impact factor, citescore
logo
 

Full Papers

 

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


1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11

 

  1. Istanbul University, Istanbul Medical Faculty, Department of Physiology, Istanbul; and Istanbul University, Department of Immunology, Institute of Health Sciences, Istanbul, Turkey.
  2. Marmara University, School of Medicine, Department Internal Medicine, Division of Rheumatology, Istanbul, Turkey.
  3. University of Health Sciences, Department of Rheumatology, Istanbul, Turkey.
  4. Istanbul University, Istanbul Medical Faculty, Department of Neurology, Istanbul, Turkey.
  5. Istanbul University, Istanbul Medical Faculty, Department of Neurology, Istanbul, Turkey.
  6. Istanbul University, Istanbul Medical Faculty, Department of Neurology, Istanbul, Turkey.
  7. University of Health Sciences, Department of Rheumatology, Istanbul, Turkey.
  8. Marmara University, School of Medicine, Department Internal Medicine, Division of Rheumatology, Istanbul, Turkey.
  9. Istanbul University, Istanbul Medical Faculty, Department Internal Medicine, Division of Rheumatology, Istanbul, Turkey.
  10. Marmara University, School of Medicine, Department Internal Medicine, Division of Rheumatology, Istanbul, Turkey.
  11. Istanbul University, Istanbul Medical Faculty, Department of Physiology, Istanbul, Turkey. gsaruhan@istanbul.edu.tr

CER19762
Full Papers

Free to view
(click on article PDF icon to read the article)

PMID: 42814600 [PubMed]

Received: 03/02/2026
Accepted : 29/04/2026
In Press: 18/09/2026

Abstract

OBJECTIVES:
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.
METHODS:
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.
RESULTS:
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.
CONCLUSIONS:
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.

DOI: https://doi.org/10.55563/clinexprheumatol/u8iusx

Rheumatology Article

Rheumatology Addendum