T_H17 cells are key drivers of pro-inflammatory responses, where they primarily provide protection against extracellular pathogens. However, they have also been implicated in the development of numerous autoimmune diseases, such as multiple sclerosis. Several studies have demonstrated that T_H17 cells possess a high degree of plasticity in both their phenotype and function where they can adopt both pro-inflammatory and regulatory states.  Recent work from our laboratory has identified a unique cell surface signature which distinguishes between pathogenic and non-pathogenic T_H17 cells. Here, we have shown that pathogenic GM-CSF- and IFNg-producing T_H17 cells express the chemokine receptor CCR2 and downregulate the canonical T_H17 chemokine receptor, CCR6, whereas non-pathogenic T_H17 cells maintain CCR6 expression. However, the stability and plasticity of these phenotypically distinct T_H17 subsets is yet to be determined. Understanding the degree of plasticity in this system as well as which factors drive the development of these cells will further enhance our understanding of T_H17 cell biology and will potentially allow for the development of novel therapeutics for T_H17-driven inflammatory diseases which target pathogenic cells whilst sparing non-pathogenic T_H17 cells.