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Ahmed N. Hegazy

M.D., Ph.D.

Marie Skłodowska-Curie Research Fellow

Immune responses in the intestine are tightly regulated to ensure host protective immunity while avoiding immune pathology due to anti-self and anti-commensal microbiota responses. A 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 between genetic, environmental, microbial and immune factors. Dysregulated effector CD4 T cell responses are involved in the immunopathology and tissue destruction of 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 are unknown.

It remains to be determined whether this polyfunctional Th17/Th1 phenotype can be therapeutically modified in favour of a homeostatic Type 17 or regulatory T cell response. 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 chronic immunepathological CD4 T cell responses can be specifically targeted in IBD.

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