Anti-CD55 monoclonal antibody, clone NFN-229 [PE]

Objectives: This study aims to examine the effect of polyherbal erythropoiesis modulatory and stimulatory agent (EMSA) Eritin administration in modulating the activity of erythropoiesis on TER-119(+)VLA-4(+) cells and complement regulators TER-119(+)CD55(+) and TER-119(+)CD59(+) cells in Balb/c mice after total body irradiation (TBI) with a dose of 500 rad. Materials and methods: EMSA Eritin was administered orally in mice after exposure to TBI with a dose of 500 rad daily for two weeks with three different doses including a low dose (1.04 mg/g BW), normal dose (3.125 mg/g BW), and high dose (9.375 mg/g BW). Mice were treated with HEMAPO Epoetin alfa twice a week as positive control with a dose of 0.21 mg/g BW. On day 15, the bone marrow was isolated and the number of TER-119(+)VLA-4(+), TER-119(+)CD55(+) and TER-119(+)CD59(+) cells were a nalyzed using flow cytometry. Examination showed marked reduction in the number of TER-119(+)VLA-4(+) cells in the bone marrow of mice after TBI with dose of 500 rad compared to those of healthy controls. The number of TER-119(+)VLA-4(+) cells in the irradiated mice was markedly increased with EMSA Eritin from low dose to high dose compared to mice with TBI and mice treated with Epoetin alfa. Results: The highest dose of EMSA Eritin was more effective to promote erythropoiesis than HEMAPO Epoetin alfa and the other dose of EMSA Eritin. Conclusion: Our study findings suggest that EMSA Eritin is a powerful medicinal herbal supplement which may serve as a protective agent to normalize homeostasis and erythropoiesis after irradiation with a dose of 500 rad.

The complement system is an innate immune defense cascade that can cause tissue damage when inappropriately activated. Evidence for complement over activation has been reported in small cohorts of patients with sickle cell disease (SCD). However, the mechanism governing complement activation in SCD has not been elucidated. Here, we observe that the plasma concentration of sC5b-9, a reliable marker for terminal complement activation, is increased at steady state in 61% of untreated SCD patients. We show that greater complement activation in vitro is promoted by SCD erythrocytes compared to normal ones, although no significant differences were observed in the regulatory proteins CD35, CD55, and CD59 in whole blood. Complement activation is positively correlated with the percentage of dense sickle cells (DRBCs). The expression levels of CD35, CD55, and CD59 are reduced in DRBCs, suggesting inefficient regulation when cell density increases. Moreover, the surface expression of the complement regulator CD46 on granulocytes was inversely correlated with the plasma sC5b-9. We also show increased complement deposition in cultured human endothelial cells incubated with SCD serum, which is diminished by the addition of the heme scavenger hemopexin. Treatment of SCD patients with hydroxyurea produces substantial reductions in complement activation, measured by sC5b-9 concentration and upregulation of CD46, as well as decreased complement activation on RBCs in vitro. In conclusion, complement over activation is a common pathogenic event in SCD that is associated with formation of DRBCs and hemolysis. And, it affects red cells, leukocytes and endothelial cells. This complement over activation is partly alleviated by hydroxyurea therapy.