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Updated: Jun 5, 2026

Evaluation of T Follicular Helper Cells and Germinal Center Response During Influenza A Virus Infection in Mice
Published on: June 27, 2020
Galectin-9 regulates T helper cell function independently of Tim-3
Ee W Su1, Shuguang Bi, Lawrence P Kane
1Department of Immunology, University of Pittsburgh School of Medicine, BST E-1056, Pittsburgh, PA 15261, USA.
Galectin-9 (a protein) can trigger pro-inflammatory cytokine production in T helper cells, independent of the Tim-3 receptor. This reveals a more complex role for galectin-9 in immune responses.
Area of Science:
- Immunology
- Molecular Biology
- Cell Biology
Background:
- Galectin-9 is a member of the galectin family, known for its role as an eosinophil chemoattractant and inducer of apoptosis.
- Galectin-9 binds to Tim-3, a receptor on T cells implicated in limiting immune responses during chronic inflammation, autoimmune diseases, and viral infections.
- The precise contribution of the galectin-9/Tim-3 interaction to these immune modulatory effects remains unclear.
Purpose of the Study:
- To investigate the multifaceted roles of galectin-9 beyond its previously known pro-apoptotic functions.
- To determine if galectin-9 influences T helper cell cytokine production.
- To elucidate the involvement of the Tim-3 receptor in galectin-9-mediated T cell responses.
Main Methods:
- Treated T helper cells with varying concentrations of galectin-9.
- Measured the production of pro-inflammatory cytokines.
- Assessed the necessity of the Tim-3 receptor for galectin-9's effects.
Main Results:
- Galectin-9 induces the production of pro-inflammatory cytokines from T helper cells in a dose-dependent manner.
- This cytokine induction occurs independently of the Tim-3 receptor.
- Galectin-9 exhibits functions beyond apoptosis induction.
Conclusions:
- Galectin-9 possesses a more complex role in modulating T cell responses than previously understood.
- Galectin-9 can activate T helper cells to produce inflammatory cytokines via Tim-3-independent pathways.
- These findings suggest the involvement of additional galectin-9 receptors on T cells.
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