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COUR Pharma Publishes Peer-Reviewed Data in Science Advances
Paper defines the mechanism by which COUR Nanoparticles induce antigen-specific immune tolerance
Jan. 29, 2026 at 1:15am
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COUR Pharma, a clinical-stage biotechnology company developing first-in-class, antigen-specific immune tolerance therapies for autoimmune diseases, announced the publication of new data in Science Advances. The paper defines the molecular and cellular mechanisms by which COUR Nanoparticles (CNPs), also referred to as tolerizing immune modifying particles (TIMPs), induce antigen-specific immune tolerance.
Why it matters
The findings establish that CNP-induced tolerance recapitulates the physiological mechanism by which the immune system establishes and maintains self-tolerance, providing a strong biological foundation for COUR's platform and supporting its continued development across a range of immune-mediated diseases.
The details
The data demonstrate that uptake of CNPs by myeloid cells leads to apoptosis and release of oxidized DNA, triggering activation of the stimulator of interferon genes (STING)/type I interferon signaling pathway. This signaling cascade drives the activity of tolerogenic antigen-presenting cells and the expansion of antigen-specific regulatory T cell populations, including disease suppressing type 1 regulatory T (Tr1) cells and FoxP3⁺ regulatory T cells. Genetic disruption of STING or the interferon receptor abrogated tolerance induction, establishing these pathways as mechanistically required.
- The paper was published on January 28, 2026.
The players
COUR Pharma
A clinical-stage biotechnology company developing first-in-class, antigen-specific immune tolerance therapies for autoimmune diseases.
Stephen D. Miller, Ph.D.
Professor of Microbiology-Immunology at the Northwestern University, coinventor of the CNP platform, and senior author of the paper.
Adam Elhofy, Ph.D.
COUR Pharma VP of Research and contributing author of the paper.
What they’re saying
“Importantly, the study shows that immune tolerance induced by antigen-coupled apoptotic splenocytes and red blood cells depends on the STING/type I interferon pathway. These findings establish that CNP-induced tolerance recapitulates the physiological mechanism by which the immune system establishes and maintains self-tolerance during the continual turnover of hematopoietic cells.”
— Stephen D. Miller, Ph.D., Professor of Microbiology-Immunology at the Northwestern University, coinventor of the CNP platform, and senior author of the paper (Science Advances)
“Although many current treatments for autoimmune diseases rely on broad immune suppression, the immune system itself has evolved precise mechanisms to maintain tolerance to self. These new findings reinforce CNPs as a unique and potent technology for the antigen-specific treatment of autoimmune diseases while preserving normal immune function.”
— Adam Elhofy, Ph.D., COUR Pharma VP of Research and contributing author of the paper (Science Advances)
What’s next
COUR is enrolling patients in two Phase 1b/2a clinical studies: one in type 1 diabetes and the other in myasthenia gravis. COUR also expects to initiate a Phase 2b clinical study in primary biliary cholangitis, a disease in which COUR has already shown positive results in a Phase 2a clinical study, in 2026.
The takeaway
By identifying a shared tolerance pathway that underlies both apoptotic cell-mediated tolerance and nanoparticle-induced antigen-specific tolerance, these findings provide a strong biological foundation for COUR's platform and support its continued development across a range of immune-mediated diseases.
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