Gamma Delta (γδ) T Cells and Their Involvement in Behçet’s Disease

Figure 1

Schematic diagram of the potential interaction of neutrophils, monocytes, and DCs with γδ T cells in BD. An infectious trigger (e.g., microbes) results in extravasation of neutrophils and following phagocytosis of the invading microbes, neutrophils release traces of HMB-PP into the microenvironment where γδ T cells sense it. Monocytes then might take up or bind this soluble HMB-PP and present it to γδ T cells. This interaction triggers TNFα secretion, a proinflammatory cytokine along with other similar cytokines including IFNγ which promotes γδ T cell expansion and drive local chemokine (CXCL8) production that further recruits new neutrophils and monocytes to the site of infection. In addition, activated γδ T cells keep providing survival and activation signals to the newly recruited neutrophils and monocytes by secreting TNFα. Furthermore, activated γδ T cells present antigen to DCs and thus initiate Th1, Th2, and Th17 differentiation and proliferation. Even if the infectious trigger is in the form of a non-HMB-PP source such as HSP60/65, γδ T cells can again respond by expanding and keep the interaction active with the neighbouring cells.