The TregTherapeutics tolerogenic approach has been developed over the past two decades, primarily using various models of experimental autoimmune encephalopathy (EAE) in laboratory animals.
These models are typical of investigational research centered on multiple sclerosis. The TregTherapeutics approach was INITIALLY developed as a possible application for MS, and its treatment and cure remain a core objective for the company. Despite this fact, it as the underlying mechanism was elucidated during development, it was discovered that the underlying principles governing the technology are equally applicable to the induction of tolerance in a wide range of disease states that have chronic inflammation as a common denominator.
The initial key research objective was to discover a way to generate a powerful, sustained tolerogenic signal on a cellular level that would translate into strong, clinically significant, disease remediation. Superb research design and execution provided important insights into various linkage mechanisms that included fusion proteins, as well as, various combinations of cytokines, antigens, and adjuvants. This work included the examination of ways to modify conventional fusion proteins to achieve the benefits of linkage but without covalent bonding, a way to link numerous proteins without the complexity of conventional restrictions, a way to convert a tolerogenic cytokine into a super-tolerogenic agent without functionally modifying its structure.
As this research continued over the years it was learned that the research objective, defined above, could indeed be achieved. Furthermore, it was discovered that by varying the linked components, a range of inflammatory conditions could be addressed. The culmination of decades of research was the discovery that under the right conditions, certain anti-inflammatory cytokines could be linked with certain adjuvants in such a way that tolerogenic induced disease remediation could be achieved, regardless of the underlying pathogenic antigens eliciting the immune response. Thus, was born the TILAC platform that creates an in-situ microenvironment that does indeed produce a powerful, sustained tolerogenic signal that has enormous downstream implications. This signal is directed towards endogenous self-antigens, pathogenic autoantigens that are driving the disease process; these are commandeered to direct that tolerogenic signal in a very specific way that initiates and maintains disease remediation. The outcome of the therapy, then, is immune tolerance and re-established immune homeostasis.