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Essential role of interferon regulatory factor 4 (IRF4) in immune cell development

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Abstract

The family of interferon regulatory factors, which includes nine mammalian members (IRF1–IRF9), acts as transcription factors for interferons and thus exerts regulatory functions in the immune system and in oncogenesis. Among these members, IRF4 expression is restricted to immune cells such as T and B lymphocytes, macrophages, and dendritic cells where it is a key factor in the regulation of differentiation and is required during the immune response for lymphocyte activation and the generation of immunoglobulin-secreting plasma cells. Consequently, dysregulation of IRF4 is associated with many lymphoid malignancies. Recent studies have demonstrated that depending on the context and stage of hematopoietic cell differentiation in which its expression is dysregulated, IRF4 may act as either an oncogene or a tumor-suppressor-like factor. In addition, it has been shown that IRF4 plays a pivotal role in the development and function of several autoimmune-associated cells. Various genetic and functional studies have also pointed to IRF4 as a master regulator for autoimmunity. In this review, the roles of IRF4 in the immune response are briefly summarized and discussed, with particular focus on its essential and distinct functions in immune cell development.

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Acknowledgements

We apologize to the colleagues whose works have not been cited due to the space constraints. This study was supported by grants from the National Research Foundation of Korea (NRF) funded by the Ministry of Science, ICT & Future Planning, Republic of Korea the Korea government (2016R1A5A1011974, 2015R1D1A1A01058051, and 2014R1A2A2A09052492). We would also like to acknowledge the financial support from the R&D Convergence Program (CAP-16-030KRIBB) of NST (National Research Council of Science & Technology) of Republic of Korea.

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Nam, S., Lim, JS. Essential role of interferon regulatory factor 4 (IRF4) in immune cell development. Arch. Pharm. Res. 39, 1548–1555 (2016). https://doi.org/10.1007/s12272-016-0854-1

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