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Peripheral gamma delta T-cell deficit in nasopharyngeal carcinoma

Previous studies identified CD56(+) and CD56(-) subsets of peripheral gamma delta T cells from healthy donors. Both subsets responded to stimulation by a myeloma cell line, XG-7 and undergo vigorous ex vivo expansion in the presence of exogenous IL-2. They are cytotoxic for different tumor targets i...

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Bibliographic Details
Published in:International journal of cancer 2002-05, Vol.99 (2), p.213-217
Main Authors: Zheng, Bo Jian, Ng, Sze Park, Chua, Daniel T T, Sham, Jonathan S T, Kwong, Dora L W, Lam, Clarence K, Ng, Mun Hon
Format: Article
Language:English
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Summary:Previous studies identified CD56(+) and CD56(-) subsets of peripheral gamma delta T cells from healthy donors. Both subsets responded to stimulation by a myeloma cell line, XG-7 and undergo vigorous ex vivo expansion in the presence of exogenous IL-2. They are cytotoxic for different tumor targets including nasopharyngeal carcinoma, but they differ from one another in that the CD56(-) subset has an additional growth requirement for IL-7 and exhibited greater cytotoxicity against nasopharyngeal carcinoma (NPC) targets. These immune cells were further shown to retard tumor growth in a nude mice NPC model. To assess if these immune cells might contribute to host defense against NPC, we compared gamma delta T-cell status of NPC patients with healthy donors and survivors who had been in clinical remission of the cancer. It was found that peripheral gamma delta T cells of patients were impaired in their response to the stimulatory effects of XG-7 and exhibited weak or essentially no cytotoxicity for the NPC targets. The deficits were present in early and advanced stages of the cancer but were restored among survivors after successful treatment of the cancer. These findings support a role for peripheral gamma delta T cells in host defense against NPC. It was noted that these immune cells comprise less than 5% of peripheral blood monocytic cells and hence it was not surprising that this component of host defense was breached early in the development of the cancer.
ISSN:0020-7136
1097-0215
DOI:10.1002/ijc.10326