{'fraction_non_alphanumeric': 0.02234258632362898, 'fraction_numerical': 0.007447528774542992, 'mean_word_length': 5.482456140350878, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[Interleukin-1 signal transduction in interaction between the nervous and immune systems].

Ligand-receptor interactions of the cytokine Interleukin-1 (IL-1) with its target cells, and further intercellular signal transduction play the key role in manifestation of its biological effects. Peculiarities of IL-1 signaling are determined by its unique structure and the composition of its receptors. The sphingomyelin pathway of IL-1beta signal transduction is one of the principle signal mechanisms providing realization of most, if not all, biological effects of cytokine. This signaling pathway is initiated by activation of the membrane enzyme neutral sphingomyelinase (nSMase), which catalyses the hydrolysis of membrane shingomyelin to the secondary cellular messenger ceramide. It has been established that IL-1beta operation in the CNS involves mechanisms mediated by IL-1 type beta1 receptor and the shingomyeline pathway of cytokine signal transduction into the cell. Type 1 IL-1 receptor is necessary for IL-1-induced activation of nSMase, the key enzyme of the sphingomyelin cascade. Change in nSMase activity in membranes of nerve and immunocompetent cells is the common link in the stress reaction of neuroendocrinal and immune system cells. nSMase activity seems to be a potential target for testing effects of various pharmaceuticals and interventions, while planning strategy of correction of immune system dysfunctions and neuro-immune interaction disturbances.