Although γδ T cells are a major component of the human intestinal mucosa, it is not clear what role they play in mucosal immunity or if they are involved in the disease process of inflammatory bowel disease (IBD).

Flow cytometry and reverse transcriptase-polymerase chain reaction (RT-PCR) assays were used to identify quantitative and qualitative changes in the repertoire of γδ T cells present in surgical and/or biopsy samples of normal and inflamed colon from individual patients with ulcerative colitis (UC) or Crohn’s disease (CD). Cytokine production and the ability to adhere to and interact with colonic fibroblasts were used to compare the functional properties of γδ T cells isolated from the normal and diseased colonic mucosa.

Increased numbers of γδ T cells localized in areas of inflammation and tissue injury were found in the majority of patients, irrespective of the type of IBD present. This expansion was attributable to an increase in Vδ1⁺ cells expressing a Vδ1-(Dδ3)-Jδ1-encoded T cell receptor and was seen in patients with severe disease as well as those with newly diagnosed or less severe forms of IBD. Among T cells present in the inflamed mucosa of patients with CD, γδ T cells, particularly Vδ1⁺ cells, were a major source of the proinflammatory cytokine interferon-γ and could interact with colonic fibroblasts.

Our results demonstrate that the chronic inflammatory immune response characteristic of IBD is associated with distinct changes in the number, distribution, composition, and function of mucosal γδ T cells. Through the production of cytokines and physical interaction with other cells, γδ T cells can perform an immunoregulatory function and contribute to the pathophysiology of IBDs.