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Updated: Jul 5, 2026
Assessment of Human Natural Killer Cell Events Driven by FcγRIIIa Engagement in the Presence of Therapeutic Antibodies
Published on: May 22, 2020
Evaluation of activatory and inhibitory natural killer cell receptors in non-segmental vitiligo: a flow cytometric
P Y Basak1, A K Adiloglu, I G Koc
1Department of Dermatology, Faculty of Medicine, Suleyman Demirel University, Isparta, Turkey. pinarbasak@hotmail.com
Background:
Recent observations established the role of altered cellular immunity and autoimmune hypothesis in the pathogenesis of vitiligo. There have been several reports discussing T-cell and natural killer (NK) cell populations, but NK cell receptors were not evaluated in vitiligo.
Objective:
The purpose of this investigation was to assess the role of T and NK cells as well as activatory and inhibitory NK cell receptor alterations in the pathogenesis of vitiligo and whether any aberrations were correlated with clinical findings of the disease.
Patients/Methods:
Fifty-three patients with non-segmental vitiligo and 45 age- and sex-matched healthy controls were enrolled in the study. The percentages of lymphocytes, granulocytes, monocytes and CD3, CD4, CD8, CD14, CD16, CD56, CD45, CD45RA, CD54RO, CD28, CD80, CD94, CD158a, KIR3DL-1 receptors as well as CD94, CD158a, KIR3DL-1 receptors on CD16(+) cells were detected by using flow cytometry. The patient and control groups were compared in terms of the results of flow cytometric analysis, and the results were assessed regarding the type and activity of vitiligo.
Results:
The percentages of CD16(+)CD56(+), CD3(+)CD16(+)CD56(+), CD8(+) and CD45RO(+) cells were significantly increased in vitiligo group compared with the controls. No difference was detected between the patients and control groups in percentages of CD3(+), CD4(+), CD3(-)CD16(+)CD56(+), CD28(+), CD45(+), CD45RA(+), CD94(+), CD158a(+) and KIR3DL-1(+) cells. The percentage of CD16(+)CD158a(+) cells was significantly decreased in a randomized selected group of vitiligo patients. There were no differences in percentage expression of studied cell surface antigens between patients in the active or stable period. CD3(+) cells were significantly increased in generalized form, and CD45RO(+) cells were significantly increased in acral/acrofacial form when compared with the other types of vitiligo.
Conclusions:
These results indicate further evidence for T and NK cell abnormalities in non-segmental vitiligo. The present data show that NK cell activation may be responsible in the pathogenesis of vitiligo in conformity with decreased inhibitory and increased activatory NK cell receptors.
