Immune complex deposition promotes NK cell accumulation in the kidney.

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.

Women's preferences for caesarean or vaginal birth with a perspective of future fertility: A discrete choice experiment.

Objective: To investigate pregnant women's preferences for risks of vaginal and caesarean birth, including possible impacts on future fertility.

Methods: In this discrete choice experiment, low-risk nulliparous pregnant women recruited after 28 weeks of gestation evaluated eight choice sets, each between two different hypothetical births scenarios which intermixed the risks of planned caesarean or vaginal birth. Scenarios consisted of six attributes: pain, maternal health, neonatal health, risk of unplanned intervention, impact on fertility and risk of complications in the next pregnancy.

Sepsis Impairs IFN-γ Production in CD8 T Cells through Changes in Local Chromatin Landscape.

Sepsis 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.

CD8 is down(regulated) for tolerance.

Activated 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.

Relevance of acquired T cell molecular defects in the immunopathogenesis of SLE.

Systemic 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.