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Published in: Comparative Clinical Pathology 5/2015

01-09-2015 | Original Article

Elevated high-mobility group box1 level is associated with alterations of interferon gamma in Egyptians with lupus nephritis

Authors: Hoiyda A. Abdel Rasol, Wafaa Gaber, Margeret A. Aziz, Abeer Galal El-Din Ahmed Rabie

Published in: Comparative Clinical Pathology | Issue 5/2015

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Abstract

High-mobility group box protein-1 (HMGB1) is identified as a pro-inflammatory mediator of tissue injury. Interferon-gamma (IFN-γ) dose dependently induced the release of HMGB1. The understanding of systemic lupus erythematosus (SLE) cytokine networks is very important for SLE treatment strategy and drug development. The purpose of this study is to determine the association of HMGB1 and IFN-γ levels to lupus nephritis and their relation to disease activity, autoantibodies, and certain laboratory parameters. The study population consisted of 50 lupus nephritis patients compared to 30 age- and sex-matched healthy controls (HC). HMGB1 and IFN-γ levels were measured by ELISA method. The plasma levels of HMGB1 and IFN-γ were significantly increased in lupus nephritis patients compared to HC (P < 0.05 and P < 0.01, respectively). Additionally, plasma HMGB1 was positively correlated with IFN-γ (P < 0.001), creatinine (P < 0.05), ESR (P < 0.05), 24-h urinary protein (P < 0.001), and negatively correlated with serum albumin (P < 0.05). HMGB1 and IFN-γ may contribute to the generation of lupus nephritis and may be a potential role for therapies targeting cytokines and HMGB1 in preventing or limiting lupus nephritis in the vulnerable SLE patients.
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Metadata
Title
Elevated high-mobility group box1 level is associated with alterations of interferon gamma in Egyptians with lupus nephritis
Authors
Hoiyda A. Abdel Rasol
Wafaa Gaber
Margeret A. Aziz
Abeer Galal El-Din Ahmed Rabie
Publication date
01-09-2015
Publisher
Springer London
Published in
Comparative Clinical Pathology / Issue 5/2015
Print ISSN: 1618-5641
Electronic ISSN: 1618-565X
DOI
https://doi.org/10.1007/s00580-014-2018-3

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