A dedicated team of researchers based at Clemson University has effectively employed an innovative multiomics approach to uncover vital immune mechanisms underlying a chronic and debilitating inflammatory skin condition known as hidradenitis suppurativa (HS).
The groundbreaking research, which was published in the prestigious journal Proceedings of the National Academy of Sciences (PNAS), presents a promising target for the development of future therapeutic interventions.
Hidradenitis suppurativa (HS) is a complex immune disease that impacts nearly 4% of the global population, leading to painful, recurring skin lesions and significant inflammation primarily located in skin folds. Notably, this condition is more prevalent among women of African American descent, highlighting a crucial demographic aspect of its impact.
Under the leadership of Shahid Mukhtar, his multidisciplinary team consisting of Bharat Mishra, Nilesh Kumar, and graduate student YiFei Gou utilized advanced single-cell sequencing techniques to identify CD2 as a pivotal immune receptor. This receptor exhibits elevated expression levels on T cells and innate lymphoid cells (ILCs), including natural killer cells, specifically within skin tissue affected by HS.
In a collaborative effort with researchers from the University of Alabama at Birmingham, Mukhtar’s team conducted organotypic skin culture experiments sourced from HS patients. Their findings revealed that the inhibition of CD2 leads to a statistically significant decrease in the production of pro-inflammatory cytokines and chemokines, alongside the suppression of critical pathogenic gene signatures associated with the disease.
This compelling discovery indicates that targeting and blocking CD2 may effectively mitigate the inflammatory response characteristic of HS, thereby opening up an exciting new therapeutic pathway aimed at managing symptoms and enhancing the overall quality of life for affected patients.
How does the immune receptor CD2 influence the systemic inflammation observed in patients with hidradenitis suppurativa (HS)?
**Interview with Shahid Mukhtar, Lead Researcher on Hidradenitis Suppurativa Study**
**Interviewer:** Thank you for joining us today, Dr. Mukhtar. Your team’s recent study published in PNAS discusses the role of the immune receptor CD2 in hidradenitis suppurativa (HS). Can you briefly explain what led to the focus on CD2?
**Shahid Mukhtar:** Thank you for having me. Our motivation stemmed from the complexities surrounding HS, a disease that significantly affects many individuals. Through our multiomics approach and advanced single-cell sequencing techniques, we discovered that CD2 was significantly upregulated in the T cells and innate lymphoid cells of HS-affected skin. This pointed to its potential role in driving the inflammatory processes associated with the condition.
**Interviewer:** Interesting! You mentioned that blocking CD2 could lead to reduced pro-inflammatory cytokines. How significant are these findings for future therapeutics?
**Shahid Mukhtar:** The implications are quite promising. By targeting CD2, we might be able to develop therapies that not only alleviate inflammation but also improve the overall quality of life for HS patients. Currently available treatments often have limitations and don’t adequately address the underlying immune mechanisms. Our findings could pave the way for new strategies tailored to the specific pathways involved in HS.
**Interviewer:** It’s estimated that HS impacts nearly 4% of the global population, particularly affecting women of African American descent. How does this demographic aspect influence your research?
**Shahid Mukhtar:** This demographic information is crucial. HS is not just a skin condition; it has profound impacts on the lives of those affected, particularly within marginalized communities. Understanding the unique immune responses in different populations will help us create more effective, personalized treatments.
**Interviewer:** Given your findings, what do you foresee as the next steps for your research team?
**Shahid Mukhtar:** Our next steps involve further validation of CD2 as a therapeutic target, including more extensive in vivo studies. We’re also looking at collaboration with pharmaceutical companies to expedite the development of a CD2-blocking therapy.
**Interviewer:** Before we wrap up, what would you say to those living with HS who are eager for new treatment options?
**Shahid Mukhtar:** I’d encourage them to stay hopeful. Research is advancing rapidly, and our understanding of HS is deepening. We are committed to translating our findings into practical therapies that can make a real difference in their lives.
**Interviewer:** Thank you, Dr. Mukhtar. This is certainly an exciting time for HS research. Now, for our readers, what do you think about the potential of targeting immune receptors like CD2 in treating chronic inflammatory diseases? Could this approach revolutionize how we handle such conditions, or do you believe there are risks involved in focusing on a single target? Let the debate begin!