Researchers have successfully synthesized a chimeric antibody against the CD36 human platelet antigen, with potential therapeutic implications for fetal and neonatal alloimmune thrombocytopenia (FNAIT), according to a recent study published in PubMed.
The authors aimed to artificially produce a chimeric antibody capable of binding to the CD36 antigen of human platelets. A chimeric antibody combines one species’ variable antibody region with another’s constant antibody region.
In this experiment, the authors used gene synthesis and recombination techniques to create the variable and constant chains of the antibody. Testing with flow cytometry and ELISA techniques demonstrated that the antibody binded to human CD36 antigen and prevents the ingestion (phagocytosis) of platelets by immune cells (monocytes).
Learn more about FNAIT therapies
“In this study, the Fc-silent chimeric antibody against human CD36 was successfully prepared, and its loss of ability to mediate CD36(+) platelet clearance was confirmed in vitro, which provides a preliminary basis for the study of modified antibodies for the therapy of CD36-antibody-mediated fetal and neonatal alloimmune thrombocytopenia(FNAIT),” the authors wrote.
Understanding the human CD36 antigen and FNAIT
The human CD36 antigen or platelet glycoprotein IV (GPIV) is a protein found in the membranes of human platelets, red blood cells, and some white blood cells. This molecule plays an important role in cellular function; however, it is also the target of maternal antibodies in FNAIT.
The binding of antibodies to CD36 begins an inflammatory immune reaction that results in platelet destruction and thrombocytopenia. The administration of an artificial antibody that binds to CD36 without initiating an immune response could inhibit the binding of deleterious maternal antibodies and prevent FNAIT complications.
This study is one of several studies that have assessed CD36 inhibition as a viable therapeutic alternative for FNAIT. Previous studies using mice and monoclonal antibodies have shown equally promising results, and CD36 inhibition will likely become a widespread therapeutic alternative in the not-so-distant future.
