Quantification of cellular poly(ADP-ribosyl)ation by stable isotope dilution mass spectrometry reveals tissue- and drug-dependent stress response dynamics.

Poly(ADP-ribosyl)ation is an essential post-translational modification with the biopolymer poly(ADP-ribose) (PAR). The reaction is catalyzed by poly(ADP-ribose) polymerases (PARPs) and plays key roles in cellular physiology and stress response. PARP inhibitors are currently being tested in clinical cancer treatment, in combination therapy, or as monotherapeutic agents by inducing synthetic lethality.

Manganese superoxide dismutase: a regulator of T cell activation-induced oxidative signaling and cell death.

Mitochondrial reactive oxygen species (ROS) are indispensible for T cell activation-induced expression of interleukin 2 (IL-2) and CD95 ligand (CD95L, FasL/Apo-1L) genes, and in turn, for CD95L-mediated activation-induced cell death (AICD). Here, we show that manganese superoxide dismutase (MnSOD/SOD2), a major mitochondrial antioxidative enzyme, constitutes an important control switch in the process of activation-induced oxidative signal generation in T cells. Analysis of the kinetics of T cell receptor (TCR)-triggered ROS production revealed a temporal association between higher MnSOD abundance/activity and a shut-down phase of oxidative signal generation.

Persistence of memory type lymphocytes in an experimental model of chronic pancreatitis in rats.

There is growing evidence that immunocompetent cells are involved in the pathogenesis of chronic pancreatitis. Using a model of chronic pancreatitis induced by dibutyltin dichloride (DBTC) in rats, we have immunohistochemically phenotyped the infiltrating T lymphocytes, CD45RC+ cells, macrophages, as well as the IL-2 receptor as an activation marker during a time course of two months. In addition, the expression of CD44, of the integrin component CD18, and of MHC class II was determined.