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Red blood cell immunity remains an obstacle to safe and effective blood transfusions in sickle cell disease (SCD), but the associated risk factors remain unclear.
blood hemolysis, which is a hallmark of SCD, releases hemoglobin with effective immunomodulation activity.
, however, the role of in-blood hemolysis on SCD body fluid response (especially the same type of immunity) is not clear.
Mouli and others found that cell-free hemolybin inhibits human B-mother/pulp cell differentiation by inhibiting the DOCK8/STAT3 signaling path, and that the DOCK8/STAT3 signaling pathline is essential for B-cell biogasing and for raising hemoerin oxygenase 1 (HO-1) through its enzyme-promoting by-products carbon monoxide and bilirubin.
SCD B cells, which affect the activation of B cells, can be inhibited by exostopic hemoglobin, while B cells of the same type of immune system do not respond to hemoglobin inhibition and are easily differentiated into plasma cells.
was consistent with the difference in blood-soluble responses of B cells, the researchers found that DOCK8 B cell base levels increased in patients with SCD who were not Immune to the same type, and that HO-1-mediated active B-cell suppression was higher than in patients with the same type of Immune SCD.
in order to overcome the insensitivity of B cells of the same type of immune to hemoglobin and quinine treatment, the researchers screened several hemoglobin binding molecules and identified quinine as an effective inhibitor of B cell activity, thereby reversing the resistance of the same immunologist to hemoglobin inhibition.
inhibition of B cells only occurs in the presence of hemohemolytin and is induced by HO-1.
all, these data suggest that hemolytic blood can inhibit the response of B-cells, which may be a factor in the same immune risk in patients with SCD.
by restoring the sensitivity of B cells to hemoglobin, quinine may have the therapeutic potential to prevent and suppress the same kind of immunity in patients with SCD.
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