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Kv1.3 and KCa3.1 channels are similar regarding the conductance properties (both channels are highly K + selective and have similar single-channel conductance in the order of 10–14 pS), however they are remarkably different in their gating and blocker sensitivity.
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Lymphocytes express predominantly two K + channels, the voltage-gated Kv1.3 (encoded by the KCNA3 gene) and the calcium-activated KCa3.1 K + channels (also known as IKCa1 encoded by the KCNN4 gene). In this review, we discuss the network of ion channels in immune cells, their role in regulating the adaptive and innate response, and the potential therapeutic value of specific channel blockers as immune modulators. IL-10) and other soluble immunosuppressive cytokines derived from immune and tumour cells, and the recruitment of immunosuppressive cells such as regulatory T cells (T reg) and myeloid-derived suppressor cells (MDSC) contribute to the failure of the immune system in controlling tumour growth. In addition to the reduction in immunogenicity of tumour cells and expression of anti-apoptotic molecules, a key contributor to escape is the development of a complex immunosuppressive network in the TM.
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Probably the most complex interaction between tumour cells and the immune system occurs during the escape phase, whereby the immune response fails to completely eliminate the tumour cancer cells that can resist, avoid or suppress the anti-tumour immune response are selected, leading to tumour-escape and a progressively growing tumour. Thus, even in the presence of continuous eradication, tumour cells resistant to killing by the immune system are generated.
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During the equilibrium phase, adaptive immune responses impose immune-selection pressure on tumour cells resulting in clones with reduced immunogenicity. The elimination phase is characterized by a concerted interplay between innate and adaptive immunity through which developing tumours are eradicated on the basis of their expression of specific antigens. Paul Ehrlich's recognition in 1909 of the importance of the host immune response to tumours led to the ‘cancer immunosurvellience’ hypothesis and its refinement, the ‘cancer immunoediting theory’, whereby cancer cells and immune cells engage in a dynamic process of elimination, equilibrium and escape (reviewed in ). The TM strongly contributes to tumour progression and influences different aspects of tumour cell behaviour via a variety of interactions including cell-to-cell or cell-to-matrix signals. TM is formed by mesenchymal, endothelial and immune cells enmeshed in a network of extracellular matrix (ECM) proteins and soluble factors. Accumulated data indicate that cancer cells cannot be studied in isolation, but should be investigated together with the surrounding ‘tumour microenvironment’ (TM). Answering these questions might lead to a better understanding of the immunosuppression phenomenon in cancer tissue and the development of drugs aimed at skewing the distribution of immune cell types towards killing of the tumour cells.Ĭancer is a complex disease in which the uncontrolled proliferation of malignantly transformed cells constitutes the major pathological picture. Understanding the immune cell subset-specific expression of ion channels along with their particular function in a given cell type, and the role of cancer tissue-dependent factors in the regulation of operation of these ion channels are emerging questions to be addressed in the fight against cancer disease. Key steps in this process, for example the generation of a proper Ca 2+ signal induced by recognition of a specific antigen, are regulated by various ion channel including voltage-gated Kv1.3 and Ca 2+-activated KCa3.1 K + channels, and the interplay between Orai and STIM to produce the Ca 2+-release-activated Ca 2+ (CRAC) current required for T-cell proliferation and function. The outcome of a malignant disease depends on the efficacy of the immune system to destroy cancer cells.