Peripheral monocytes and soluble biomarkers in autoimmune encephalitis

Autoimmune encephalitis (AE) is an inflammatory disease of the central nervous system which can result in long-term seizures and cognitive dysfunction despite treatment with immunotherapy. The role of the innate immune system in AE is not well established. To investigate the contribution of innate i...

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Veröffentlicht in:Journal of autoimmunity 2023-02, Vol.135, p.103000-103000, Article 103000
Hauptverfasser: Wesselingh, Robb, Griffith, Sarah, Broadley, James, Tarlinton, David, Buzzard, Katherine, Seneviratne, Udaya, Butzkueven, Helmut, O'Brien, Terence J., Monif, Mastura
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container_start_page 103000
container_title Journal of autoimmunity
container_volume 135
creator Wesselingh, Robb
Griffith, Sarah
Broadley, James
Tarlinton, David
Buzzard, Katherine
Seneviratne, Udaya
Butzkueven, Helmut
O'Brien, Terence J.
Monif, Mastura
description Autoimmune encephalitis (AE) is an inflammatory disease of the central nervous system which can result in long-term seizures and cognitive dysfunction despite treatment with immunotherapy. The role of the innate immune system in AE is not well established. To investigate the contribution of innate immunity to AE and its long-term outcomes we evaluated peripheral monocytes and serum cytokines in the periphery of patients with AE. We recruited 40 patients with previously diagnosed AE and 28 healthy volunteers to our cross-sectional observation study and evaluated their peripheral blood monocytes via flow cytometry and serum cytokines (CCL-2, CCL-17, G-CSF, GM-CSF, IFNγ, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-17, TNFα) via ELISA.Compared with controls the AE cohort had expansion of the ‘pro-inflammatory’ CD14+CD16+ monocyte sub-population (7.13% vs 5.46%, p 
doi_str_mv 10.1016/j.jaut.2023.103000
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The role of the innate immune system in AE is not well established. To investigate the contribution of innate immunity to AE and its long-term outcomes we evaluated peripheral monocytes and serum cytokines in the periphery of patients with AE. We recruited 40 patients with previously diagnosed AE and 28 healthy volunteers to our cross-sectional observation study and evaluated their peripheral blood monocytes via flow cytometry and serum cytokines (CCL-2, CCL-17, G-CSF, GM-CSF, IFNγ, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-17, TNFα) via ELISA.Compared with controls the AE cohort had expansion of the ‘pro-inflammatory’ CD14+CD16+ monocyte sub-population (7.13% vs 5.46%, p &lt; 0.01) with higher levels of serum IL-6 (2.34 pg/mL vs 0.54 pg/mL, p &lt; 0.001). These changes were most significant in anti-LGI-1 antibody mediated AE, an AE subtype with poor long-term cognitive outcomes. Expansion of the peripheral CD14+CD16+ monocyte population and increased serum IL-6 in AE is reflective of changes seen in other systemic inflammatory and neurodegenerative conditions. These changes may indicate a persistent pro-inflammatory state in AE and may contribute to poor long-term outcomes. •Pro-inflammatory peripheral monocytes are increased in autoimmune encephalitis.•IL-6 is also elevated in the serum despite treatment with immunotherapy.•Changes in inflammatory biomarkers are most marked in the LGI-1 autoimmune encephalitis subset.</description><identifier>ISSN: 0896-8411</identifier><identifier>EISSN: 1095-9157</identifier><identifier>DOI: 10.1016/j.jaut.2023.103000</identifier><identifier>PMID: 36753921</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Autoimmune Diseases of the Nervous System ; Autoimmune encephalitis ; Biomarkers ; Cross-Sectional Studies ; Cytokines ; Humans ; Innate immunity ; Interleukin-6 ; LGI-1 ; Monocytes ; Receptors, IgG</subject><ispartof>Journal of autoimmunity, 2023-02, Vol.135, p.103000-103000, Article 103000</ispartof><rights>2023 Elsevier Ltd</rights><rights>Copyright © 2023 Elsevier Ltd. 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The role of the innate immune system in AE is not well established. To investigate the contribution of innate immunity to AE and its long-term outcomes we evaluated peripheral monocytes and serum cytokines in the periphery of patients with AE. We recruited 40 patients with previously diagnosed AE and 28 healthy volunteers to our cross-sectional observation study and evaluated their peripheral blood monocytes via flow cytometry and serum cytokines (CCL-2, CCL-17, G-CSF, GM-CSF, IFNγ, IL-1α, IL-1β, IL-2, IL-4, IL-5, IL-6, IL-10, IL-17, TNFα) via ELISA.Compared with controls the AE cohort had expansion of the ‘pro-inflammatory’ CD14+CD16+ monocyte sub-population (7.13% vs 5.46%, p &lt; 0.01) with higher levels of serum IL-6 (2.34 pg/mL vs 0.54 pg/mL, p &lt; 0.001). These changes were most significant in anti-LGI-1 antibody mediated AE, an AE subtype with poor long-term cognitive outcomes. Expansion of the peripheral CD14+CD16+ monocyte population and increased serum IL-6 in AE is reflective of changes seen in other systemic inflammatory and neurodegenerative conditions. These changes may indicate a persistent pro-inflammatory state in AE and may contribute to poor long-term outcomes. •Pro-inflammatory peripheral monocytes are increased in autoimmune encephalitis.•IL-6 is also elevated in the serum despite treatment with immunotherapy.•Changes in inflammatory biomarkers are most marked in the LGI-1 autoimmune encephalitis subset.</description><subject>Autoimmune Diseases of the Nervous System</subject><subject>Autoimmune encephalitis</subject><subject>Biomarkers</subject><subject>Cross-Sectional Studies</subject><subject>Cytokines</subject><subject>Humans</subject><subject>Innate immunity</subject><subject>Interleukin-6</subject><subject>LGI-1</subject><subject>Monocytes</subject><subject>Receptors, IgG</subject><issn>0896-8411</issn><issn>1095-9157</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kDFPwzAQhS0EoqXwBxhQRpYUnxPbscSCKgpIlWCA2XKci-qSxMVOkPrvSdXCyHTS6b139z5CroHOgYK428w3ZujnjLJsXGSU0hMyBap4qoDLUzKlhRJpkQNMyEWMG0oBOOfnZJIJyTPFYEqWbxjcdo3BNEnrO293PcbEdFUSfTOUDSal860Jnxhi4rpkPOhd2w4dJthZ3K5N43oXL8lZbZqIV8c5Ix_Lx_fFc7p6fXpZPKxSm3HRp8KiKY2VwooSVF1XvOQgC17kdHyzRJRMqZpZASWrQORQG6DcqKpmBjMpshm5PeRug_8aMPa6ddFi05gO_RA1kzIvlBS8GKXsILXBxxiw1tvgxiY7DVTv-emN3vPTe376wG803Rzzh7LF6s_yC2wU3B8EOLb8dhh0tG5PonIBba8r7_7L_wEzroIR</recordid><startdate>202302</startdate><enddate>202302</enddate><creator>Wesselingh, Robb</creator><creator>Griffith, Sarah</creator><creator>Broadley, James</creator><creator>Tarlinton, David</creator><creator>Buzzard, Katherine</creator><creator>Seneviratne, Udaya</creator><creator>Butzkueven, Helmut</creator><creator>O'Brien, Terence J.</creator><creator>Monif, Mastura</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-5898-3287</orcidid></search><sort><creationdate>202302</creationdate><title>Peripheral monocytes and soluble biomarkers in autoimmune encephalitis</title><author>Wesselingh, Robb ; Griffith, Sarah ; Broadley, James ; Tarlinton, David ; Buzzard, Katherine ; Seneviratne, Udaya ; Butzkueven, Helmut ; O'Brien, Terence J. ; Monif, Mastura</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-6ceabac76c6b19ffd5b51785840841bee7299f2c61b2d1641fa105a9df2ae3763</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Autoimmune Diseases of the Nervous System</topic><topic>Autoimmune encephalitis</topic><topic>Biomarkers</topic><topic>Cross-Sectional Studies</topic><topic>Cytokines</topic><topic>Humans</topic><topic>Innate immunity</topic><topic>Interleukin-6</topic><topic>LGI-1</topic><topic>Monocytes</topic><topic>Receptors, IgG</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wesselingh, Robb</creatorcontrib><creatorcontrib>Griffith, Sarah</creatorcontrib><creatorcontrib>Broadley, James</creatorcontrib><creatorcontrib>Tarlinton, David</creatorcontrib><creatorcontrib>Buzzard, Katherine</creatorcontrib><creatorcontrib>Seneviratne, Udaya</creatorcontrib><creatorcontrib>Butzkueven, Helmut</creatorcontrib><creatorcontrib>O'Brien, Terence J.</creatorcontrib><creatorcontrib>Monif, Mastura</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of autoimmunity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wesselingh, Robb</au><au>Griffith, Sarah</au><au>Broadley, James</au><au>Tarlinton, David</au><au>Buzzard, Katherine</au><au>Seneviratne, Udaya</au><au>Butzkueven, Helmut</au><au>O'Brien, Terence J.</au><au>Monif, Mastura</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Peripheral monocytes and soluble biomarkers in autoimmune encephalitis</atitle><jtitle>Journal of autoimmunity</jtitle><addtitle>J Autoimmun</addtitle><date>2023-02</date><risdate>2023</risdate><volume>135</volume><spage>103000</spage><epage>103000</epage><pages>103000-103000</pages><artnum>103000</artnum><issn>0896-8411</issn><eissn>1095-9157</eissn><abstract>Autoimmune encephalitis (AE) is an inflammatory disease of the central nervous system which can result in long-term seizures and cognitive dysfunction despite treatment with immunotherapy. 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subjects Autoimmune Diseases of the Nervous System
Autoimmune encephalitis
Biomarkers
Cross-Sectional Studies
Cytokines
Humans
Innate immunity
Interleukin-6
LGI-1
Monocytes
Receptors, IgG
title Peripheral monocytes and soluble biomarkers in autoimmune encephalitis
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