Researchers at the Hospital for Special Surgery in New York City have identified a therapeutic intervention that could potentially slow or reverse skin fibrosis associated with scleroderma.
The study, published in the Journal of Clinical Investigation, is generating hope that a duplication of the results could yield a treatment for scleroderma where currently there lacks efficacious treatment. The lead researcher and author of the study is Theresa T. Lu, MD.
Scleroderma comprises a group of autoimmune skin-hardening diseases that can extend to the fibrosis of blood vessels and internal organs – such as the lungs or kidneys – and can result in death. The disorder is also associated with numerous comorbidities, including severe joint problems, pain and loss of hand function.
In the present study, Lu and colleagues describe the mechanisms of skin fibrosis; specifically, that normal layers of fat beneath the skin undergo a loss of dermal white adipose tissue (DWAT). In addition, they note that when skin fibrosis is present, there is also a reduction of adipose-derived stromal cells (ADSCs), cells that would normally exhibit regenerative and repair functions, concluding that the loss of ADSCs contributes to the skin fibrosis. The team then focussed on the remaining ADSCs to learn more about how these cells survive.
What they discovered is that remaining ADSCs are dependent on immune cells called dendritic cells, which release a compound called lymphotoxin B. This led to the researchers’ hypothesis for a therapeutic intervention that might promote ADSC survival.
After injecting antibodies that stimulate the lymphotoxin B receptor, ADSC survival increased, suggesting a method to slow or possibly reverse skin fibrosis.
Dr. Lu concludes by stating similar strategies could prove useful for treating rheumatological and other diseases, such as rheumatoid arthritis and lupus.
Written by: MaryAnne Pankhurst
Dendritic cells maintain dermal adipose–derived stromal cells in skin fibrosis
Published in Volume 126, Issue 11 (November 1, 2016)
J Clin Invest. 2016;126(11):4331–4345. doi:10.1172/JCI85740.