Mechanism of Anti-Cluster of Differentiation 47 Monoclonal Antibody on Acute Graft vs. Host Disease in Haploid Transplanted Mice.

Cluster of differentiation 47-thrombospondin 1 is newly discovered pathway as T-cell stimulatory signal can induce immune tolerance that provides a new idea for the therapy of acute graft vs. host disease after transplantation haploid. However, numerous studies have found the regulation of cluster of differentiation 47-thrombospondin 1 on the immune system is bi-directional. Currently the specific mechanisms of cluster of differentiation 47-thrombospondin 1 pathway promotes immune tolerance is unclear. The acute graft vs. host disease model with cluster of differentiation 47 monoclonal antibody was occurred to test the function of the cluster of differentiation 47-thrombospondin 1 in acute graft vs. host disease. The consequences of the investigation affirmed that the application of cluster of differentiation 47 monoclonal antibody lessened the pathological manifestations and associated clinical symptoms of acute graft vs. host disease. Cluster of differentiation 47 monoclonal antibody has no significant impact on the proliferation of donor T lymphocytes, but it promotes the apoptosis of donor T lymphocytes. It favors the secretion of interleukin-4 and diminishes the secretion of interferon gamma and interleukin-17a. These data exhibit that the mechanisms by which cluster of differentiation 47-thrombospondin 1 inhibits the progress of acute graft vs. host disease are multifaceted, including promoting the secretion of inhibited inflammatory factors, discouraging the secretion of inflammatory factors, and promoting and frustrating the expression of transcription factors. Cluster of differentiation 47 therapeutic antibodies can convert a distinct way of treating acute graft vs. host disease by inhibiting the development of inflammation. Cluster of differentiation 47 therapeutic antibodies can improve a distinct idea for the therapy of acute graft vs. host disease by inducing immune tolerance of donor T cells. [ABSTRACT FROM AUTHOR]