The transmembrane protein CD83 expressed on antigen presenting cells can be expressed as a soluble form generated by alternative splice variants and/or by shedding. The soluble form of CD83 (sCD83) has been shown to be involved in negatively regulating the immune response and shows promising activity as an efficient immunosuppressant. sCD83 inhibits T cell proliferation in vitro, supports allograft survival, prevents corneal transplant rejection and attenuates the progression and severity of autoimmune diseases and experimental colitis in in vivo mouse models.

Coimmune has identified the binding partner for sCD83 on monocytes, a type of antigen presenting cell. By interacting with this binding partner, we propose the tolerogenic mechanism of action of sCD83 is dependent on initial interaction with antigen presenting cells, altering early cytokine signal pathways leading to T cell unresponsiveness. Thus, our preclinical data supports the potential usefulness of sCD83 having therapeutic efficacy to treat autoimmune and inflammatory diseases as well as alleviate transplant rejection.