Mechanisms of immune suppression in patients with head and neck cancer: Influence on the immune infiltrate of the cancer

Incomplete Th2 skewing of cytokines in plasma of patients with squamous cell carcinoma of the head and neck

“…Of note was the absence of a significant increase in plasma levels of active TGF-␤. This was a surprise because we had previously reported that HNSCC secrete TGF-␤ [16,20]. Also, others had demonstrated increased levels of TGF-␤ in patients with other malignancies, such as colorectal or prostate cancer [21][22][23].…”

Immunobiology of head and neck cancer

“…Phenotypically, TIL look like activated T cells, but these cells are functionally compromised [12]. In situ immunostaining with antibodies specific for T cell receptor (TcR)-associated signaling molecules as well as functional assays with TIL isolated from the tumor bed identified the following defects in these cells: absent or low expression of the ζ chain, which is the key signaling molecule in the TcR pathway [12,13]; decreased proliferation in response to mitogens or IL-2 [11,12]; inability to kill tumor cell targets [11]; imbalance in the cytokine profile, with the striking absence of IL-2 or IFN-γ production [14]; and evidence for DNA fragmentation in a considerable proportion of infiltrating T cells [12]. More recent studies confirm and extend these findings, as summarized in Table 2.…”

Mechanisms of Tumor Growth and Metastasis in Head and Neck Squamous Cell Carcinoma

“…Not only do HNSCC tumors evade the immune system, they actively suppress anti-tumor immune responses through production of immune suppressive soluble factors and induction of immune inhibitory cells. The production of immune suppressive soluble factors, including TGF-b [53,54], prostaglandins [55], and FasL [56], actively suppresses anti-tumor effector mechanisms. The presence of immune inhibitory cells, including CD34 + progenitor cells, inhibitory macrophages, and T-regulatory cells, within the tumor and peripheral blood of HNSCC patients contribute to continued tumor survival and metastases by actively inhibiting T-cell anti-tumor effector mechanisms [4,57].…”