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Murine Model of Epicutaneously-Induced Immunomodulation
Published on: June 24, 2025
Receptor usage by the Acanthocheilonema viteae-derived immunomodulator, ES-62
William Harnett1, Helen S Goodridge, Janet M Allen
1Strathclyde Institute of Pharmacy and Biomedical Sciences, University of Strathclyde, Glasgow G4 0RE, UK. w.harnett@strath.ac.uk
Experimental Parasitology
|September 20, 2011
Summary
ES-62, an immunomodulatory glycoprotein, binds to different proteins on various immune cells. Phosphatidylcholine (PC) is key for this binding, and Toll-like receptor 4 (TLR4) influences ES-62 internalization in macrophages.
Area of Science:
- Immunology
- Parasitology
- Molecular Biology
Background:
- ES-62 is an immunomodulatory glycoprotein from Acanthocheilonema viteae.
- Previous studies indicated Toll-like receptor 4 (TLR4) dependence for ES-62 effects on macrophages and dendritic cells.
- Potential for ES-62 to interact with diverse cell surface proteins, leading to varied receptor usage.
Purpose of the Study:
- To identify proteins interacting with ES-62 across different immune cell types.
- To investigate the role of phosphatidylcholine (PC) in ES-62 binding.
- To determine the involvement of TLR4 in ES-62 internalization.
Main Methods:
- Protein identification by molecular weight after ES-62 interaction.
- Assessment of PC's effect on ES-62 binding.
- Analysis of ES-62 internalization in the presence or absence of TLR4.
Main Results:
- Lymphocytes show ES-62 interaction with proteins at ~135 kDa and ~82 kDa.
- U937 monocytes exhibit ES-62 binding to an ~82 kDa protein.
- PC blocked ES-62 binding to B cells and U937 cells, highlighting PC's role.
- ES-62 internalization occurred in macrophages and B cells; TLR4 absence blocked it only in macrophages.
Conclusions:
- ES-62 exhibits differential receptor usage across immune cell types.
- Phosphatidylcholine is crucial for ES-62-mediated cell interactions.
- TLR4 plays a cell-specific role in ES-62 internalization.

