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Muromoto R, Shimoda K, Oritani K, et al. Therapeutic Advantage of Tyk2 Inhibition for Treating Autoimmune and Chronic Inflammatory Diseases. Biol Pharm Bull. 2021;44(11):1585-1592doi: 10.1248/bpb.b21-00609.
Muromoto, R., Shimoda, K., Oritani, K., & Matsuda, T. (2021). Therapeutic Advantage of Tyk2 Inhibition for Treating Autoimmune and Chronic Inflammatory Diseases. Biological & pharmaceutical bulletin, 44(11), 1585-1592. https://doi.org/10.1248/bpb.b21-00609
Muromoto, Ryuta, et al. "Therapeutic Advantage of Tyk2 Inhibition for Treating Autoimmune and Chronic Inflammatory Diseases." Biological & pharmaceutical bulletin vol. 44,11 (2021): 1585-1592. doi: https://doi.org/10.1248/bpb.b21-00609
Muromoto R, Shimoda K, Oritani K, Matsuda T. Therapeutic Advantage of Tyk2 Inhibition for Treating Autoimmune and Chronic Inflammatory Diseases. Biol Pharm Bull. 2021;44(11):1585-1592. doi: 10.1248/bpb.b21-00609. PMID: 34719635.
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Biol Pharm Bull. 2021;44(11):1585-1592. doi: 10.1248/bpb.b21-00609.

Therapeutic Advantage of Tyk2 Inhibition for Treating Autoimmune and Chronic Inflammatory Diseases.

Biological & pharmaceutical bulletin

Ryuta Muromoto, Kazuya Shimoda, Kenji Oritani, Tadashi Matsuda

Affiliations

  1. Department of Immunology, Graduate School of Pharmaceutical Sciences Hokkaido University.
  2. Department of Internal Medicine II, Faculty of Medicine, University of Miyazaki.
  3. Department of Hematology, International University of Health and Welfare.

PMID: 34719635 DOI: 10.1248/bpb.b21-00609

Abstract

Tyrosine kinase 2 (Tyk2) is a member of the Janus family of protein tyrosine kinases (Jaks). Tyk2 associates with interferon (IFN)-α, IFN-β, interleukin (IL)-6, IL-10, IL-12, and IL-23 receptors and mediates their downstream signaling pathways. Based on our data using Tyk2-deficient mice and cells, Tyk2 plays crucial roles in the differentiation, maintenance, and function of T helper 1 (Th1) and Th17 cells, and its dysregulation may promote autoimmune and/or inflammatory diseases. IFN-α-induced growth inhibition of B lymphocyte progenitors is dependent on Tyk2-mediated signals to regulate death-associated protein (Daxx) nuclear localization and Daxx-promyelocytic leukemia protein interactions. Tyk2-deficient mice show impaired constitutive production of type I IFNs by macrophages under steady-state conditions. When heat-killed Cutibacterium acnes is injected intraperitoneally, Tyk2-deficient mice show less granuloma formation through enhanced prostaglandin E

Keywords: Janus family of protein tyrosine kinase (Jak) inhibitor; cytokine; immune system; signal transduction; therapy; tyrosine kinase 2 (Tyk2)

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