PD-1 on CD8+T cells are low in Behçet's disease and is not normalised with type-I interferon

Programmed cell death-1 (PD-1) protein on CD8+T cells may affect disease development as a regulatory molecule through various mechanisms. On the other hand, type-I interferons (IFN-I) are used in autoimmune and autoinflammatory diseases to induce regulatory mechanisms. This study aims to investigate PD-1 molecules on CD8+T cells in Behçet's disease (BD) and their response to IFN-I.

BD (n=37) patients were compared with age- and sex-matched healthy (n=24) and diseased controls (n=29). Peripheral mononuclear cells (PBMCs) were stained for PD-1, CD45RA and CCR7 molecules on CD3+CD8+T cells. Cells from patients and controls were further activated in vitro by anti-CD3 and interferon (IFN-α/2α1b) and the induction of PD-1, TIM-3 and TIGIT on CD8+T cells was analysed.

PD-1 on CD8+T cells with potentially regulatory functions were significantly lower in BD patients, regardless of disease activity, than in controls. CD3 stimulation of PBMCs induced PD-1 expression in all groups, whereas the addition of interferon to stimulated CD8+T cells produced differential responses: the increase of PD-1 on CD8+T cells in controls was not observed in BD patients. The responsive increase of similar co-inhibitory molecules, TIM-3 and TIGIT, in controls was not seen in BD patients either.

The decreased PD-1 expression on CD8+T cells, along with the decreased PD-1, TIM-3 and TIGIT responses of CD8+T cells upon IFN-I stimulation, demonstrated an altered immune response in BD.