Hidradenitis suppurativa, (HS) is a condition that causes chronic inflammation on the surface of the skin. It’s characterized by painful bumps that form under the skin and can sometimes rupture.

In a study published in Proceedings of the National Academy of Sciences, UAB Department of Dermatology professors Chander Raman, PhD and Mohammad Athar, PhD revealed that by disrupting the protein CD2’s interaction with CD58, the gene expressions that result in HS symptoms could be suppressed, resulting in potential novel treatment options for HS.

Current treatments for HS mainly reduce some symptoms, but they don’t cure or arrest the progression of the disease.

The Raman and Athar team’s study uncovered that the lymphocyte cell surface protein CD2 is expressed at elevated levels on T lymphocytes and innate lymphocytes, including natural killer cells (NK), natural killer T cells (NKT) and mucosal-associated invariant T cells (MAIT) in HS lesions. The understanding that innate lymphocyte populations, specifically NKT cells and natural killer cells, express high levels of CD2 and are the predominant lymphocyte population in HS lesions helped demonstrate that the blockade of cognate interaction between CD2 and CD58 had profound effects in mitigating gene expression and secretion of proteins (cytokines, chemokines, growth factors) that are relevant to the pathogenesis of HS.

“Our study identifies CD2:CD58 interaction along with NKT and NK cells as major drivers of HS pathogenesis,” Raman said. “Targeting of CD2:CD58 therapeutically offers an opportunity to treat HS, an incurable debilitating skin disease impacting quality of life among young patients, particularly women.”

According to the HS Foundation, HS impacts about one percent to two percent of people, particularly between the age group of 16 to 40, in the United States. The disease commonly affects women of African American descent.