136

EP - 1144

JO - Journal of Rheumatology

JF - Journal of Rheumatology

SN - 0315-162X

IS - 8

ER -