Cancer Treatments

IL-17: The Game-Changing Molecule for Autoimmune and Cancer Treatments


A breakthrough study in Signal Transduction and Targeted Therapy highlights the tremendous potential of interleukin-17 (IL-17) in revolutionizing treatments for autoimmune diseases and cancer. IL-17, a family of six molecules, including IL-17A, IL-17B, IL-17C, IL-17D, IL-17E (IL-25), and IL-17F, plays a crucial role in various physiological and pathological processes.

IL-17A, also known as cytotoxic T-lymphocyte-associated antigen 8 (CTLA-8), has been extensively studied due to its wide-ranging effects. The IL-17 family functions through different receptor types, formed by five receptor subunits, offering diverse ligands and receptors. This multifunctionality provides IL-17 with the ability to perform multiple crucial roles within the body.

IL-17 is primarily expressed by a subset of CD4+ T helper cells (Th17), but it is also produced by other immune cells such as natural killer (NK) cells, CD8+ T-cells, dendritic cells, macrophages, and neutrophils during infections. CD4+ and CD8+ T-cells produce IL-17 in response to T-cell receptor (TCR) activation, while innate immune cells generate IL-17 in response to pro-inflammatory cytokines, particularly IL-1 and IL-23.

IL-17 binds to its receptor, IL-17R, via the adapter molecule Act1, initiating downstream pathways. These pathways involve tumor necrosis factor (TNF) receptor-associated factors (TRAFs) and E3 ligase-mediated ribonucleic acid (RNA) binding, resulting in transcription and post-transcriptional gene activation.

One of the key roles of IL-17 is its ability to enhance the inflammatory response by activating the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and mitogen-activated protein kinase (MAPK) pathways. This leads to the transcription of target messenger RNA (mRNA) and the production of inflammatory cytokines. Importantly, IL-17 is subject to feedback regulation, preventing an excessively prolonged or hyperactive inflammatory response.

Regulation of genes within the IL-17 pathways is also achieved through the stability of mRNA transcripts. Both the MAPK and NF-κB pathways produce mRNA with an unstable 3′ untranslated region (UTR). RNA-binding proteins (RBP) like Act1 can bind to these regions, enhancing stability and promoting the translation of inflammatory cytokines. Conversely, another RBP called ribonuclease regnase-1 facilitates the breakdown of IL-17 mRNA.

The multifaceted role of IL-17 in the body, its ability to modulate the inflammatory response, and its potential to act as a target for treating autoimmune diseases and cancer make it a promising molecule for future therapeutic developments. With further research and understanding of IL-17’s precise mechanisms, it has the potential to revolutionize the field of medicine and improve patient outcomes.


1. Source: Coherent Market Insights, Public sources, Desk research
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