Quantitative and qualitative deficits of peripheral gd T cells in patients with active nasopharyngeal carcinoma

BJ Zheng1 MD, PhD, SP Ng1 PhD, D Chua2 MD, JST Sham2 MD, D Kwong2 MD, CK Lam3 MD, MH Ng1 PhD

1Department of Microbiology, 2Department of Radiation Oncology, The University of Hong Kong, 3Hematology Section, Department of Pathology, Queen Mary Hospital, Hong Kong SAR, Peoples Republic of China

Abstract Aims: To assess the contribution of peripheral gd T cells might to host defense against nasopharyngeal carcinoma (NPC). Methods: gd T cell status of patients with active NPC was compared with those of healthy donors and survivors who had been in clinical remission of the cancer by their activation in response to the tumor (XG-7) stimulation and cytotoxicity to NPC. Results: The quantitative deficit of peripheral gd T cells of patients was characterized by that their peripheral blood monocytic cells (PBMC) contained less responder for stimulation of XG-7, which is a well-know stimulator of gd T cells. The qualitative deficit was demonstrated by that the expanded and purified gd T cells of patients exhibited quite weak cytotoxicity for the NPC targets. It was additionally found that gd T cells from patients contained much less of the CD56- subset, which had been shown to exhibit greater cytotoxicity against NPC targets than CD56+ subset (Scand J Immunol 2001; 53:40-48) and to be capable of retarding tumor growth in a nude mice NPC model (Int J Cancer 2001; 93:421-425). The deficits were present in both early and advanced stages of the cancer, but were restored among survivors after successful treatment of the cancer. Conclusions: These findings support a role for peripheral gd T cells in host defense against NPC. It was noted that these immune cells comprise less than 5% of PBMC, and hence it was not surprising that this component of host defense was breached early in the development of the cancer.

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Paper presented at the International Symposium on Predictive Oncology and Intervention Strategies; Paris, France; February 9 - 12, 2002; in the section on Immunotherapy.