October 22, 2026
Every immune cell in the body has a role to play. Together, they form something like a band, where each type of cell is a musician. When the system is working in balance, they deliver a harmonious performance and protect the body.
But sometimes in immune-mediated kidney diseases, such as antibody-mediated rejection (AMR) and IgA nephropathy (IgAN), some musicians can begin to play off-key. Certain immune cells, including plasma cells and plasmablasts, can produce harmful antibodies that attack the body’s own tissues, and natural killer cells can drive direct tissue injury.1 The performance starts to break down.
For patients, that can mean kidney function gradually declines or worsens, potentially leading to serious long-term consequences.1
That’s where CD38 comes into play. CD38 is a protein expressed on the surface of those disruptive immune cells, a signal of the musicians who are playing off-key.2 While many treatment approaches for immune-mediated diseases work by broadly suppressing the entire immune system, this can also quiet the cells that are doing exactly what they should, leaving patients more vulnerable in the process.3 Biogen believes that by selectively targeting CD38, it may be possible to deplete the cells driving disease, while preserving the rest of the immune system’s ability to function, bringing things back into harmony.
“What makes CD38 a compelling target is that it gives us a way to better understand and potentially address the cells that drive immune-mediated kidney diseases, without broadly silencing the immune system as a whole,” said Daniel Quirk, MD, Chief Medical Officer at Biogen. “By studying how CD38-expressing cells contribute to kidney damage, we are uncovering broader insights into the immune mechanisms that drive kidney disease.”
CD38-expressing cells are connected to a range of immune-mediated diseases,2 and Biogen is committed to advancing research that expands our understanding of disease biology and the immune mechanisms that drive kidney damage and other serious immune-mediated conditions. In doing so, we hope to better understand how each musician, or immune cell, contributes to the immune system's performance and why it sometimes falls out of tune.
1. Schinstock et al. (2018) Kidney Transplant with Low Levels of DSA or Low Positive B-Flow Crossmatch: An Underappreciated Option for Highly-Sensitized Transplant Candidates (Page 8). Available at: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5481511/pdf/nihms837168.pdf#page=8; Ciancio et al. 2018 Antibody-Mediated Rejection Implies a Poor Prognosis in Kidney Transplantation: Results From a Single Center. Available at: https://onlinelibrary.wiley.com/doi/10.1111/ctr.13392
2. Piedra-Quintero, Z. L., et al. (2020). CD38: An Immunomodulatory Molecule in Inflammation and Autoimmunity. Frontiers in immunology, 11, 597959. https://doi.org/10.3389/fimmu.2020.597959
3. Immunosuppressants. Cleveland Clinic. (2025, September 30). https://my.clevelandclinic.org/health/treatments/10418-immunosuppressants