Application of CD177 positive neutrophil in liver regeneration

By regulating the content of CD177-positive neutrophils and utilizing their agonists or inhibitors, combined with cell reinfusion technology, the problems of insufficient liver regeneration rate and high risk after ALPPS surgery were solved, thereby increasing the hepatocyte proliferation rate and reducing the risk of liver failure.

CN121868338APending Publication Date: 2026-04-17ZHONGSHAN HOSPITAL FUDAN UNIV
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Patent Information

Application Number
CN202511785994.7
Authority / Receiving Office
CN · China
Patent Type
Applications(China)
Current Assignee / Owner
Filing Date
2025-12-01
Publication Date
2026-04-17

AI Technical Summary

Technical Problem

Current technologies for promoting liver regeneration in liver resection surgery, especially after ALPPS surgery, still face challenges such as insufficient speed and high risks. Furthermore, the regulatory mechanisms of the liver's immune microenvironment are unclear, and the functional heterogeneity and specific subtypes of neutrophils have not been fully explored.

Method used

Using CD177-positive neutrophils as a target, their levels in vivo are regulated by injecting exogenous cells or using agonists/inhibitors to promote or inhibit hepatocyte proliferation. Combined with cell reinfusion technology, this precisely enhances liver regeneration and can be used independently or as an adjunct to ALPPS surgery.

Benefits of technology

It significantly improved hepatocyte proliferation rate and residual liver volume growth, reduced the risk of liver failure, increased surgical success rate, and provided flexible intervention methods to accelerate liver regeneration.

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Abstract

The invention belongs to the field of biological medicine, and particularly relates to application of CD177 positive neutrophil in liver regeneration. A series of experiments reveal that neutrophil is an immune cell necessary for liver regeneration after a liver resection operation, especially after a two-step liver resection operation (ALPPS) combining liver separation and portal vein ligation, and after the neutrophil is depleted by an antibody, liver cell proliferation and liver volume increase are remarkably inhibited. The invention further finds that the CD177 positive neutrophil is a specific functional subgroup which plays a key role in the CD177 positive neutrophil. Liver regeneration can be obviously inhibited by clearing the CD177 positive neutrophil in the mouse body, and inhibited liver regeneration can be recovered by in-vivo feedback of the CD177 positive neutrophil. The invention discloses an unknown effect of the CD177 positive neutrophil in promotion of ALPPS induced liver regeneration previously. The research lays a foundation for a strategy taking the neutrophil as a target spot, and a regenerative liver microenvironment is expected to be established and is used for preventing and treating hepatic failure.
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