ImmunomodulationCosting more than $100 billion annually in the U.S., autoimmune diseases arise and persist due to the loss of immune tolerance to one’s own tissues. Immune tolerance is propagated through a variety of mechanisms, including suppression of self-reactive T effector cells and auto (self)-antigen presenting cells by T regulatory cells (Tregs). A numerical or functional deficit of Tregs curtails immune tolerance to self-tissues and innocuous external antigens, underpinning autoimmune and allergic diseases. Caladrius' technology to enhance autologous Treg number and function therefore leverages the native immune regulatory mechanisms, offering a path to true disease modification.
The Potential of T Regulatory CellsThe potential of Tregs as a therapeutic platform differentiates itself from available therapeutics, and almost all investigational agents in development through:
- Disease modification via restoration of immune tolerance as the most proximal/root cause of the autoimmune disease pathways, in contrast to targeting less pivotal and redundant downstream effects.
- Freedom from indiscriminate immune suppression of vital effector functions of the immune system.
- Specific homing to disease affected organs, thus targeting tolerance to where it is needed most.
- Limited dosing regimen.
Caladrius has launched a Phase 2 study (The Sanford Project: T-Rex Study, a collaboration with Sanford Research) of CLBS03, a Treg based therapeutic being developed to treat type 1 diabetes mellitus (T1DM) in adolescents. We are evaluating other clinical indications into which we may advance this program, including graft versus host disease, chronic obstructive pulmonary disease (COPD), multiple sclerosis (MS), inflammatory bowel disease (IBD) and steroid resistant asthma.