Profiling Complement System Components in Primary CNS Vasculitis
Complement activation has been implicated in the pathogenesis of many vasculitic syndromes such as anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides. Using an array-based multiplex system, we simultaneously quantified serum and CSF levels of activated and regulatory complement syst...
Main Authors: | , , , , , , |
---|---|
Format: | Article |
Language: | English |
Published: |
MDPI AG
2021-05-01
|
Series: | Cells |
Subjects: | |
Online Access: | https://www.mdpi.com/2073-4409/10/5/1139 |
_version_ | 1797534856809283584 |
---|---|
author | Milani Deb-Chatterji Christian W. Keller Simon Koch Heinz Wiendl Christian Gerloff Tim Magnus Jan D. Lünemann |
author_facet | Milani Deb-Chatterji Christian W. Keller Simon Koch Heinz Wiendl Christian Gerloff Tim Magnus Jan D. Lünemann |
author_sort | Milani Deb-Chatterji |
collection | DOAJ |
description | Complement activation has been implicated in the pathogenesis of many vasculitic syndromes such as anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides. Using an array-based multiplex system, we simultaneously quantified serum and CSF levels of activated and regulatory complement system proteins in patients with primary CNS vasculitis (PACNS; <i>n</i> = 20) compared to patients with non-inflammatory conditions (<i>n</i> = 16). Compared to non-inflammatory controls, levels of C3a, C5a, and SC5b-9, indicative for general activation of the complement system, of C4a, specific for the activation of the classical pathway, Ba and Bb, reflective for alternative complement activation as well as concentrations of complement-inhibitory proteins factor H and factor I were unchanged in patients with PACNS. Our study does not support the hypothesis that complement activation is systemically increased in patients with PACNS. |
first_indexed | 2024-03-10T11:36:23Z |
format | Article |
id | doaj.art-3b191c5e2a3140318420e2536c0cc83e |
institution | Directory Open Access Journal |
issn | 2073-4409 |
language | English |
last_indexed | 2024-03-10T11:36:23Z |
publishDate | 2021-05-01 |
publisher | MDPI AG |
record_format | Article |
series | Cells |
spelling | doaj.art-3b191c5e2a3140318420e2536c0cc83e2023-11-21T18:50:54ZengMDPI AGCells2073-44092021-05-01105113910.3390/cells10051139Profiling Complement System Components in Primary CNS VasculitisMilani Deb-Chatterji0Christian W. Keller1Simon Koch2Heinz Wiendl3Christian Gerloff4Tim Magnus5Jan D. Lünemann6Department of Neurology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, GermanyDepartment of Neurology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, GermanyDepartment of Neurology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Neurology, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, GermanyDepartment of Neurology with Institute of Translational Neurology, University Hospital Münster, 48149 Münster, GermanyComplement activation has been implicated in the pathogenesis of many vasculitic syndromes such as anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitides. Using an array-based multiplex system, we simultaneously quantified serum and CSF levels of activated and regulatory complement system proteins in patients with primary CNS vasculitis (PACNS; <i>n</i> = 20) compared to patients with non-inflammatory conditions (<i>n</i> = 16). Compared to non-inflammatory controls, levels of C3a, C5a, and SC5b-9, indicative for general activation of the complement system, of C4a, specific for the activation of the classical pathway, Ba and Bb, reflective for alternative complement activation as well as concentrations of complement-inhibitory proteins factor H and factor I were unchanged in patients with PACNS. Our study does not support the hypothesis that complement activation is systemically increased in patients with PACNS.https://www.mdpi.com/2073-4409/10/5/1139complement systemvasculitisPACNSCSFneuroinflammation |
spellingShingle | Milani Deb-Chatterji Christian W. Keller Simon Koch Heinz Wiendl Christian Gerloff Tim Magnus Jan D. Lünemann Profiling Complement System Components in Primary CNS Vasculitis Cells complement system vasculitis PACNS CSF neuroinflammation |
title | Profiling Complement System Components in Primary CNS Vasculitis |
title_full | Profiling Complement System Components in Primary CNS Vasculitis |
title_fullStr | Profiling Complement System Components in Primary CNS Vasculitis |
title_full_unstemmed | Profiling Complement System Components in Primary CNS Vasculitis |
title_short | Profiling Complement System Components in Primary CNS Vasculitis |
title_sort | profiling complement system components in primary cns vasculitis |
topic | complement system vasculitis PACNS CSF neuroinflammation |
url | https://www.mdpi.com/2073-4409/10/5/1139 |
work_keys_str_mv | AT milanidebchatterji profilingcomplementsystemcomponentsinprimarycnsvasculitis AT christianwkeller profilingcomplementsystemcomponentsinprimarycnsvasculitis AT simonkoch profilingcomplementsystemcomponentsinprimarycnsvasculitis AT heinzwiendl profilingcomplementsystemcomponentsinprimarycnsvasculitis AT christiangerloff profilingcomplementsystemcomponentsinprimarycnsvasculitis AT timmagnus profilingcomplementsystemcomponentsinprimarycnsvasculitis AT jandlunemann profilingcomplementsystemcomponentsinprimarycnsvasculitis |