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Intestinal Microfold Cells Play a Critical Role in the Uptake and Oral Tolerance Mediated by

Vincent Chak¹, Sujay Harne¹, Jason G Kay^2,3

¹Department of Pharmaceutical Sciences, School of Pharmacy and Pharmaceutical Sciences, University at Buffalo, The State University of New York, 359 Pharmacy Building, Buffalo, NY 14214, USA.

Nanomaterials (Basel, Switzerland)

|April 13, 2026

Summary

This summary is machine-generated.

Single-chain phosphatidylserine (PS) nanoparticles induce oral tolerance by enhancing immune cell exposure and microfold cell (M-cell) uptake. This tolerance is dependent on M-cells, as shown in M-cell-deficient mice.

Keywords:

apoptosis immune regulation intestinal-M-cells nanoparticle oral tolerance phosphatidylserine regulatory T cells

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Area of Science:

Immunology
Cell Biology
Nanotechnology

Background:

Phosphatidylserine (PS) externalization during apoptosis signals immune tolerance.
Single-chain PS (LysoPS) nanoparticles induce oral tolerance, unlike double-chain PS.
Microfold cells (M-cells) transport antigens to Peyer's patches for immune surveillance.

Purpose of the Study:

Investigate the role of M-cell uptake in LysoPS-mediated oral tolerance.
Determine if structural differences in PS affect M-cell interaction and tolerogenicity.
Elucidate the mechanism behind LysoPS nanoparticles' tolerogenic potential.

Main Methods:

In vitro and ex vivo studies to assess M-cell uptake of PS nanoparticles.
Oral tolerance induction studies using ovalbumin (OVA) in M-cell-deficient mice.
Comparison of LysoPS and double-chain PS nanoparticle uptake and immune cell exposure.

Main Results:

LysoPS nanoparticles showed a 2-fold increase in immune cell exposure and M-cell uptake compared to double-chain PS.
LysoPS-mediated oral tolerance was abrogated in M-cell-deficient mice.
M-cell-deficient mice exhibited higher anti-OVA antibody titers.

Conclusions:

M-cell-mediated uptake is crucial for LysoPS nanoparticle-induced oral tolerance.
Enhanced PS exposure on LysoPS nanoparticles facilitates M-cell interaction.
The structural form of PS significantly impacts its tolerogenic efficacy via M-cells.