The immunological synapse is a transient junction that occurs when the plasma membrane of a T cell comes in close contact with an APC after recognizing a peptide from the antigen‐MHC. The interaction starts when CRAC channels embedded in the T cell membrane open, flowing calcium ions into the cell. To counterbalance the ion influx and subsequent depolarization, K_v1.3 and KCa3.1 channels are recruited to the immunological synapse, increasing the extracellular K⁺ concentration. These processes are crucial as they initiate gene expression that drives T cell activation and proliferation. The T cell‐specific function of the K_2P channel family member TASK2 channels and their role in autoimmune processes remains unclear. Using mass spectrometry analysis together with epifluorescence and super‐resolution single‐molecule localization microscopy, we identified TASK2 channels as novel players recruited to the immunological synapse upon stimulation. TASK2 localizes at the immunological synapse, upon stimulation with CD3 antibodies, likely interacting with these molecules. Our findings suggest that, together with K_v1.3 and KCa3.1 channels, TASK2 channels contribute to the proper functioning of the immunological synapse, and represent an interesting treatment target for T cell‐mediated autoimmune disorders.

中文翻译：

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TASK2通道在人类免疫突触中的作用

免疫突触是一个短暂的连接，当T细胞的质膜从抗原MHC识别出肽后与APC紧密接触时发生。当嵌在T细胞膜中的CRAC通道打开并使钙离子流入细胞时，相互作用开始。为了平衡离子流入和随后的去极化，将K _v 1.3和KCa3.1通道募集到免疫突触，以增加细胞外K ⁺浓度。这些过程至关重要，因为它们启动了驱动T细胞活化和增殖的基因表达。K _2P的T细胞特异性功能通道家族成员TASK2通道及其在自身免疫过程中的作用尚不清楚。使用质谱分析，落射荧光和超分辨率单分子定位显微镜，我们将TASK2通道鉴定为刺激后被募集到免疫突触的新型参与者。在用CD3抗体刺激后，TASK2定位于免疫突触，可能与这些分子相互作用。我们的发现表明，TASK2通道与K _v 1.3和KCa3.1通道一起有助于免疫突触的正常运行，并代表T细胞介导的自身免疫性疾病的有趣治疗靶标。