Vol.:(0123456789) 1 3 Infammation Research https://doi.org/10.1007/s00011-020-01339-9 REVIEW Interleukin 23 and autoimmune diseases: current and possible future therapies Ahmad Ismail Khaled Abdo 1  · Gee Jun Tye 1 Received: 22 November 2019 / Revised: 21 February 2020 / Accepted: 16 March 2020 © Springer Nature Switzerland AG 2020 Abstract Purpose IL-23 is a central proinfammatory cytokine with a wide range of infuence over immune response. It is implicated in several autoimmune diseases due to the infnite infammatory loops it can create through the positive feedbacks of both IL-17 and IL-22 arms. This made IL-23 a key target of autoimmune disorders therapy, which indeed was proven to inhibit infammation and ameliorate diseases. Current autoimmune treatments targeting IL-23 are either by preventing IL-23 liga- tion to its receptor (IL-23R) via antibodies or inhibiting IL-23 signaling by signaling downstream mediators’ inhibitors, with each approach having its own pros and cons. Methods Literature review was done to further understand the biology of IL-23 and current therapies. Results In this review, we discuss the biological features of IL-23 and its role in the pathogenesis of autoimmune diseases including psoriasis, rheumatoid arthritis and infammatory bowel diseases. Advantages, limitations and side efects of each concept will be reviewed, suggesting several advanced IL-23-based bio-techniques to generate new and possible future therapies to overcome current treatments problems. Keywords IL-23 · Autoimmune diseases · Psoriasis · Rheumatoid arthritis · Infammatory bowel disease Introduction The immune system’s cells are activated upon receiving a danger signal or recognizing non-self-antigens, which can be pathogens or diseases such as cancers. This activation initiates several infammatory mechanisms including cytokines and anti- microbial peptides (AMPs) secretion, phagocytosis, antibody production and cell-mediated cytotoxicity [1]. Excessive efec- tor infammatory mechanisms, however, can injure the host. Hence, infammation is tightly regulated by anti-infammatory mediators. Both infammatory and anti-infammatory reactions shape the immune response. A balanced immune response can eliminate harmful and unwanted molecules or cells; while, dys- regulation and shifting the equilibrium towards one side can result in fatal diseases. Immune-mediated disorders are conditions characterized by an uncontrolled immune response that leads to body dam- age. For example, overexpression of immune suppressive T regulatory cells (Treg), a subset of T cells which secrete anti-inflammatory cytokines such as TGF-β, IL-10 and IL-35, can attenuate cancer immune surveillance and con- tribute in tumor development [2]. On the other hand, con- tinuous infammation leads to a deleterious impact on body tissues which can diminish or completely halt tissue function such as in rheumatism and type 1 diabetes. This can be due to B cell receptor (BCR) and T cell receptor (TCR) rec- ognizing self-antigens, creating autoreactive lymphocytes; or by positive feedbacks infammatory signaling through cytokine cross-talk among immune cells that keeps infam- mation ongoing [3]. In both cases, the body own molecules are the “fuels” for infammation which create “auto” immune response activation leading to life-time chronic diseases. In other words, autoimmune diseases are conditions where the body attacks and destroys itself. Several risk fac- tors have been correlated with autoimmunity development. The genetic make-up of infammatory mediators such as human leukocyte antigen (HLA), infections, tissue injuries and environmental factors such as UV and toxic chemicals Inflammation Research * Gee Jun Tye geejun@usm.my Ahmad Ismail Khaled Abdo ahmad_ik_abdo@outlook.com 1 Institute for Research in Molecular Medicine (INFORMM), Universiti Sains Malaysia, 11800 Minden, Penang, Malaysia