ArticleInternational journal of molecular sciences2017
Therapeutic Effect of Exogenous Truncated IK Protein in Inflammatory Arthritis.
Article in International journal of molecular sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Structural Studies of Expressed tIK, Anti-Inflammatory Peptide.International journal of molecular sciences · 2022Article
- MiR-141-3p and miR-200a-3p are involved in Th17 cell differentiation by negatively regulating RARB expression.Human cell · 2021Article
- Suppressive Effects of a Truncated Inhibitor K562 Protein-Derived Peptide on Two Proinflammatory Cytokines, IL-17 and TNF-α.Journal of microbiology and biotechnology · 2020Article
- Homology Modeling and Optimized Expression of Truncated IK Protein, tIK, as an Anti-Inflammatory Peptide.Molecules (Basel, Switzerland) · 2020Article
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Authors and funding
11 authors.
Funding
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Abstract
Inhibitor K562 (IK) protein was first isolated from the culture medium of K562, a leukemia cell line. It is known to be an inhibitory regulator of interferon-γ-induced major histocompatibility complex class (MHC) II expression. Previously, we found that transgenic (Tg) mice constitutively expressing truncated IK (tIK) showed reduced numbers of pathogenic Th1 and Th17 cells, which are known to be involved in the development of rheumatoid arthritis (RA). Here, we investigated whether exogenous tIK protein has a therapeutic effect in arthritis in disease models and analyzed its mechanism. Exogenous tIK protein was produced in an insect expression system and applied to the collagen antibody-induced arthritis (CAIA) mouse disease model. Injection of tIK protein alleviated the symptoms of arthritis in the CAIA model and reduced Th1 and Th17 cell populations. In addition, treatment of cultured T cells with tIK protein induced expression of A20, a negative regulator of nuclear factor-κB (NFκB)-induced inflammation, and reduced expression of several transcription factors related to T cell activation. We conclude that exogenous tIK protein has the potential to act as a new therapeutic agent for RA patients, because it has a different mode of action to biopharmaceutical agents, such as tumor necrosis factor antagonists, that are currently used to treat RA.
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