2020
DOI: 10.1007/s00011-020-01339-9
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Interleukin 23 and autoimmune diseases: current and possible future therapies

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Cited by 29 publications
(18 citation statements)
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“…The efficacy of IL-23 blockade was further supported by reduction in IL-17 and IL-22 levels through the sequestration of IL-23 by a decoy protein containing the IL-23 receptor cytokine-binding homology region [84]. Such evidence provides support for potential development of an IL-23 receptor-Fc fusion protein, similar to etanercept [85].…”
Section: Discussionmentioning
confidence: 85%
“…The efficacy of IL-23 blockade was further supported by reduction in IL-17 and IL-22 levels through the sequestration of IL-23 by a decoy protein containing the IL-23 receptor cytokine-binding homology region [84]. Such evidence provides support for potential development of an IL-23 receptor-Fc fusion protein, similar to etanercept [85].…”
Section: Discussionmentioning
confidence: 85%
“…There are several mAbs targeting cytokines or their receptors developed to reduce inflammatory response in autoimmune disorders. IL-17 as a major cytokine Introduction on Monoclonal Antibodies DOI: http://dx.doi.org/10.5772/intechopen.98378 of Th17 cells, plays crucial roles in immune response against bacterial and fungal infections, as well as in the pathogenesis of autoimmune diseases, importantly in psoriasis [55]. Secukinumab (Cosentyx®), an IgG1 human mAb, binds to IL-17A and is approved for the treatment of psoriasis and ankylosing spondylitis.…”
Section: Other Monoclonal Antibodies For Treating Autoimmune Diseasesmentioning
confidence: 99%
“…IL-23 is also a key proinflammatory cytokine playing an important role in Th-17 differentiation and activation. Guselkumab (Tremfya®), Risankizumab (SKYRIZI®), and Tildrakizumab (Ilumya®) are IgG1 mAbs targeting IL-23 p19 approved for the treatment of patients with plaque psoriasis [55].…”
Section: Other Monoclonal Antibodies For Treating Autoimmune Diseasesmentioning
confidence: 99%
“…Existen diversos elementos compartidos por estas enfermedades, entre los que podemos incluir: la ausencia de un autoantígeno claro que indique la naturaleza autoinmune de estas enfermedades (por ello se prefiere el término «autoinflamatorias»), su profunda relación con la disbiosis intestinal [3][4][5][6] y la participación del eje IL-23/IL-17 en su patogenia [7][8][9][10] . Otro elemento compartido entre estas enfermedades es el fondo genético, en el que se comparten varios polimorfismos de un solo nucleótido (SNP, single nucleotide polymorphism) 2 y la presencia de moléculas de histocompatibilidad como el HLA-B27.…”
Section: Introductionunclassified