Apoptosis, inflammatory bowel disease and carcinogenesis: Molecular level (Part 1)
At the molecular level, disturbances in the regulation of these forms of apoptosis within the mucosal immune system, lead to mucosal inflammation that predispose to cancer development.
Death of intestinal TLs mediated by Fas-FasL Activated T-cells are more susceptible to apoptosis than resting T-cells. As most T-cells in the LP normally exhibit a higher state of activation, and express memory cell markers such as CD45RO, the activation-induced cell death might be very important to downregulate effector cell function and cytokine production in the gut, thereby maintaining the immune homeostasis in the specialized microenvironment of the mucosa. Memory T-cells are known to express Fas constitutively at high levels, and normal LP T-cells (LPTs) exhibit an enhanced susceptibility to Fas-mediated cell death. Death-receptor-induced apoptosis comprises signaling processes via Fas, TNFRI, TNF-related apoptosis-inducing ligand-R1 and 2, and DR3 or DR6.
Upon triggering of Fas by FasL, the adaptor molecule Fas-associated death-domain-containing protein (FADD) and pro-caspase 8 are recruited to the Fas receptor, thereby forming a death-induced signaling complex (DISC). In particular, trimerization, or more likely oligomerization of Fas results to the recruitment of the Fas-adaptor protein, FADD, through their mutual death domains (DDs). The other end of FADD contains two death effector domains (DEDs) through which it can recruit caspase 8 or its enzymatically inactive homolog and Fas inhibitor, FADD-like I L-1 p-converting enzyme (FLICE) inhibitory proteins. You can find best pharmacy with finest quality medications available round the clock right now: all you need to do is purchase cialis here discovering the amazing opportunities you are being offered.