Anti-Cytokine Autoantibodies in Systemic Lupus Erythematosus
Identifieur interne : 000933 ( Pmc/Curation ); précédent : 000932; suivant : 000934Anti-Cytokine Autoantibodies in Systemic Lupus Erythematosus
Auteurs : Hwee Siew Howe ; Bernard Pui Lam Leung [Singapour]Source :
- Cells [ 2073-4409 ] ; 2019.
Abstract
Cytokine dysregulation is characteristic of systemic lupus erythematosus (SLE), a systemic autoimmune disease of considerable heterogeneity. Insights gained about the cytokine dysregulation in SLE have the potential for identifying patient subsets before the onset of clinical disease and during established disease. Clustering patients by cytokine and disease activity subsets is more informative than isolated cytokine studies, as both pro inflammatory and immunoregulatory cytokines contribute to the cytokine dysregulated state in SLE. Endogenous anti-cytokine autoantibodies (ACAAs) may be involved in the regulation of cytokine biology by reducing excessive production or by prolonging their half-life in the circulation through the formation of cytokine-antibody immune complexes. Although endogenous ACAAs may have deleterious effects such as contributing to immunodeficiency states, their role in the pathophysiology of autoimmune conditions such as SLE has yet to be clearly elucidated. The aim of the present article is to provide a focused review of the current knowledge of ACAAs in SLE.
Url:
DOI: 10.3390/cells9010072
PubMed: 31892200
PubMed Central: 7016754
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Anti-Cytokine Autoantibodies in Systemic Lupus Erythematosus</title><author><name sortKey="Howe, Hwee Siew" sort="Howe, Hwee Siew" uniqKey="Howe H" first="Hwee Siew" last="Howe">Hwee Siew Howe</name><affiliation><nlm:aff id="af1-cells-09-00072">Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, Singapore 308433, Singapore;<email>Bernard.Leung@SingaporeTech.edu.sg</email></nlm:aff></affiliation></author><author><name sortKey="Leung, Bernard Pui Lam" sort="Leung, Bernard Pui Lam" uniqKey="Leung B" first="Bernard Pui Lam" last="Leung">Bernard Pui Lam Leung</name><affiliation><nlm:aff id="af1-cells-09-00072">Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, Singapore 308433, Singapore;<email>Bernard.Leung@SingaporeTech.edu.sg</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-cells-09-00072">Singapore Institute of Technology, Singapore 138683, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Singapore Institute of Technology, Singapore 138683</wicri:regionArea></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31892200</idno><idno type="pmc">7016754</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7016754</idno><idno type="RBID">PMC:7016754</idno><idno type="doi">10.3390/cells9010072</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000933</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000933</idno><idno type="wicri:Area/Pmc/Curation">000933</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000933</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Anti-Cytokine Autoantibodies in Systemic Lupus Erythematosus</title><author><name sortKey="Howe, Hwee Siew" sort="Howe, Hwee Siew" uniqKey="Howe H" first="Hwee Siew" last="Howe">Hwee Siew Howe</name><affiliation><nlm:aff id="af1-cells-09-00072">Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, Singapore 308433, Singapore;<email>Bernard.Leung@SingaporeTech.edu.sg</email></nlm:aff></affiliation></author><author><name sortKey="Leung, Bernard Pui Lam" sort="Leung, Bernard Pui Lam" uniqKey="Leung B" first="Bernard Pui Lam" last="Leung">Bernard Pui Lam Leung</name><affiliation><nlm:aff id="af1-cells-09-00072">Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, Singapore 308433, Singapore;<email>Bernard.Leung@SingaporeTech.edu.sg</email></nlm:aff></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-cells-09-00072">Singapore Institute of Technology, Singapore 138683, Singapore</nlm:aff><country xml:lang="fr">Singapour</country><wicri:regionArea>Singapore Institute of Technology, Singapore 138683</wicri:regionArea></affiliation></author></analytic><series><title level="j">Cells</title><idno type="eISSN">2073-4409</idno><imprint><date when="2019">2019</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p>Cytokine dysregulation is characteristic of systemic lupus erythematosus (SLE), a systemic autoimmune disease of considerable heterogeneity. Insights gained about the cytokine dysregulation in SLE have the potential for identifying patient subsets before the onset of clinical disease and during established disease. Clustering patients by cytokine and disease activity subsets is more informative than isolated cytokine studies, as both pro inflammatory and immunoregulatory cytokines contribute to the cytokine dysregulated state in SLE. Endogenous anti-cytokine autoantibodies (ACAAs) may be involved in the regulation of cytokine biology by reducing excessive production or by prolonging their half-life in the circulation through the formation of cytokine-antibody immune complexes. Although endogenous ACAAs may have deleterious effects such as contributing to immunodeficiency states, their role in the pathophysiology of autoimmune conditions such as SLE has yet to be clearly elucidated. The aim of the present article is to provide a focused review of the current knowledge of ACAAs in SLE.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="Lu, R" uniqKey="Lu R">R. Lu</name></author><author><name sortKey="Munroe, M E" uniqKey="Munroe M">M.E. Munroe</name></author><author><name sortKey="Guthridge, J M" uniqKey="Guthridge J">J.M. Guthridge</name></author><author><name sortKey="Bean, K M" uniqKey="Bean K">K.M. Bean</name></author><author><name sortKey="Fife, D A" uniqKey="Fife D">D.A. Fife</name></author><author><name sortKey="Chen, H" uniqKey="Chen H">H. Chen</name></author><author><name sortKey="Slight Webb, S R" uniqKey="Slight Webb S">S.R. Slight-Webb</name></author><author><name sortKey="Keith, M P" uniqKey="Keith M">M.P. Keith</name></author><author><name sortKey="Harley, J B" uniqKey="Harley J">J.B. Harley</name></author><author><name sortKey="James, J A" uniqKey="James J">J.A. 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<front><journal-meta><journal-id journal-id-type="nlm-ta">Cells</journal-id><journal-id journal-id-type="iso-abbrev">Cells</journal-id><journal-id journal-id-type="publisher-id">cells</journal-id><journal-title-group><journal-title>Cells</journal-title></journal-title-group><issn pub-type="epub">2073-4409</issn><publisher><publisher-name>MDPI</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">31892200</article-id><article-id pub-id-type="pmc">7016754</article-id><article-id pub-id-type="doi">10.3390/cells9010072</article-id><article-id pub-id-type="publisher-id">cells-09-00072</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Anti-Cytokine Autoantibodies in Systemic Lupus Erythematosus</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0003-2656-136X</contrib-id><name><surname>Howe</surname><given-names>Hwee Siew</given-names></name><xref ref-type="aff" rid="af1-cells-09-00072">1</xref><xref rid="c1-cells-09-00072" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Leung</surname><given-names>Bernard Pui Lam</given-names></name><xref ref-type="aff" rid="af1-cells-09-00072">1</xref><xref ref-type="aff" rid="af2-cells-09-00072">2</xref></contrib></contrib-group><aff id="af1-cells-09-00072"><label>1</label>Department of Rheumatology, Allergy and Immunology, Tan Tock Seng Hospital, Singapore 308433, Singapore;<email>Bernard.Leung@SingaporeTech.edu.sg</email></aff><aff id="af2-cells-09-00072"><label>2</label>Singapore Institute of Technology, Singapore 138683, Singapore</aff><author-notes><corresp id="c1-cells-09-00072"><label>*</label>Correspondence: <email>hwee_siew_howe@ttsh.com.sg</email>; Tel.: +65-63577822; Fax: +65-63577837</corresp></author-notes><pub-date pub-type="epub"><day>27</day><month>12</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>1</month><year>2020</year></pub-date><volume>9</volume><issue>1</issue><elocation-id>72</elocation-id><history><date date-type="received"><day>15</day><month>10</month><year>2019</year></date><date date-type="accepted"><day>17</day><month>12</month><year>2019</year></date></history><permissions><copyright-statement>© 2019 by the authors.</copyright-statement><copyright-year>2019</copyright-year><license license-type="open-access"><license-p>Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (<ext-link ext-link-type="uri" xlink:href="http://creativecommons.org/licenses/by/4.0/">http://creativecommons.org/licenses/by/4.0/</ext-link>).</license-p></license></permissions><abstract><p>Cytokine dysregulation is characteristic of systemic lupus erythematosus (SLE), a systemic autoimmune disease of considerable heterogeneity. Insights gained about the cytokine dysregulation in SLE have the potential for identifying patient subsets before the onset of clinical disease and during established disease. Clustering patients by cytokine and disease activity subsets is more informative than isolated cytokine studies, as both pro inflammatory and immunoregulatory cytokines contribute to the cytokine dysregulated state in SLE. Endogenous anti-cytokine autoantibodies (ACAAs) may be involved in the regulation of cytokine biology by reducing excessive production or by prolonging their half-life in the circulation through the formation of cytokine-antibody immune complexes. Although endogenous ACAAs may have deleterious effects such as contributing to immunodeficiency states, their role in the pathophysiology of autoimmune conditions such as SLE has yet to be clearly elucidated. The aim of the present article is to provide a focused review of the current knowledge of ACAAs in SLE.</p></abstract><kwd-group><kwd>autoantibodies</kwd><kwd>cytokines</kwd><kwd>autoimmunity</kwd><kwd>systemic lupus erythematosus</kwd></kwd-group></article-meta></front><floats-group><table-wrap id="cells-09-00072-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">cells-09-00072-t001_Table 1</object-id><label>Table 1</label><caption><p>Anti-cytokine autoantibodies in systemic lupus erythematosus.</p></caption><table frame="hsides" rules="groups"><thead><tr><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Cytokine Autoantibody </th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">%Prevalence in SLE pts (No.)</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Correlation with Corresponding Cytokine Levels</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Functional Assays</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Clinical Associations</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">References</th></tr></thead><tbody><tr><td rowspan="2" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">IFNα</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">27 (49)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Associated with decreased biological activity of circulating IFNα and lowered disease severity</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B10-cells-09-00072" ref-type="bibr">10</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">42 (76)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Higher levels in clinically quiescent disease. Clinically quiescent disease demonstrated higher levels of anti-IFNα autoantibodies</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B46-cells-09-00072" ref-type="bibr">46</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Granulocyte Colony-Stimulating Factor (G-CSF)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">50 (32)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">A neutralizing effect of anti–GCSF antibodies on its target molecule was found in 3 of the 9 patients tested</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Exaggerated serum level of G-CSF, low neutrophil count</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B47-cells-09-00072" ref-type="bibr">47</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">TNF-α</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Serum levels of autoantibodies to IL-1, IL-6, IL-10 and TNFα were not significantly correlated with circulating levels of their corresponding cytokines </td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Significantly lower levels of anti-TNFαantibodies were found at disease exacerbation</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B48-cells-09-00072" ref-type="bibr">48</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">IL-1α</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">4.7 (64)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Neutralizing</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B49-cells-09-00072" ref-type="bibr">49</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">IL-6</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">-</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">No</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B50-cells-09-00072" ref-type="bibr">50</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">IL-10</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">17.5 (14)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">No</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B51-cells-09-00072" ref-type="bibr">51</xref>]</td></tr><tr><td rowspan="4" align="center" valign="middle" style="border-bottom:solid thin" colspan="1">BAFF</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Weakly correlated, and with levels of BAFF–IgG complexes</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B13-cells-09-00072" ref-type="bibr">13</xref>] </td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">No</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">IgG anti-BAFF autoantibodies in some individuals were capable of blocking BAFF signaling through the BAFF receptor</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Associated with a more severe SLE disease profile and elevated IFN signature</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B53-cells-09-00072" ref-type="bibr">53</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">100 (121)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Negatively correlated with BAFF levels</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">negatively correlated with clinical disease activity, antidsDNA and BAFF levels</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B54-cells-09-00072" ref-type="bibr">54</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">62.2 (28)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Correlated with disease activity</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B55-cells-09-00072" ref-type="bibr">55</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">IL-2</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">18.4 (152)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1"></td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Higher serum anti-IL-2 IgG present in SLE patients with alopecia</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B56-cells-09-00072" ref-type="bibr">56</xref>]</td></tr></tbody></table></table-wrap></floats-group></pmc></record>Pour manipuler ce document sous Unix (Dilib)
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