Scleroderma Treatment Breakthrough? New Study Hints At Way To Slow Skin Fibrosis

New and ongoing research at Hospital for Special Surgery (HSS) in New York City has identified a possible mechanism behind the fibrosis that occurs in scleroderma – a mechanism that may one day lead to a treatment for the disease.

The findings appear in the Journal of Clinical Investigation. 

In laboratory research, adipose-derived stromal cells (ADSCs) are reduced in the layer of fat sitting under the skin, and the loss of these ADSCs may contribute to the skin fibrosis of scleroderma.

Moreover, the survival of the ADSCs that do remain beneath the skin in scleroderma are dependent on dendritic cells which release a compound called lymphotoxin B that promotes ADSC survival. When antibodies that stimulate the lymphotoxin B receptor were administered with ADSCs to replenish the lost supply, ADSC survival was increased, suggesting a means for reversing the fibrosis of the skin.

“Injecting ADSCs is being tried in scleroderma; the possibility of stimulating the lymphotoxin B pathway to increase the survival of these stem cells is very exciting,” says lead study author Theresa T. Lu, MD, PhD, an associate scientist in the Autoimmunity and Inflammation Program at HSS. “By uncovering these mechanisms and targeting them with treatments, perhaps one day we can better treat the disease."

Dr. Lu also feels this strategy could be used to target stem-cells from other tissue sources in order to treat rheumatological and other conditions -- such as lupus and rheumatoid arthritis – and also to facilitate bone and cartilage repair.

In the coming years, Dr. Lu and her colleagues hope to test the applicability of their work in human cells. “Improving ADSC therapy would be a major benefit to the field of rheumatology and to patients suffering from scleroderma,” she says.

Photo: Theresa Lu, MD, PhD

Photo Credit: Hospital for Special Surgery