IL17

IL17 Full Name

Interleukin 17

IL17 Introduction

Interleukin-17 (IL-17) primarily refers to the cytokine IL-17A, the founding member of the IL-17 family which includes six members (IL-17A through IL-17F). It is a homodimeric glycoprotein secreted predominantly by a distinct subset of helper T cells, known as Th17 cells. IL-17A signals through a receptor complex composed of IL-17RA and IL-17RC subunits, which are widely expressed on epithelial cells, fibroblasts, and myeloid cells. Unlike classical Th1 or Th2 cytokines, its signaling activates unique pathways such as NF-κB and MAPK, leading to the production of antimicrobial peptides and pro-inflammatory mediators.

Figure 1. Strcuture of Interleukin-17.

Cellular Sources and Regulation
The primary producers of IL-17A are CD4+ Th17 cells, whose differentiation from naïve T cells is driven by cytokines like TGF-β, IL-6, IL-1β, and IL-23. Other important cellular sources include γδ T cells, innate lymphoid cells (ILC3s), neutrophils, and natural killer T (NKT) cells. The development and stability of Th17 cells are critically dependent on the master transcription factor RORγt. The production of IL-17 is tightly controlled, with anti-inflammatory cytokines like IL-10 and interferon-gamma (IFN-γ) from Th1 cells acting as key negative regulators to prevent excessive inflammation.

Role in Autoimmunity and Chronic Inflammation
While crucial for host defense, dysregulated or persistent IL-17 signaling is a central driver of chronic inflammatory and autoimmune diseases. Its pathogenic role is well-established in psoriasis, psoriatic arthritis, and ankylosing spondylitis. IL-17 promotes disease by stimulating keratinocyte proliferation, osteoclastogenesis, and the production of other inflammatory mediators that lead to tissue damage. Evidence also implicates it in the pathogenesis of multiple sclerosis, rheumatoid arthritis, and inflammatory bowel diseases (IBD), making it a major focus in immunopathology research.