# NIH grant: A Bioengineered Probiotic for Resetting Immune Function in Rheumatoid Arthritis (1R44AR087173-01) — retained record

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NIH grant 1R44AR087173-01: A Bioengineered Probiotic for Resetting Immune Function in Rheumatoid Arthritis
Institute: {'code': 'AR', 'abbreviation': 'NIAMS', 'name': 'National Institute of Arthritis and Musculoskeletal and Skin Diseases', 'admin_org_id': '12500006', 'admin_funding_url': ''}. PI: Neil A Fanger. Award: $306341.
Start: 2026-08-26T00:00:00.
Project Summary
Our goal is to commercialize VTC-B35 as a novel, orally administered therapy for long-term disease remission
of rheumatoid arthritis (RA). RA is a chronic, systemic inflammatory disorder affecting up to 1% of the US
population1-3. While many organs are affected, the main targets of RA are synovial joints. As the disease
progresses, approximately half of RA patients become disabled6. RA patients also face higher unemployment
and double the risk of depression of the general population9.
Treatment of RA remains a significant unmet medical need. Despite the advent of a number of effective but
costly biologic therapies, less than half of RA patients achieve sustained remission, with many non-responsive
or experiencing relapse10 . Further, tolerability of biologics is limited by immunosuppressive side effects, such
as increased risk of serious infections, cancer and, in rare instances, neurological complications11-14
Therapies that redirect immune responses to produce immune tolerance instead of inflammation have potential
to treat the cause rather than the symptoms of disease, and so represent superior treatments for RA. For these
reasons, we are developing an oral immunotherapeutic that regulates auto-antigen specific regulatory T cells
(Tregs) and B cells (Bregs) to provide disease-specific tolerance. This approach has the potential to 1) “switch
off” the immune response against the patient’s own tissues specific to RA in an enduring manner, and; 2)
maximally balance the relationships between effector cells of different lineages to prevent relapses of
inflammation. As such, our approach will provide patients long-term remission and increased safety without
systemic immunosuppression.
Our team recently demonstrated that oral administration of a probiotic bacterial strain expressing the
cytokine IL-35 effectively induced Treg cells, reduced disease severity, and generated a tolerogenic
response in the mouse model of CIA22.
Building from this initial work, we have engineered a clinical strain of the probiotic yeast S. boulardii (termed
VTC-B35) that expresses human IL-35 from a genome-integrated operon. The use of S. boulardii allows us
to leverage a well-accepted, GRAS (generally regarded as safe) probiotic strain with unique immune
regulation, protein expression, and protein processing attributes. This application is designed to advance
VTC-B35 towards the clinic by establishing its manufacturing, therapeutic activity, and animal safety.
Successful commercialization of VTC-B35 will ultimately provide a profound front-line medical advancement
in the treatment of RA, and potentially other autoimmune diseases as well.
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