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Reading: Immunomodulatory Protein Derived from Parasites Enhances Regeneration in Mice – Fight Aging!
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P-HealthX > Blog > Senior Health > Immunomodulatory Protein Derived from Parasites Enhances Regeneration in Mice – Fight Aging!
Senior Health

Immunomodulatory Protein Derived from Parasites Enhances Regeneration in Mice – Fight Aging!

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Last updated: 2024/08/31 at 6:13 AM
By admin 2 Min Read
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Immunomodulatory Protein Derived from Parasites Enhances Regeneration in Mice


Researchers have discovered a promising immunomodulatory protein derived from parasitic worms that shows potential in enhancing regeneration in mice. This protein inhibits TGF-β signaling, leading to a shift in innate immune cells towards a pro-regenerative state at the site of injury. This process enables tissue regeneration with reduced scarring, promoting the regrowth of hair follicles instead of scar tissue in wounded skin. The findings open up new avenues for regenerative medicine, especially in addressing age-related healing impairments.



The delicate balance between tissue scarring and regeneration is heavily influenced by immune cell activity at the wound site. Emerging research indicates that molecules from parasitic worms could modulate the host’s immune response to favor tissue regeneration. A recent study focused on a protein called TGF-β mimic (TGM) produced by Heligmosomoides polygyrus, a gut-dwelling roundworm in rodents. Treatment with TGM led to accelerated wound closure, reduced scarring, and enhanced skin regeneration in mice, including the formation of new hair follicles.



Further investigation revealed that TGM interacts with the TGF-β receptor on cell surfaces, particularly immune cells like macrophages. This interaction drives immune cell recruitment to wounds and reprograms them to support tissue regeneration. The potential of parasitic worm-derived proteins like TGM in promoting regeneration highlights a promising direction in regenerative medicine research.


Link: https://www.eurekalert.org/news-releases/1055270

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admin August 31, 2024 August 31, 2024
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