Adalimumab is an antibody that binds to tumor necrosis factor alpha. Antibodies have high-affinity binding sites for their antigen, and for a small antigen such as TNF-alpha, would bind to it and prevent it from binding to its target receptors. Antibodies, like all proteins, degrade after a certain period of time and are removed from circulation, and since the body does not produce more of this antibody, it must be re-administered every few weeks.
The mechanism of this pharmacological is in a sense somewhat ironic in that in nature the chief role of antibodies is binding and neutralization of foreign and potentially dangerous antigens, however, this antibody binds and neutralizes a feature of the immune system itself. This element of the immune system is a cytokine, TNF-alpha, whose function is to promote inflammation, which draws white blood cells to the site of the inflammation and activates them. TNF-alpha also induces fever, and suppresses tumor formation and viral replication by activating programmed cell death pathways.
Aggressive immune responses always cause collateral damage to surrounding tissues, however, in autoimmune diseases such as rheumatoid arthritis the damage is compounded by the fact that the target of the immune response is an element of the body itself. A central function of the immune system is to induce tolerance to self; sometimes tolerance fails and while there are genetic components involved, the process is yet to be well-understood.