Like getting a tan? Your immune system doesn’t. September 26, 2006Posted by Hegemony in Health, Science.
Several studies recently have examined the mechanisms by which UV radiation causes immunosuppression. The immune system in the skin relies on a specific class of dendritic cells known as Langerhans cells. When an antigen (i.e. a bacterium) is present in the skin these cells phagocytose and process the antigen. It is then presented on cell surface receptors. The Langerhans cell will make its way back to a Lymph node where it can activate T-cells. These T-cells then direct the immune response against the antigen via the release of cytokines.
Much in the way of specifics in this situation are as yet unknown. However, it is relatively certain that the process starts with the absorbtion of UV radiation by “chromophores” near the surface of the skin. In this case DNA as it in a known chromophore for UV radiation. This causes damage to the nucleic acid. When this damage occurs in immune cells there is a marked decrease in immune system function in that area.
The usual way to test for immune function in the skin is to use Contact Hypersensitivity. A simple antigen known as a “contact sensitizer” is introduced under the skin. After an immune response has had time to occur the contact sensitizer is presented again. In a normal immune response there will be an inflammatory response. In instances where there had been reasonable UV exposure the inflammatory response is not as strong. This indicates a weakness in the immune system.
The mechanism by which this nucleic acid damage causes immunosuppression is still questionable. The current theory is that these damaged dendritic cells produce cytokines that favor the activation of Th2 type T-cells. These are not as well suited for dealing with Hypersensitivity responses and cancer. Research also shows that these damaged dendritic cells have a tendency to stimulate suppressor T-cells. These cells release IL-10 which suppresses cellular immunity.
The consequences for this are great. All signs point to the fact that this mechanism can increase one’s risk of developing skin cancer. In a study from 1990 nearly all of those participants who demonstrated no suppressed contact hypersensitivity could be made to do so with exposure to UV radiation. In those with histories of melanoma the effect was universal. Clearly there is a connection.
Additionally it was found that contact hypersensitivity could be suppressed in people that were both “darker-skinned” and “lighter-skinned” if the UV dose was such that it could cause burning of the skin. If the dose was lowered to levels that would not cause a burn, the lighter skinned individuals had much more susceptibility to immune suppression.
The potential also exists for this process to affect infectious disease and vaccination. These findings are based largely on rodent models. Many infections have been shown to be more severe in UV exposed animals. Observation of human disease has yielded some interesting results though. The Netherlands has reported a seasonal change in the number of cervical smears positive for human papiloma virus. There is a positive correlation between the number of positive tests and the amount of UV radiation.
This is a very interesting process but requires further study. For instance, what is the role of vitamin D in immunity? Some studies indicate that vitamin D interferes with dendritic cell maturation. The future may well bring surprising discoveries in this area.