Polypeptide Blocks Chemokine and GAG Interactions and Decreases Long-Term Damage Done by Immune System
This viral anti-inflammatory protein inhibits the interaction between chemokines and glycosaminoglycans (GAGs), decreasing immune system response and reducing the number of late transplant rejections. About 17 percent of kidney transplants are rejected within the first three years. Chronic rejection, a progressive form of allograft injury that usually results in the failure of transplanted organs, is the most common reason that kidney transplants are rejected. It is caused by long-term damage inflicted by the body’s immune system. Available treatments to reduce organ rejection only target the host’s T and B cells (defender cells that fight infection) in an attempt to limit their roles in immune responses. University of Florida researchers have developed a viral anti-inflammatory protein that reduces transplant rejection by preventing inflammatory macrophage reactions, which are the driving force behind chronic rejection. This protein reduces or inhibits the body’s natural immune response after a transplant. By treating the donor or organ before implantation, the chance of rejection significantly decreases. The treatment was tested on renal transplants but is not limited to only this type of transplant.
Application
Viral anti-inflammatory protein reduces the body’s immune response to organ transplants
Advantages
- Decreases the body’s immune response to organ transplants, reducing the number of late transplant rejections
- Allows for customization of therapy and pathway of administration, leading to optimal therapeutic responses and improved results for patients
- Allows for uses beyond human medicine, applicable to veterinary medicine as well
Technology
These polypeptides are derived from a Myxoma Virus Virulence factor (M-T7) to inhibit chemokine and glycosaminoglycans (GAGs) interactions. The polypeptides contain point mutations that increase the effectiveness of the inhibition. GAG is highly charged and contains many heparin sulfate molecules. After an organ is transplanted, inflammatory response cells become and remain active for long periods of time. This response induces transplant vasculopathy (TV), which is responsible for late transplant loss. Chemokines and GAGs interact and become directional signals for migrating cells, such as inflammatory response cells. Blocking or inhibiting this interaction significantly decreases the levels of inflammatory cell invasion and thus the number of transplant rejections. The polypeptides can be used to treat either the donor or the transplant, and they can be administered through a number of pathways, such as oral, topical, transdermal, pulmonary, and parenteral. The polypeptides also reduce T cell receptor (TCR) expression as compared to a reference level. TCR, a molecule found on the surface of a T cell, recognizes antigens bound to major histocompatibility complex molecules as host or donor cells. Reducing TCR expression helps minimize the chance that donor cells will be recognized and rejected.
Brochure
