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Si us plau utilitzeu sempre aquest identificador per citar o enllaçar aquest document: https://hdl.handle.net/2445/186239
KCNE4-dependent functional consequences of Kv1.3-related leukocyte physiology.
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The voltage-dependent potassium channel Kv1.3 plays essential roles in the immune system, participating in leukocyte activation, proliferation and apoptosis. The regulatory subunit KCNE4 acts as an ancillary peptide of Kv1.3, modulates K+ currents and controls channel abundance at the cell surface. KCNE4-dependent regulation of the oligomeric complex fne-tunes the physiological role of Kv1.3. Thus, KCNE4 is crucial for Ca2+-dependent Kv1.3-related leukocyte functions. To better understand the role of KCNE4 in the regulation of the immune system, we manipulated its expression in various leukocyte cell lines. Jurkat T lymphocytes exhibit low KCNE4 levels, whereas CY15 dendritic cells, a model of professional antigen-presenting cells, robustly express KCNE4. When the cellular KCNE4 abundance was increased in T cells, the interaction between KCNE4 and Kv1.3 afected important T cell physiological features, such as channel rearrangement in the immunological synapse, cell growth, apoptosis and activation, as indicated by decreased IL-2 production. Conversely, ablation of KCNE4 in dendritic cells augmented proliferation. Furthermore, the LPS-dependent activation of CY15 cells, which induced Kv1.3 but not KCNE4, increased the Kv1.3-KCNE4 ratio and increased the expression of free Kv1.3 without KCNE4 interaction. Our results demonstrate that KCNE4 is a pivotal regulator of the Kv1.3 channelosome, which fne-tunes immune system physiology by modulating Kv1.3-associated leukocyte functions.
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VALLEJO-GRACIA, Albert, SASTRE MARTINEZ, Daniel, COLOMER-MOLERA, Magalí, SOLÉ, Laura, NAVARRO-PÉREZ, María, CAPERA ARAGONÉS, Jesusa, ROIG, Sara r., PEDRÓS-GÁMEZ, Oriol, ESTADELLA, Irene, SZILÁGYI, Orsolya, PANYI, Gyorgy, HAJDÚ, Péter, FELIPE CAMPO, Antonio. KCNE4-dependent functional consequences of Kv1.3-related leukocyte physiology.. _Scientific Reports_. 2021. Vol. 11, núm. 14632. [consulta: 21 de gener de 2026]. ISSN: 2045-2322. [Disponible a: https://hdl.handle.net/2445/186239]