Systemic and local granzyme B levels are associated with disease activity, kidney damage and interferon signature in systemic lupus erythematosus
Kok, Helena M.; van den Hoogen, Lucas L.; van Roon, Joel A.G.; Adriaansen, Elisabeth J M; Fritsch-Stork, Ruth D.E.; Nguyen, Tri Q.; Goldschmeding, Roel; Radstake, Timothy R.D.J.; Bovenschen, Niels
(2017) Rheumatology (Oxford, England), volume 56, issue 12, pp. 2129 - 2134
(Article)
Abstract
Objectives: Granzymes (Grs) are serine proteases that eliminate virally infected or tumour cells by inducing apoptosis. GrB has been shown to be associated to the pathophysiology of SLE, whereas the role of the other Grs in SLE remain unknown. Methods: Gr levels were determined in the serum of SLE patients
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and controls and linked to SLE activity parameters, including the IFN signature. In addition, GrB expression was investigated in LN biopsies and correlated to kidney function parameters and disease severity. Results: Serum GrK and GrM levels were not elevated in SLE and did not correlate with disease activity. In contrast, GrB was increased in SLE serum, which correlated to both the SLEDAI and IFN signature. GrB expression was detected in LN tissue biopsies. The number of GrB-positive cells in tissue correlated to several kidney function parameters (e.g. serum creatinine, proteinuria) and to the LN chronicity index. Conclusion: GrB, but not GrK and GrM, is increased in the serum and kidney of patients with SLE and correlates with measures of poor prognosis in LN. These data suggest that GrB may contribute to the pathogenesis of SLE/LN, which indicates the possibility that GrB might be used as a biomarker and/or a therapeutic target.
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Keywords: granzyme, interferon signature, lupus nephritis, systemic lupus erythematosus, Interferon signature, Systemic lupus erythematosus, Granzyme, Lupus nephritis, Severity of Illness Index, Humans, Kidney Diseases/enzymology, Male, Lupus Nephritis/blood, Granzymes/blood, Interferons/blood, Biomarkers/blood, Female, Lupus Erythematosus, Systemic/blood, Pharmacology (medical), Rheumatology, Journal Article, Research Support, Non-U.S. Gov't
ISSN: 1462-0324
Publisher: Oxford University Press
Note: © The Author 2017. Published by Oxford University Press on behalf of the British Society for Rheumatology. All rights reserved. For Permissions, please email: journals.permissions@oup.com
(Peer reviewed)