The exact cause of psoriasis is still unknown. Two processes—rapid skin growth and inflammation—com-bine to cause the skin changes that lead to psoriasis. The initiating trigger for these processes—what makes the process begin in a particular person—remains obscure, and active research is ongoing to identify these events. Under the microscope, skin affected by psoriasis is thicker than normal skin, with dramatic thickening of the epidermis (hyperkeratinization) and inflammation caused by a type of white blood cell called T cells. These T cells react against parts of the skin where the disease is active.
The T cells and other immune system cells make cytokines, immune-system chemicals with names like TNFα (tumor necrosis factor alpha) and IL 23 (interleukin 23), that aid in their communication and activation. Chronic inflammation in these areas causes skin cells to divide and turn over much more rapidly, up to four to five times as quickly as in normal skin. The rapid buildup of these skin cells, called keratinocytes, can lead to thick white scales on top of psoriatic skin.
Over time, new, small blood vessels develop in the deeper layers of the skin. These blood vessels support the actively developing psoriatic plaques and may cause a persistent reddening of affected skin even after treatment. It is not yet clear why the T cells become activated in the skin in psoriasis and other immune diseases, but once the process starts, it seems to persist for life. How to inactivate or “turn off ” these particular T cells permanently without impairing the immune sys-tem as a whole or causing serious side effects is a significant treatment challenge and is the focus of active immunology research. Studies of people and their relatives with psoriasis show that there is a genetic or familial predisposition to the disease, but not all people with certain genes or affected siblings will get the disease.
So far, most of the possible genes associated with psoriasis are part of the immune system. Different genes and groups of genes are more common in people with psoriasis, but most people with these genes do not develop psoriasis, and many people with psoriasis do not have these genes. Some researchers have found that you need to have a group of relatively common genes to be susceptible. One gene that seems consistently important, however, is called HLA-C. For these reasons, genetic testing is only used for research at this point and cannot offer useful information about psoriasis diagnosis, treatment, or prognosis. Active research into the cause of psoriasis has shown that certain immune system genes are associated with this and other immune processes. The next step, using this information to develop new therapies, is underway.