Abstract
Innate immunity represents the semi-specific first line of defense and provides the initial host response to tissue injury, trauma, and pathogens. Innate immunity activates the adaptive immunity, and both act highly regulated together to establish and maintain tissue homeostasis. Any dysregulation of this interaction can result in chronic inflammation and autoimmunity and is thought to be a major underlying cause in the initiation and progression of highly prevalent immune-mediated inflammatory diseases (IMIDs) such as psoriasis, rheumatoid arthritis, inflammatory bowel diseases among others, and periodontitis. Th1 and Th2 cells of the adaptive immune system are the major players in the pathogenesis of IMIDs. In addition, Th17 cells, their key cytokine IL-17, and IL-23 seem to play pivotal roles. This review aims to provide an overview of the current knowledge about the differentiation of Th17 cells and the role of the IL-17/IL-23 axis in the pathogenesis of IMIDs. Moreover, it aims to review the association of these IMIDs with periodontitis and briefly discusses the therapeutic potential of agents that modulate the IL-17/IL-23 axis.
Highlights
Innate immunity represents the semi-specific first line of defense for all primitive and complex multicellular organisms and provides the initial acute inflammatory reaction to tissue injury, trauma, or pathogens [1]
There is still much to be elucidated, this review aims to provide an overview of the current knowledge about the T helper 17 (Th17) cell lineage, the role of its key cytokine IL-17, the IL-17/IL-23 axis in health and disease, and strategies that target IL-17 related pathways
IL-23 is produced by antigen-presenting cells, such as dendritic cells and monocytes/macrophages upon activation and initiates signaling by binding to IL-23 receptor (IL-23R), which in return increases the expression of receptor γt (RORγt) and IL-17 via STAT3 (Figures 1c and 2) [39]
Summary
Innate immunity represents the semi-specific first line of defense for all primitive and complex multicellular organisms and provides the initial acute inflammatory reaction to tissue injury, trauma, or pathogens [1]. Innate immunity is a rather unspecific and immediate reaction that recruits immune cells to the injury or infection site through various cytokines (e.g., prostaglandins, tumor necrosis factor (TNF), interleukin (IL)-1β, and others) It promotes phagocytosis, and activates the complement and adaptive immune system [2]. In contrast to the innate immune system, the activation of the adaptive immune system results in an antigen specific host response that is mediated by T and B cells. An alteration of the regular immune response may result in persistence of the acute inflammation, its transition into chronic inflammation, and could even induce autoimmune reactions in susceptible individuals This altered inflammatory response is believed to be a major underlying cause in the initiation and progression of disorders, such as immune-mediated inflammatory diseases (IMIDs) [5]. Understanding the similar mechanisms that drive the pathogenesis of these diseases will support an interdisciplinary approach between medical doctors and dentists, and allow proper screening, prevention, and early treatment
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