Immune response in the intestine are tightly regulated to ensure host protective immunity in the absence of immune pathology. A permanent disturbance of this delicate balance can lead to the development of inflammatory bowel disease (IBD) comprising Crohn’s disease (CD) and ulcerative colitis (UC). The aetiology of IBD is unknown, but it is thought to involve a complex interplay among genetic, environmental, microbial and immune factors. Dysregulated effector CD4 T cell responses can be causative in IBD irrespective of the initiating events that promote them. There is compelling evidence that pathogenic CD4 T cells accumulate in the inflamed intestine and contribute to the chronicity of disease. Additionally at the onset of IBD, mucosal effector CD4 T cells acquire a pathogenic polyfunctional Th17/Th1 phenotype. However the signals and molecular events that induce and regulate the pathogenic switch in human T cells, remain unknown. Whether this phenotype can be modified in favour of a homeostatic Type 17 or regulatory T cell response also remains to be determined. Revealing the signals and mechanisms by which the differentiation programs of pathogenic CD4 T cells are induced, maintained and modulated, might open new avenues by which pathogenic and chronic CD4 T cell responses can be specifically targeted in IBD.