Results: Patients with SCCHN had significantly lower absolute numbers of CD3؉ CD4؉, and CD8؉ T cells than normal controls. However, no differences in the percentages of T-cell subsets between patients and normal controls were observed. Patients with active disease had significantly lower CD3؉ and CD4؉ T-cell counts than those with NED. Patients who had NED after surgery and radiotherapy had the lowest T-cell counts among the NED cohort. Patients who had NED for >2 years did not recover their T-cell counts, and the T-cell imbalance was evident many years after curative surgery. The tumor-node-metastasis (TNM) stage or site of the disease was not related to the absolute T-cell count. Patients with recurrent disease at the time of blood draw tended to have the lowest CD4؉ T-cell counts. Conclusions:Patients with SCCHN have altered lymphocyte homeostasis, which persists for months or years after curative therapies.

Natural killer (NK) cells (CD56 + /CD3-) in the circulation of cancer patients were reported to have low NK activity and undergo spontaneous apoptosis. A possible relationship between apoptosis and impaired NK activity was studied by Annexin V-binding and NK-cell assays performed with peripheral blood mononuclear cells of patients with head and neck cancer (HNC), breast cancer (BC) and normal controls (NC). Cells stained with Annexin V (Anx) and antibodies to CD56, CD3, CD95, CD25, CD122 or CD132 were examined by flow cytometry. NK activity was tested against K562 targets in 4-h 51 Cr-release assays.

A subset of circulating T cells (CD8 + CD45RO À CD27 À ) with a naïve phenotype, but mediating effector function, is considered to play an important role in host antitumour defence. To investigate the attributes of these effector T cells in patients with squamous cell carcinoma (SCC) of the head and neck cancer, venous blood was obtained from 39 individuals with cancer and 45 normal controls (NC). Peripheral blood mononuclear cells were isolated, stained with labelled monoclonal antibodies specific for CD8, CD45RO, CD45RA, CD62L, CD27, TCR-z as well as isotype controls and examined by multicolour flow cytometry. Annexin V binding to CD8 + T cells and PMA/ionomycin-induced IFN-g expression were also evaluated in patients and NC. The proportions of CD45RA + CD45RO À (naïve) and CD45RA À CD45RO + (memory) cells were found to be comparable within the CD8 + T-cell subset. However, relative to NC, the frequency of effector CD8 + CD45RO À CD27 À cells was strikingly increased in all SCC patients regardless of the disease status (P ¼ 0.0003). The proportion of these cells was found to increase with age in both patients and NC. In NC, stimulated IFN-g expression was largely restricted to CD8 + CD45RO À CD27 + cells, while in patients CD8 + CD45RO À CD27 À expressed IFN-g after ex vivo stimulation. Expression of the TCR-associated z chain was decreased or absent in freshly isolated CD8 + CD45RO À CD27 À T cells in patients (Po0.0001). Annexin V was found to bind to a higher proportion of circulating CD8 + T cells in patients than NC (Po0.006), and significantly more Annexin V + T cells were present in the effector (Po0.0059) than the naïve subset within the CD8 + CD45RO À compartment. The data indicate that the expanded CD8 + CD45RO À CD27 À T cells, which contain precursors of IFN-g-producing T cells, are z-negative and sensitive to apoptosis in the circulation of patients with HNC.

Apoptosis of circulating CD8+T cells seen in patients with squamous cell carcinoma of the head and neck (HNSCC) suggests a possibility of lymphocyte imbalance. Therefore, absolute numbers and percentages of T lymphocyte subsets were examined in the peripheral blood of patients with HNSCC and age-matched controls. Venous blood was obtained from 148 patients with HNSCC and 54 normal volunteers. Absolute numbers of CD3+, CD4+ and CD8+ T lymphocytes were determined using fluorobeads in a flow-cytometry-based technique. Percentages of T lymphocyte subsets were also evaluated by flow cytometry. The patients were grouped, at the time of blood draw (active vs. no evident disease, NED), type of therapy administered and the length of follow-up. Patients with HNSCC were found to have significantly lower absolute numbers of CD3+, CD4+and CD8+T cells than normal controls (NC). However, no differences in the percentages of T cell subsets between patients and NC were observed. Patients with active disease had significantly lower CD3+ and CD4+ T cell counts than those with NED. Patients with NED after surgery and radiotherapy had lower T cell counts than those treated by surgery alone. Patients who remained without evident disease for more than 2 years did not recover their T cell counts, and the T cell imbalance was evident many years after curative surgery. Patients with recurrent disease at the time of blood draw tended to have the lowest CD4+T cell counts. The TNM stage or site of the disease were not related to the absolute T cell count. Our data indicate that patients with HNSCC have altered lymphocyte homeostasis, which persists for months or years after curative therapies.

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