Scientists Exploring How the Interplay between UVB Rays and "Programmed Cell Death" May Promote Lupus Disease Activity
Arthritis Research & Therapy, Volume 8, Issue 6, October 2, 2006, R156
Is disturbed clearance of apoptotic keratinocytes responsible for UVB-induced inflammatory skin lesions in systemic lupus erythematosus?
When cells die in an orderly manner in a healthy body, they undergo a series of changes and then a clean-up procedure, which are collectively called apoptosis. This complex process, which helps the body eliminate and replace older or damaged cells, involves changes in the structure of the cell and the release of chemicals that act as signals. In response to these signals, proteins rise to the surface of the cell, attracting antibodies and white blood cells called macrophages, which surround the apoptotic cells, ingest them, and then transport them away for disposal. Apoptotic cells may also break into pieces, and the macrophages swallow these cell fragments (apopototic bodies) as well. Macrophages are inflammatory white blood cells, but under normal circumstances, clearance of apoptotic cells does not promote excessive inflammation.
UVB light rays are known to induce apoptosis. UVB light rays also can trigger reactions in people with lupus. And apoptosis has been linked to certain autoimmune processes, including lupus. The intriguing interplay of these processes led a group of researchers in The Netherlands to study whether apoptosis after exposure to UVB rays was somehow different in lupus patients and if it could be a factor in promoting inflammation.
For their study, the researchers exposed 15 lupus patients and 13 healthy control subjects to two small doses of UVB light rays. They then conducted skin biopsies over the next ten days, comparing the number of apoptotic cells, macrophages, and immune-related proteins in the samples of the two study groups.
There was no difference between lupus patients and healthy people found in this study in the rate at which apoptotic cells were cleared up after exposure to UVB. However, the lupus patients had a greater influx of macrophages into the areas of skin that were exposed to the light, and the researchers determined that these macrophages were ingesting lots of apoptotic bodies.
The authors concluded that the elimination of inflammatory-stimulating debris from dead cells may be relatively normal in the skin of lupus patients that has been exposed to UVB light; but they speculate that the higher number of white blood cells that are present may trigger enough inflammation to set off the sun-exposure-related rash that may occur with lupus.
This research adds an interesting perspective to other ongoing research that is pointing to ways apoptosis may be involved in the development of lupus and a number of its symptoms.