Sujet(s) Antinéoplasiques immunologiques/effets indésirables In a broader perspective, the iatrogenic side effects of immunotherapy provide a unique opportunity to explore the genetic, humoral and cytotoxic immune confounders. What makes the endocrine system a prominent target when facing an unleashed immune system? Why are the endocrine irAEs mostly irreversible and unresponsive to glucocorticoid therapy? Is it possible to identify those prone to develop irAEs? The presents review describes the unique characteristics of the endocrine system and its crosstalk with the immune system. Disruption of the innate immune inhibition has introduced a large and growing spectrum of immune-related adverse effects (irAEs), with the endocrine system being a prominent target to autoimmune damage. Immunotherapy has transformed the treatment of cancer by restoring the power of the immune system against tumor cells. , Facteur de nécrose tumorale alpha/métabolisme , Effets secondaires indésirables des médicaments/thérapie LncRNA XLOC_032768 is a potential novel agent to reduce cisplatin-induced nephrotoxicity. As such, XLOC_032768 suppressed cisplatin-induced apoptosis and inflammatory response of renal tubular epithelial cells through TNF-α. TNF-α inhibition also ameliorated cisplatin-induced apoptosis of renal tubular epithelial cells and renal structural damage. RNA sequencing analysis further confirmed that XLOC_032768 could regulate tumor necrosis factor (TNF)-α in the cisplatin-induced apoptosis of HK-2 cells in trans-manner. The overexpression of XLOC_032768 significantly inhibited the cisplatin-induced apoptosis and inflammatory response in HK-2 cells and mouse exposed to cisplatin. This result was validated by an RT-qPCR experiment on in vivo and in vitro models. The differentially expressed genes (DEGs) of the transcriptome data were determined, and the results showed that lncRNA XLOC_032768 expression was significantly repressed by cisplatin treatment. Cisplatin treatment resulted in the apoptosis of the renal tubular epithelial cells and inflammatory response in a mouse model and human renal proximal tubular epithelial cells (HK-2). We explored the functions and underlying mechanisms of a novel lncRNA XLOC_032768 in cisplatin-induced nephrotoxicity. However, the role of long non-coding RNAs (lncRNAs) in cisplatin-induced nephrotoxicity is not well known. The cellular and molecular mechanisms through which cisplatin induces nephrotoxicity have been investigated extensively.
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