Therapeutic potential of targeting TBK1 in autoimmune diseases and interferonopathies

Pharmacol Res. 2016 Sep:111:336-342. doi: 10.1016/j.phrs.2016.04.008.

Maroof Hasan ¹, Nan Yan ²

Affiliations

1 Autoimmunity, Transplantation and Inflammation, Novartis Institute of Biomedical Research, CH?4056 Basel, Switzerland. Electronic address: [email protected].
2 Departments of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX, USA; Departments of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX, USA. Electronic address: [email protected].

PMID: 27353409 DOI: 10.1016/j.phrs.2016.04.008

Abstract

The serine/threonine protein kinase, TBK1, plays a crucial role as the hub for many innate immune signaling pathways that lead to the induction of type I interferon (IFN) and interferon-stimulated genes (ISGs). Due to its key function in maintaining homeostasis of the immune system, cell survival and proliferation, TBK1 activity is tightly regulated. Dysregulation of TBK1 activity is often associated with autoimmune diseases and Cancer, implicating the potential therapeutic benefit for targeting TBK1. Tremendous effort from both academic institutions and private sectors during the past few years has led to the development of many potent and selective TBK1 inhibitors, many of which have shown great promise in disease models in vivo. This review summarizes recent advance on the pharmacological inhibition of TBK1 and its potential for treating autoimmune diseases and interferonopathies.

Keywords

Autoimmune disease; Interferonopathy; Lupus; TBK1; Type I interferon.

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