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Int. J. Mol. Sci. 2017, 18(9), 1976; doi:10.3390/ijms18091976

Therapeutic Effect of Exogenous Truncated IK Protein in Inflammatory Arthritis

1
Department of Biotechnology, The Catholic University of Korea, Bucheon 14662, Korea
2
The Rheumatism Research Center, Catholic Research Institute of Medical Science, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea
3
Division of Rheumatology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea
4
Department of Biotechnology, Chonbuk National University, Iksan 54596, Korea
5
Biomaterials Research Center, Cellinbio, Suwon 16680, Korea
These authors contributed equally to this work.
*
Author to whom correspondence should be addressed.
Received: 31 August 2017 / Revised: 10 September 2017 / Accepted: 11 September 2017 / Published: 14 September 2017
(This article belongs to the Special Issue T Cell Signaling and Autoimmunity)
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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. View Full-Text
Keywords: autoimmune disease; rheumatoid arthritis; T cells; truncated IK autoimmune disease; rheumatoid arthritis; T cells; truncated IK
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

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MDPI and ACS Style

Choi, S.; Park, H.; Jung, S.; Kim, E.-K.; Cho, M.-L.; Min, J.-K.; Moon, S.-J.; Lee, S.-M.; Cho, J.-H.; Lee, D.-H.; Nam, J.-H. Therapeutic Effect of Exogenous Truncated IK Protein in Inflammatory Arthritis. Int. J. Mol. Sci. 2017, 18, 1976.

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