Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis
Identifieur interne : 000343 ( Pmc/Checkpoint ); précédent : 000342; suivant : 000344Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis
Auteurs : Jenn-Haung Lai [Taïwan] ; Shue-Fen Luo [Taïwan] ; Ling-Jun Ho [Taïwan]Source :
- Cells [ 2073-4409 ] ; 2019.
Abstract
Full activation of T lymphocytes requires signals from both T cell receptors and costimulatory molecules. In addition to CD28, several T cell molecules could deliver costimulatory signals, including CD154, which primarily interacts with CD40 on B-cells. CD40 is a critical molecule regulating several B-cell functions, such as antibody production, germinal center formation and cellular proliferation. Upregulated expression of CD40 and CD154 occurs in immune effector cells and non-immune cells in different autoimmune diseases. In addition, therapeutic benefits have been observed by blocking the CD40-CD154 interaction in animals with collagen-induced arthritis. Given the therapeutic success of the biologics abatacept, which blocks CD28 costimulation, and rituximab, which deletes B cells in the treatment of autoimmune arthritis, the inhibition of the CD40-CD154 axis has two advantages, namely, attenuating CD154-mediated T cell costimulation and suppressing CD40-mediated B-cell stimulation. Furthermore, blockade of the CD40-CD154 interaction drives the conversion of CD4+ T cells to regulatory T cells that mediate immunosuppression. Currently, several biological products targeting the CD40-CD154 axis have been developed and are undergoing early phase clinical trials with encouraging success in several autoimmune disorders, including autoimmune arthritis. This review addresses the roles of the CD40-CD154 axis in the pathogenesis of autoimmune arthritis and its potential as a therapeutic target.
Url:
DOI: 10.3390/cells8080927
PubMed: 31426619
PubMed Central: 6721639
Affiliations:
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<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis</title><author><name sortKey="Lai, Jenn Haung" sort="Lai, Jenn Haung" uniqKey="Lai J" first="Jenn-Haung" last="Lai">Jenn-Haung Lai</name><affiliation wicri:level="1"><nlm:aff id="af1-cells-08-00927">Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305</wicri:regionArea><wicri:noRegion>Taoyuan 33305</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-cells-08-00927">Graduate Institute of Medical Science, National Defense Medical Center, Taipei 11490, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Medical Science, National Defense Medical Center, Taipei 11490</wicri:regionArea><wicri:noRegion>Taipei 11490</wicri:noRegion></affiliation></author><author><name sortKey="Luo, Shue Fen" sort="Luo, Shue Fen" uniqKey="Luo S" first="Shue-Fen" last="Luo">Shue-Fen Luo</name><affiliation wicri:level="1"><nlm:aff id="af1-cells-08-00927">Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305</wicri:regionArea><wicri:noRegion>Taoyuan 33305</wicri:noRegion></affiliation></author><author><name sortKey="Ho, Ling Jun" sort="Ho, Ling Jun" uniqKey="Ho L" first="Ling-Jun" last="Ho">Ling-Jun Ho</name><affiliation wicri:level="1"><nlm:aff id="af3-cells-08-00927">Institute of Cellular and System Medicine, National Health Research Institute, Zhunan 35053, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Cellular and System Medicine, National Health Research Institute, Zhunan 35053</wicri:regionArea><wicri:noRegion>Zhunan 35053</wicri:noRegion></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">31426619</idno><idno type="pmc">6721639</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6721639</idno><idno type="RBID">PMC:6721639</idno><idno type="doi">10.3390/cells8080927</idno><date when="2019">2019</date><idno type="wicri:Area/Pmc/Corpus">000922</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Corpus" wicri:corpus="PMC">000922</idno><idno type="wicri:Area/Pmc/Curation">000922</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Curation">000922</idno><idno type="wicri:Area/Pmc/Checkpoint">000343</idno><idno type="wicri:explorRef" wicri:stream="Pmc" wicri:step="Checkpoint">000343</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis</title><author><name sortKey="Lai, Jenn Haung" sort="Lai, Jenn Haung" uniqKey="Lai J" first="Jenn-Haung" last="Lai">Jenn-Haung Lai</name><affiliation wicri:level="1"><nlm:aff id="af1-cells-08-00927">Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305</wicri:regionArea><wicri:noRegion>Taoyuan 33305</wicri:noRegion></affiliation><affiliation wicri:level="1"><nlm:aff id="af2-cells-08-00927">Graduate Institute of Medical Science, National Defense Medical Center, Taipei 11490, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Graduate Institute of Medical Science, National Defense Medical Center, Taipei 11490</wicri:regionArea><wicri:noRegion>Taipei 11490</wicri:noRegion></affiliation></author><author><name sortKey="Luo, Shue Fen" sort="Luo, Shue Fen" uniqKey="Luo S" first="Shue-Fen" last="Luo">Shue-Fen Luo</name><affiliation wicri:level="1"><nlm:aff id="af1-cells-08-00927">Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305</wicri:regionArea><wicri:noRegion>Taoyuan 33305</wicri:noRegion></affiliation></author><author><name sortKey="Ho, Ling Jun" sort="Ho, Ling Jun" uniqKey="Ho L" first="Ling-Jun" last="Ho">Ling-Jun Ho</name><affiliation wicri:level="1"><nlm:aff id="af3-cells-08-00927">Institute of Cellular and System Medicine, National Health Research Institute, Zhunan 35053, Taiwan</nlm:aff><country xml:lang="fr">Taïwan</country><wicri:regionArea>Institute of Cellular and System Medicine, National Health Research Institute, Zhunan 35053</wicri:regionArea><wicri:noRegion>Zhunan 35053</wicri:noRegion></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>Full activation of T lymphocytes requires signals from both T cell receptors and costimulatory molecules. In addition to CD28, several T cell molecules could deliver costimulatory signals, including CD154, which primarily interacts with CD40 on B-cells. CD40 is a critical molecule regulating several B-cell functions, such as antibody production, germinal center formation and cellular proliferation. Upregulated expression of CD40 and CD154 occurs in immune effector cells and non-immune cells in different autoimmune diseases. In addition, therapeutic benefits have been observed by blocking the CD40-CD154 interaction in animals with collagen-induced arthritis. Given the therapeutic success of the biologics abatacept, which blocks CD28 costimulation, and rituximab, which deletes B cells in the treatment of autoimmune arthritis, the inhibition of the CD40-CD154 axis has two advantages, namely, attenuating CD154-mediated T cell costimulation and suppressing CD40-mediated B-cell stimulation. Furthermore, blockade of the CD40-CD154 interaction drives the conversion of CD4+ T cells to regulatory T cells that mediate immunosuppression. Currently, several biological products targeting the CD40-CD154 axis have been developed and are undergoing early phase clinical trials with encouraging success in several autoimmune disorders, including autoimmune arthritis. This review addresses the roles of the CD40-CD154 axis in the pathogenesis of autoimmune arthritis and its potential as a therapeutic target.</p></div></front><back><div1 type="bibliography"><listBibl><biblStruct><analytic><author><name sortKey="O Ell, J R" uniqKey="O Ell J">J.R. O’Dell</name></author><author><name sortKey="Mikuls, T R" uniqKey="Mikuls T">T.R. Mikuls</name></author><author><name sortKey="Taylor, T H" uniqKey="Taylor T">T.H. Taylor</name></author><author><name sortKey="Ahluwalia, V" uniqKey="Ahluwalia V">V. Ahluwalia</name></author><author><name sortKey="Brophy, M" uniqKey="Brophy M">M. 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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">31426619</article-id><article-id pub-id-type="pmc">6721639</article-id><article-id pub-id-type="doi">10.3390/cells8080927</article-id><article-id pub-id-type="publisher-id">cells-08-00927</article-id><article-categories><subj-group subj-group-type="heading"><subject>Review</subject></subj-group></article-categories><title-group><article-title>Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis</article-title></title-group><contrib-group><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0002-6266-705X</contrib-id><name><surname>Lai</surname><given-names>Jenn-Haung</given-names></name><xref ref-type="aff" rid="af1-cells-08-00927">1</xref><xref ref-type="aff" rid="af2-cells-08-00927">2</xref><xref rid="c1-cells-08-00927" ref-type="corresp">*</xref></contrib><contrib contrib-type="author"><name><surname>Luo</surname><given-names>Shue-Fen</given-names></name><xref ref-type="aff" rid="af1-cells-08-00927">1</xref></contrib><contrib contrib-type="author"><contrib-id contrib-id-type="orcid" authenticated="true">https://orcid.org/0000-0003-3453-2913</contrib-id><name><surname>Ho</surname><given-names>Ling-Jun</given-names></name><xref ref-type="aff" rid="af3-cells-08-00927">3</xref><xref rid="c1-cells-08-00927" ref-type="corresp">*</xref></contrib></contrib-group><aff id="af1-cells-08-00927"><label>1</label>Division of Allergy, Immunology, and Rheumatology, Department of Internal Medicine, Chang Gung Memorial Hospital, Chang Gung University, Taoyuan 33305, Taiwan</aff><aff id="af2-cells-08-00927"><label>2</label>Graduate Institute of Medical Science, National Defense Medical Center, Taipei 11490, Taiwan</aff><aff id="af3-cells-08-00927"><label>3</label>Institute of Cellular and System Medicine, National Health Research Institute, Zhunan 35053, Taiwan</aff><author-notes><corresp id="c1-cells-08-00927"><label>*</label>Correspondence: <email>laiandho@gmail.com</email> (J.-H.L.); <email>lingjunho@nhri.org.tw</email> (L.-J.H.); Tel.: +886-2-8791-8382 (L.-J.H.); Fax: +886-2-8791-8382 (L.-J.H.)</corresp></author-notes><pub-date pub-type="epub"><day>18</day><month>8</month><year>2019</year></pub-date><pub-date pub-type="collection"><month>8</month><year>2019</year></pub-date><volume>8</volume><issue>8</issue><elocation-id>927</elocation-id><history><date date-type="received"><day>18</day><month>7</month><year>2019</year></date><date date-type="accepted"><day>17</day><month>8</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>Full activation of T lymphocytes requires signals from both T cell receptors and costimulatory molecules. In addition to CD28, several T cell molecules could deliver costimulatory signals, including CD154, which primarily interacts with CD40 on B-cells. CD40 is a critical molecule regulating several B-cell functions, such as antibody production, germinal center formation and cellular proliferation. Upregulated expression of CD40 and CD154 occurs in immune effector cells and non-immune cells in different autoimmune diseases. In addition, therapeutic benefits have been observed by blocking the CD40-CD154 interaction in animals with collagen-induced arthritis. Given the therapeutic success of the biologics abatacept, which blocks CD28 costimulation, and rituximab, which deletes B cells in the treatment of autoimmune arthritis, the inhibition of the CD40-CD154 axis has two advantages, namely, attenuating CD154-mediated T cell costimulation and suppressing CD40-mediated B-cell stimulation. Furthermore, blockade of the CD40-CD154 interaction drives the conversion of CD4+ T cells to regulatory T cells that mediate immunosuppression. Currently, several biological products targeting the CD40-CD154 axis have been developed and are undergoing early phase clinical trials with encouraging success in several autoimmune disorders, including autoimmune arthritis. This review addresses the roles of the CD40-CD154 axis in the pathogenesis of autoimmune arthritis and its potential as a therapeutic target.</p></abstract><kwd-group><kwd>CD40</kwd><kwd>CD154</kwd><kwd>costimulation</kwd><kwd>autoimmune</kwd><kwd>arthritis</kwd></kwd-group></article-meta></front><floats-group><fig id="cells-08-00927-f001" orientation="portrait" position="float"><label>Figure 1</label><caption><p>After interacting with CD154, CD40 recruits and interacts with several adapter proteins, including TRAF1, 2, 3, 5 and 6. The accumulated signaling of TRAFs leads to the activation of canonical NF-κB and noncanonical NF-κB signaling pathways. The noncanonical NF-κB signaling pathway involves the processing of p100 and the nuclear translocation of the p52 and RelB heterodimers. TRAF3 is constitutively associated with NIK, leading to its degradation by the proteasome, and CD40 signaling causes TRAF3 degradation and activation of NIK as well as the downstream noncanonical NF-κB signaling pathway. TRAF3 also functions as a resident nuclear protein via association with the transcriptional regulator CREB and Mcl-1. In comparison, the activation of the canonical NF-κB signaling pathway involves the degradation of IκBα and the nuclear translocation of the p50 and RelA heterodimers. Overall, CD40 signaling activates MAPKs and PI3K. The activation of the CD154-CD40 axis results in several events, including cytokine production, immunoglobulin gene switching, prevention of B-cell apoptosis, increased expression of costimulatory molecules such as CD80 and CD86, germinal center formation, production of high-affinity antibodies and formation of B memory cells. TRAF, TNF receptor (TNFR)-associated factor; NF-κB, nuclear factor-kappaB; IκBα, inhibitor of NF-κB; CREB, cAMP response element binding protein; MAPK, mitogen-activated protein kinase, PI3K, phosphoinositide 3-kinases.</p></caption><graphic xlink:href="cells-08-00927-g001"></graphic></fig><table-wrap id="cells-08-00927-t001" orientation="portrait" position="float"><object-id pub-id-type="pii">cells-08-00927-t001_Table 1</object-id><label>Table 1</label><caption><p>Clinical experience with pivotal CD40-CD154 blockers for patients with rheumatic autoimmune disorders.</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">Aimed Target</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Drugs</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Structure</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Aimed Diseases</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Trial Designs</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Patient No./Study Period</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Results and Comments</th><th align="center" valign="middle" style="border-top:solid thin;border-bottom:solid thin" rowspan="1" colspan="1">Ref.</th></tr></thead><tbody><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CD154</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">IDEC-131</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Humanized mAb</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">SLE *</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Phase I & Phase II, DB, PC</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">23/3 months and 85/7 months</td><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Safe and well-tolerated and no clinical benefits compared to baseline</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B91-cells-08-00927" ref-type="bibr">91</xref>,<xref rid="B92-cells-08-00927" ref-type="bibr">92</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CD154</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BG9588</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Humanized mAb</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">SLE (PLN)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">phase II, open-label</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">28/22–24 wks</td><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Early termination of the trial due to thromboembolic AE although clinical benefits noted</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B93-cells-08-00927" ref-type="bibr">93</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CD154</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Dapirolizumab pegol</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Fab</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">SLE</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Phase I, DB & Phase IIb, DB, PC</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">16/12 wks and 182/24 wks</td><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Clinical benefits in high disease activity group at baseline & Fail to meet the primary endpoint (noted in press release)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B94-cells-08-00927" ref-type="bibr">94</xref>,<xref rid="B95-cells-08-00927" ref-type="bibr">95</xref>,<xref rid="B96-cells-08-00927" ref-type="bibr">96</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CD154</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">VIB4920 (MEDI4920)</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Tn3 fusion protein</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">RA</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Phase Ib, DB, PC</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">57/12 wks</td><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Significant benefits in clinical and laboratorial assessment</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B97-cells-08-00927" ref-type="bibr">97</xref>]</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CD40</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CFZ533</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Humanized mAb</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">SS; RA</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Phase IIa, DB, PC & Phase I, DB, PC</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">44/12 wks and 75/20 wks (estimated)</td><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Clinical benefits in SS patients & The drug was well-tolerated in RA patients</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B18-cells-08-00927" ref-type="bibr">18</xref>,<xref rid="B98-cells-08-00927" ref-type="bibr">98</xref>], NCT02-089087</td></tr><tr><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">CD40</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">BI 655064</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Humanized mAb</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">RA, fail with MTX</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Phase IIa, DB, PC</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">67/12 wks</td><td align="left" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">Improvement in laboratorial parameters but no significant clinical efficacy</td><td align="center" valign="middle" style="border-bottom:solid thin" rowspan="1" colspan="1">[<xref rid="B99-cells-08-00927" ref-type="bibr">99</xref>]</td></tr></tbody></table><table-wrap-foot><fn><p>* Abbreviations: SLE, systemic lupus erythematosus; PLN, proliferative lupus nephritis; RA, rheumatoid arthritis; SS, Sjögren’s syndrome; mAb, monoclonal antibody; Fab, Fab portion of antibody; MTX, methotrexate. DB, double-blinded; PC, placebo-controlled; wks: weeks.</p></fn></table-wrap-foot></table-wrap></floats-group></pmc><affiliations><list><country><li>Taïwan</li></country></list><tree><country name="Taïwan"><noRegion><name sortKey="Lai, Jenn Haung" sort="Lai, Jenn Haung" uniqKey="Lai J" first="Jenn-Haung" last="Lai">Jenn-Haung Lai</name></noRegion><name sortKey="Ho, Ling Jun" sort="Ho, Ling Jun" uniqKey="Ho L" first="Ling-Jun" last="Ho">Ling-Jun Ho</name><name sortKey="Lai, Jenn Haung" sort="Lai, Jenn Haung" uniqKey="Lai J" first="Jenn-Haung" last="Lai">Jenn-Haung Lai</name><name sortKey="Luo, Shue Fen" sort="Luo, Shue Fen" uniqKey="Luo S" first="Shue-Fen" last="Luo">Shue-Fen Luo</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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