In systemic lupus erythematosus, immune complexes deposited in the kidney vasculature represent a potent inflammatory trigger with a high potential to progress to glomerulonephritis and organ failure. These immune complexes can be recognized by multiple effector cells via complement and Fcγ receptors. The transcriptome of CD16-bearing NK cells has been documented in kidneys from patients with SLE.
View Article and Find Full Text PDFSepsis is a complex condition of inflammatory and immune dysregulation, triggered by severe infection. In survivors, chronic inflammation and immune dysregulation linger, facilitating the emergence of infections. CD8 dysfunction contributes to immunosuppression in sepsis survivors.
View Article and Find Full Text PDFActivated CD8 T cells directly kill target cells. Therefore, the regulation of their function is central to avoiding immunopathology. Mechanisms that curb effector functions in CD4 and CD8 T cells are mostly shared, yet important differences occur.
View Article and Find Full Text PDFSystemic lupus erythematosus (SLE) and other autoimmune diseases are thought to develop in genetically predisposed individuals when triggered by environmental factors. This paradigm does not fully explain disease development, as it fails to consider the delay between birth and disease expression. In this review, we discuss observations described in T cells from patients with SLE that are not related to hereditary factors and have therefore been considered secondary to the disease process itself.
View Article and Find Full Text PDFSodium-glucose cotransporter 2 (SGLT2) inhibitor, dapagliflozin (Dapa), exhibited nephroprotective effects in patients with chronic kidney disease (CKD). We assessed the efficacy of short-term Dapa administration following acute kidney injury (AKI) in preventing CKD. Male Wistar rats were randomly assigned to Sham surgery, bilateral ischemia for 30 minutes (abbreviated as IR), and IR + Dapa groups.
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