The lymphokines produced by TH1 and TH2 subsets of CD4+ T helper (TH) cells are critical to the effectiveness of the immune response. In vivo and in vitro studies have demonstrated that environmental cytokines determine the development of naive T cells into TH1 or TH2 effector cells. Unregulated expansion of one subset or the other may contribute to the development of certain diseases.
To establish if this was the case in colon cancer, we examined cytokine serum levels and cytokine production by peripheral blood mononuclear cells (PBMCs), tumour-draining lymph node lymphocytes (LNLs) and tumour cells (TCs). Levels of soluble (s) carcinoembryonic antigen (CEA), sCD30, sIL2 receptor (R) and sIL6R; the PBMC expression of T, B, NK, APC cells and activation phenotypic antigens: CD3, CD4, CD8, CD19, CD16, CD56, CD57, DR, and CD25; and the proliferative responses of PBMC to IL2, IL4 and anti-CD3 monoclonal antibody (mCD3) were also studied.
Our data leads us to believe that the suppressive effect of cytokines in the peripheral blood of cancer patients causes disregulation in the functionality of TH1 and TH2 subsets of CD4+ T cells, with an expansion of TH2 cells and a malfunctioning of TH1 cells. This immunological disregulation appears to increase with stage progression suggesting a direct role in the mechanisms that allow the tumour to expand within the host. In order to generate an immune response in vivo that corrects the imbalance between TH1 and TH2 cells, we need to understand how tumour mechanisms cause this imbalance in the first place.
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