Origins of T-cell-mediated autoimmunity in acquired aplastic anaemia.

Acquired aplastic anaemia (AA) is an autoimmune bone marrow failure disease resulting from a cytotoxic T-cell-mediated attack on haematopoietic stem and progenitor cells (HSPCs). Despite significant progress in understanding the T-cell repertoire alterations in AA, identifying specific pathogenic T cells in AA patients has remained elusive, primarily due to the unknown antigenic targets of the autoimmune attack. In this review, we will synthesize findings from several decades of research to critically evaluate the current knowledge on T-cell repertoires in AA.

A novel combinatorial approach integrating experimental and computational analysis of antioxidant activity: Evaluating catechin and L-ascorbic acid in serum.

Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality globally, with oxidative stress playing a pivotal role in its progression. Free radicals produced via oxidative stress contribute to lipid peroxidation, leading to subsequent inflammatory responses, which then result in atherosclerosis. Antioxidants inhibit these harmful effects through their reducing ability, thereby preventing oxidative damage.

TET2 regulates early and late transitions in exhausted CD8 T cell differentiation and limits CAR T cell function.

CD8 T cell exhaustion hampers control of cancer and chronic infections and limits chimeric antigen receptor (CAR) T cell efficacy. Targeting in CAR T cells provides therapeutic benefit; however, TET2's role in exhausted T cell (T) development is unclear. In chronic lymphocytic choriomeningitis virus (LCMV) infection, TET2 drove conversion from stem cell-like T progenitors toward terminally differentiated and effector (T)-like T.