γδ T cells lyse autologous and allogenic oesophageal tumours: involvement of heat-shock proteins in the tumour cell lysis

T cells expressing γδ receptors were isolated from the peripheral blood of oesophageal cancer patients and analysed for their potential to lyse tumour targets. Immunophenotyping by flow cytometry showed that the dominant population of γδ T cells expressed the Vγ9 and the Vδ2 T cell receptor, and a m...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Cancer Immunology, Immunotherapy Immunotherapy, 2000, Vol.48 (11), p.653-659
Hauptverfasser: THOMAS, M. L, SAMANT, U. C, RAMAKANT KRISHNAJI DESHPANDE, SHUBHADA VIVEK CHIPLUNKAR
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:T cells expressing γδ receptors were isolated from the peripheral blood of oesophageal cancer patients and analysed for their potential to lyse tumour targets. Immunophenotyping by flow cytometry showed that the dominant population of γδ T cells expressed the Vγ9 and the Vδ2 T cell receptor, and a minor population expressed the Vδ1 receptor. Cytotoxicity assays revealed that activated γδ T cells lysed Daudi Burkitt's lymphoma and K562 cells. Lysis of autologous oesophageal tumours was higher than of allogenic tumours. Anti-hsp60 and anti-hsp70 mAb significantly inhibited the cytotoxicity of γδ T cells to both autologous and allogenic oesophageal tumours. Surface expression of hsp60 and hsp70 on oesophageal tumours and Daudi cells was demonstrated by flow cytometry. In conclusion, γδ T cells isolated from the peripheral blood of oesophageal cancer patients have the ability of kill oesophageal tumour cells. The lysis of tumour targets by the γδ T cells is brought about via recognition of heat-shock proteins expressed on the surface of tumour cells. γδ T cells isolated from the peripheral blood may have applications in adoptive immunotherapy of oesophageal cancer.
ISSN:0340-7004
1432-0851
DOI:10.1007/s002620050014