Targeting the CD40-CD154 Signaling Pathway for Treatment of Autoimmune Arthritis
Identifieur interne : 000381 ( Main/Exploration ); précédent : 000380; suivant : 000382Targeting 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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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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Long</name></author></analytic></biblStruct></listBibl></div1></back></TEI><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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