New York City Blood Center Enterprises today announced that their researchers have uncovered a critical mechanism that could potentially transform treatment approaches for Sickle Cell Disease. The findings, published as the cover article in the most recent issue of the medical journal Blood, underscore the nature of immune responses in SCD, suggesting that therapies targeting specific immune pathways could improve outcomes.
“This research provides crucial insights into how the immune system functions in sickle cell disease,” said Dr. Karina Yazdanbakhsh, Vice President and Director of Research at New York Blood Center Enterprises. “By understanding these complex immune mechanisms, we can develop more targeted treatments for SCD patients, potentially reducing their vulnerability to infections while managing immune system complications.”
Using sophisticated mouse models, NYBCe researchers systematically examined the role of key immune cell subsets and discovered that SCD mice exhibited enhanced immune responses to specific T-cell independent antigens. B-1 cells, particularly the B-1b subset, played a critical role in these immune responses, while type I interferons emerged as pivotal factors in modulating immune responses and contributing to autoantibody production. The study was funded through NIH grants awarded to NYBCe researchers by the National Heart, Lung, and Blood Institute.
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“The findings from Dr. Yazdanbakhsh’s lab are truly exciting and novel,” said Dr. Banu Aygun, Associate Chief of Hematology and Section Head of Sickle Cell Disease at New York’s Northwell Health Cohen Children’s Medical Center. “The team’s discovery of anti-red blood cell (RBC) autoantibodies, and the underlying mechanisms through type I interferon and B1b cell subsets, provide crucial insights for future therapeutic interventions.” “This research builds on her team’s continued work developing novel approaches for treating vaso-occlusive episodes and modifying the course of SCD”, said Jay Mohr, Chief Business Officer at New York Blood Center Enterprises.
SOURCE: GlobeNewswire