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In Vitro Differentiation of Naive CD4+ T Cells into Pathogenic Th17 Cells in Mouse
Published on: October 25, 2024
Galectin-3 modulates Th17 responses by regulating dendritic cell cytokines.
Agnes Fermin Lee1, Huan-Yuan Chen2, Lei Wan3
1Department of Dermatology, University of California, Davis, School of Medicine, Sacramento, California.
The American Journal of Pathology
|August 7, 2013
Summary
Galectin-3 negatively regulates T helper 17 (Th17) cell development by controlling dendritic cell cytokine production. This finding is crucial for understanding autoimmune diseases and fungal infections.
Area of Science:
- Immunology
- Cell Biology
Background:
- Galectin-3, a β-galactoside-binding lectin, influences T helper cell responses.
- Dendritic cells (DCs) expressing galectin-3 may play a role in immune regulation.
- Th17 cells are critical in autoimmune inflammation and fungal defense, but galectin-3's role in their development is unclear.
Purpose of the Study:
- To investigate the role of galectin-3 in the induction of Th17 immunity.
- To determine how galectin-3 deficiency affects DC function and Th17 polarization.
Main Methods:
- Compared galectin-3-deficient (gal3(-/-)) and wild-type (gal3(+/+)) mouse bone marrow-derived DCs.
- Stimulated DCs with dectin-1 agonist curdlan and lipopolysaccharide.
- Analyzed Th17-axis cytokine (IL-23) and NF-κB pathway components (c-Rel, Raf-1).
- Assessed Th17 responses and protection against Candida albicans via adoptive transfer of DCs.
Main Results:
- Intracellular galectin-3 negatively regulates Th17 polarization.
- gal3(-/-) DCs secreted higher IL-23 levels and had increased activated c-Rel.
- Impaired active Raf-1 levels were observed in gal3(-/-) DCs.
- Adoptive transfer of gal3(-/-) DCs enhanced Th17 responses and fungal protection.
Conclusions:
- Galectin-3 suppresses Th17 responses by regulating DC cytokine production.
- Galectin-3 plays a critical role in modulating Th17 immunity in both in vitro and in vivo settings.
- Understanding galectin-3's function in DCs offers insights into autoimmune and infectious disease mechanisms.
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