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In a recent study, researchers from Australia found that soluble CD52 inhibits Toll-like receptors
and tumor necrosis factor receptor signaling and limits NF- κ B activation, thereby inhibiting
macrophages, monocytes and dendritic cells inflammatory cytokine synthesis. The results also
show that when the concentration of CD52 is elevated, soluble CD52 depletes the short-lived
promyelocytic MCL-1 and promotes the apoptosis of BH3-only pro-apoptotic proteins BAX and
BAK. In vivo experiments showed that administration of soluble CD52 inhibited LPS-induced
cytokine secretion and other characteristics of endotoxic shock, while knockdown of CD52
aggravated LPS response.
Previous studies have confirmed that humanized anti-CD52 monoclonal antibodies produced by
gene recombination followed by monoclonal technology can be used to treat alkylating agents
and fludarabine-resistant chronic lymphocytic leukemia. The study shows that soluble CD52 has a
wide range of immunosuppressive effects, the future is expected to be used for the development
of immunotherapy drugs.