A recent study published in Proceedings of the National Academy of Sciences reveals that targeting the interaction between two proteins, CD2 and CD58, may provide new therapeutic avenues for individuals suffering from hidradenitis suppurativa (HS), a chronic and painful skin condition.
HS, which affects around 1-2% of the U.S. population, is characterized by recurrent, inflamed bumps or boils, typically appearing in skin-fold areas such as the armpits, groin, and buttocks. The condition significantly impacts both the physical and social well-being of those affected, and current treatments only offer partial symptom relief without halting the disease’s progression.
In a breakthrough study, researchers from the University of Alabama at Birmingham (UAB), led by Professors Chander Raman, Ph.D., and Mohammad Athar, Ph.D., uncovered a potential new approach for treating HS by disrupting the interaction between the proteins CD2 and CD58. The findings suggest that this disruption could suppress the gene expressions responsible for HS symptoms, paving the way for novel treatment options.
The study demonstrated that CD2, a lymphocyte cell surface protein, is expressed at elevated levels on T lymphocytes and innate lymphocytes, including natural killer (NK) cells and natural killer T (NKT) cells, in HS lesions. These cells play a central role in the inflammatory response seen in HS. The researchers found that blocking the interaction between CD2 and CD58 significantly reduced the expression of cytokines, chemokines, and growth factors that contribute to HS pathogenesis.
“Targeting the CD2
interaction, along with NKT and NK cells, provides a promising therapeutic approach for HS, an incurable disease that severely impacts quality of life, particularly among young women,” said Raman.
The study also highlights that HS disproportionately affects women, especially those of African American descent, and typically manifests in individuals between the ages of 16 and 40. Despite existing treatments, no cure for HS currently exists, and the disease continues to affect patients’ quality of life.
Athar emphasized the importance of understanding the immune cell landscape of HS at different stages of the disease. “Defining these molecular signatures will help us develop therapies that not only manage symptoms but may eventually cure the disease,” he said.
The research team included dermatology experts from UAB, including Boni Elewski, M.D., and Craig Elmets, M.D., with Mahendra Kashyap, Ph.D., serving as the study’s first author. In collaboration with Clemson University’s Shahid Mukhtar, Ph.D., and his team, the study also employed multi-omics analysis to deepen the understanding of HS pathology.
The study was further supported by contributions from Erik Berglund, M.D., and David Berglund, M.D., co-founders of ITB-MED, developers of TCD601 (siplizumab), a monoclonal antibody targeting CD2. This antibody may soon play a role in the development of effective HS treatments.
As the research progresses, the hope is to provide much-needed relief for HS patients through targeted therapies that address the underlying immune mechanisms of the disease.
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