How does IL-17 cause inflammation?
How does IL-17 cause inflammation?
Interleukin-17 (IL-17, also known as IL-17A) is a key cytokine that links T cell activation to neutrophil mobilization and activation. As such, IL-17 can mediate protective innate immunity to pathogens or contribute to the pathogenesis of inflammatory diseases, such as psoriasis and rheumatoid arthritis.
What does IL-23 do in the body?
IL-23 functions in innate and adaptive immunity, and is a key cytokine for promoting inflammatory responses in a variety of target organs. The most important function ascribed to IL-23 is its role in the development and differentiation of effector Th17 cells via activation of STAT3.
What produces il21?
IL-21 is a pleiotropic type I cytokine that is produced mainly by T cells and natural killer T (NKT) cells. This cytokine has diverse effects on a broad range of cell types including, but not limited to, CD4 + and CD8 + T cells, B cells, macrophages, monocytes, and dendritic cells (DCs) 1 ( Figure 1).
What does IL 17 do in psoriasis?
In psoriatic lesions, IL-17A, IL-17E, and IL-17F are involved in neutrophil accumulation, followed by the formation of epidermal micro abscesses. IL-17A together with other Th17 cytokines also upregulates the production of several chemokines that are implicated in psoriasis pathogenesis.
What is the difference between IL 17 and IL-17A?
IL17C shows only 23% homology with IL-17A, and unlike IL-17A, is expressed mainly by epithelial cells rather than immune cells. Much evidence links IL-17C to skin inflammation. Importantly, IL-17C is overexpressed in lesional skin of psoriatic (91, 92) and atopic dermatitis patients (93).
What is an IL-17 inhibitor?
Abstract. Secukinumab, ixekizumab and brodalumab are monoclonal antibody therapies that inhibit interleukin (IL)-17 activity and are widely used for the treatment of psoriasis, psoriatic arthritis and ankylosing spondylitis.
Is the IL-23 / IL-17 axis critical for inflammatory diseases?
The IL-23/IL-17, but not IL-12/IFN-γ, axis is critical for the development of autoimmune inflammatory diseases. The development of autoimmune diseases, such as RA, MS, and IBD, is thought to be mediated by Th1 cells because high levels of IL-12 and IFN-γ are detected in inflammatory sites (9).
Why are IL-23 and IFN γ important?
IL-23 and IL-17 are also important in host defenses against infection. It should be noted that IL-12/IFN-γ are primarily involved in host defenses against intracellular pathogens while IL-23/IL-17 are important for defenses against extracellular pathogens, including Klebsiella pneumoniae ( 28 ).
What is the role of IMQ in dermatitis?
IMQ induced epidermal expression of IL-23, IL-17A, and IL-17F, as well as an increase in splenic Th17 cells. IMQ-induced dermatitis was partially dependent on the presence of T cells, whereas disease development was almost completely blocked in mice deficient for IL-23 or the IL-17 receptor, demonstrating a pivotal role of the IL-23/IL-17 axis.
How does IL-4 inhibit Th17 cell expansion?
Although IL-4 also inhibits Th17 cell expansion, the mechanism governing this suppression is not known (2, 4). Thus, the identification of the signals that induce IL-23R expression on naive CD4 + T cells is crucial in elucidating the mechanisms of Th17/Th IL-17 cell lineage differentiation.
