What is the function of IL-17A?
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 is the difference between IL-17A and IL 17F?
Despite the large number of double- positive cells in these models, IL-17F is dispensable for autoimmune tissue inflammation whereas IL-17A-deficient mice show reduced disease (Ishigame et al., 2009).
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.
What activates Th17?
The secretion of IL-23 from antigen-presenting cells such as dendritic cells, which have been activated by the uptake and processing of pathogens, in turn activates Th17 cells.
Where is IL-17 produced?
As predicated by the original studies, it has been shown that innate IL-17-producing cells predominantly reside in the skin and mucosal tissues that separate the host from the environment — where they serve as the sentinels of the immune system8,17,25,26,27,28.
Is IL-17 an inflammatory cytokine?
Interleukin-17 (IL-17) induces the production of granulocyte colony-stimulating factor (G-CSF) and chemokines such as CXCL1 and CXCL2 and is a cytokine that acts as an inflammation mediator.
Is IL-17A proinflammatory?
IL-17A promotes inflammation by inducing various proinflammatory cytokines and chemokines, recruiting neutrophils, enhancing antibody production, and activating T cells. IL-17A expression is also augmented in autoimmune diseases such as multiple sclerosis and rheumatoid arthritis.
Which cytokine is a precursor to IL-17?
Cytokines released from DCs stimulate dying keratinocytes to secrete TNF-alpha, IL-1 and IL-6 leading to the chemotaxis of T cells, natural killer cells and monocytes to the epidermis. These cells release IL-23 which induce Th17 cells to produce IL-17.
What are IL-17 drugs?
Secukinumab, ixekizumab, and brodalumab are three anti-IL-17 medications used for treating psoriasis, of which only secukinumab is FDA approved; ixekizumab and brodalumab remain under clinical development.
Is Humira an IL-17?
Two newer classes of biologics, the interleukin 23 (IL-23) and interleukin 17 (IL-17) inhibitors are challenging the longstanding supremacy of tumor necrosis factor (TNF) inhibitors like Humira (adalimumab), Enbrel (etanercept), and Remicade (infliximab).
Do Th17 cells produce IL-17?
IL-17 is believed to be mainly produced by T helper 17 (Th17) cells, a unique helper T-cell subset different from Th1 and Th2 cells. Other subsets of T cells such as γδT and natural killer T (NKT) cells have also been found to produce IL-17 in response to innate stimuli.
What is a polarizing cytokine?
Cytokines determine T-cell polarization. The presence of IL-12 and/or interferon γ drives previously uncommitted T cells to become polarized to produce T1 cytokines, while IL-4 drives them to become polarized to secrete T2 cytokines.
How does IL-17 affect the left ventricle?
Th17 cells were markedly increased in the ischemic HF rabbit model. IL-17 directly induced VA in vivo and in vitro in a dose-dependent manner. IL-17 decreased conduction velocity, lengthened action potential duration, and increased the slope of the left ventricle (LV) restitution curve.
What is the role of interleukin-17 in ischemic heart failure?
Background: We aimed to investigate the impact of interleukin (IL)-17 on ventricular remodeling and the genesis of ventricular arrhythmia (VA) in an ischemic heart failure (HF) model. The expression of the proinflammatory cytokine IL-17 is upregulated during myocardial ischemia and plays a fundamental role in post-infarct inflammation.
How is Th17 cell expression measured in ischemic HF?
Methods and results: The level of inflammation and Th17 cell (CD4 + IL-17 +) expression in the rabbit model of ischemic HF were studied by flow cytometry, quantitative polymerase chain reaction (qPCR), and enzyme-linked immunosorbent assay (ELISA).