Assessing the effects of TNF-α on dendritic cells

Autoimmune diseases are described as an immunological response against self-tissue. Major symptoms of autoimmune diseases include chronic or prolonged inflammation. One of the major mediators of inflammation is tumor necrosis factor-alpha (TNF-α). TNF-α has also been implicated in autoimmune diseases. TNF-α has been called a contradictory cytokine in that it can induce either cell death or survival after TNF-α binds to its receptor TNF-receptor one (TNFR1). We propose that TNF-α prolongs survival of resident dendritic cells (DC). Here we demonstrate that TNF-α has an anti-apoptotic effect on DC. TNF-α reduces the activation of caspase 8, 9, and 3, which are critical components of the death pathway. TNF-α also reduces activation of pro-apoptotic proteins such as Poly (ADP-ribose) polymerase (PARP). Moreover, we also demonstrate that TNF-α does not affect the activation status of DC. These findings provide support for the role of TNF-α and a link between inflammation and autoimmunity