Invariant Natural Killer T cells resilience to paradoxical sleep deprivation-associated stress
| Autor: | Alexandre S. Basso, Beatriz M. Freire, Edgar Ruz Fernandes, Michelangelo Bauwelz Gonzatti, Alexandre C. Keller, Maria Eduarda Perrud Sousa, Monica L. Andersen, Daniela Santoro Rosa, Marcia G. Guereschi |
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| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
medicine.medical_treatment Immunology Sleep REM Stimulation Spleen Mice 03 medical and health sciences Behavioral Neuroscience 0302 clinical medicine Immune system Antigen medicine Animals biology Endocrine and Autonomic Systems Immunotherapy Killer Cells Natural Mice Inbred C57BL 030104 developmental biology Cytokine medicine.anatomical_structure CD1D biology.protein Cytokines Natural Killer T-Cells 030217 neurology & neurosurgery Glucocorticoid medicine.drug |
| Zdroj: | Brain, Behavior, and Immunity. 90:208-215 |
| ISSN: | 0889-1591 |
| Popis: | Although several studies demonstrate that stressful situations, such as sleep disturbances, negatively impact the innate and adaptive arms of the immune system, their influence on invariant Natural Killer T (iNKT) cells remains unclear. iNKT cells are CD1d-restricted innate T cells that recognize glycolipid antigens and rapidly produce polarizing cytokines being key players in several immune responses, and a potential target for immunotherapy. iNKT cells differ in several aspects from conventional T lymphocytes, including a unique dependence on CD1d-expressing double-positive (DP) thymocytes for intrathymic maturation. As a consequence of stress, DP thymocytes undergo glucocorticoid-induced apoptosis, which might compromise iNKT developmental pathway. Therefore, we used a paradoxical sleep deprivation (SD) model to determine the impact of sleep disturbance on iNKT cell biology. After 72 h of SD, C57Bl/6 mice exhibited a significant increase in systemic glucocorticoid levels and thymus atrophy. Despite marked decrease in the number of DP thymocytes, the ratio CD1d+/CD1d− was higher in SD mice, and the number of thymic iNKT cells remained unaltered, suggesting that SD did not compromise the iNKT developmental pathway. In contrast, SD reduced hepatic IFN-γ, but not, IL-4-producing iNKT cells, without further effect in the spleen. Despite this fact, SD did not affect stimulation of IFN-γ production by iNKT cells, or cytokine release, in response to α-galactosylceramide, a specific antigen. Furthermore, although SD impaired splenic NK cells activity against tumor cells, it did not affect iNKT cell-specific cytotoxicity. Thus, our study shows that SD-induced stress did not impair the iNKT cells’ responses to a cognate antigen. |
| Databáze: | OpenAIRE |
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