Editorial: To channel or not to channel? Functioning of nicotinic acetylcholine receptors in leukocytes Maryna V. Skok 1 Department of Molecular Immunology, Palladin Institute of Biochemistry, Kyiv, Ukraine 1. Correspondence: Department of Molecular Immunology, Palladin Institute of Biochemistry, 9, Leontovicha str., 01601 Kyiv, Ukraine. E-mail: skok@biochem.kiev.ua trafficking/migration innate immunity adaptive immunity Cholinergic signaling plays an important role in inflammation and immune response. Leukocytes produce endogenous acetylcholine, which affects their activation through nAChRs in an auto/paracrine way. However, the mode of nAChR signaling in the leukocytes is different from classical ion channel functioning in excitable (nerve and muscle) cells. Although the nAChRs expressed in hematopoietic cells seem to be permeable for ions, the ion contribution to the nAChR signaling in these cells is minimal. Instead, binding of agonists or competitive antagonists affects the activity of adjacent (purinergic or antigen-specific) receptors and influences the intracellular Ca 2+ fluxes evoked by their stimulation. These data indicate that not all signaling events triggered by nAChRs require the ion channel opening and that ligation of the acetylcholine-binding site induces allosteric transition sufficient for certain types of receptor signaling. The multiple ways of nAChR functioning in the cells of different origin regarding the universal
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