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Related Experiment Video

Updated: Jan 13, 2026

In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction

In Vivo Augmentation of Gut-Homing Regulatory T Cell Induction

Published on: January 22, 2020

Lactic acid improves Treg manufacturing and in vivo function.

Karoliina Tuomela^1,2, Emily S Y Leong^1,2, Manjurul Haque^1,2

¹Department of Surgery, University of British Columbia, Vancouver, BC V5Z 1M9, Canada.

Molecular Therapy. Methods & Clinical Development

|October 28, 2025

Summary

Lactic acid (LA) enhances the purity, viability, and suppressive function of regulatory T cells (Tregs) for cell therapy. This method improves Treg stability and efficacy in preclinical models, offering a promising approach for treating autoimmune diseases and transplant rejection.

Keywords:

autoimmunity cell manufacture exhaustion lactate lactic acid metabolism regulatory T cell transplantation

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Published on: December 30, 2016

Area of Science:

Immunology
Cell Therapy
Biochemistry

Background:

Adoptive cell therapy using regulatory T cells (Tregs) shows promise for autoimmunity and transplantation.
Expanding pure and highly suppressive Tregs remains a significant challenge in cell therapy development.
Lactic acid (LA) is known to enhance Treg function in tumor microenvironments.

Purpose of the Study:

To investigate the potential benefits of lactic acid (LA) during the expansion of regulatory T cells (Tregs).
To determine if LA improves Treg purity, viability, suppressive function, and reduces exhaustion markers.
To evaluate the efficacy of LA-conditioned Tregs in preclinical models of immune-mediated diseases.

Main Methods:

Human polyclonal and chimeric antigen receptor (CAR)-Tregs were expanded with or without lactic acid (LA).
Treg viability, purity, glycolysis, and suppressive function were assessed post-expansion and upon re-stimulation.
Expression of exhaustion markers (PD-1, TIM-3, LAG-3, TOX, BLIMP-1) was analyzed in CAR-Tregs.
LA-conditioned Tregs were tested in immunodeficient mouse models of chronic stimulation and xenogeneic graft-versus-host disease.

Main Results:

Addition of LA from day 3 onwards significantly improved Treg viability and purity.
LA enhanced Treg glycolysis upon re-stimulation and led to superior suppressive function.
In CAR-Tregs, LA reduced tonic signaling-associated expression of exhaustion markers.
LA-conditioned Tregs showed enhanced stability, reduced exhaustion, and improved efficacy in mouse models.

Conclusions:

Lactic acid (LA) has a multimodal beneficial effect on human Treg expansion and function for cell therapy.
LA improves Treg purity, viability, and suppressive capacity, while mitigating exhaustion.
LA represents a novel method for generating an optimal Treg product for therapeutic applications in autoimmunity and transplantation.