Cited by 63Galectins and Cancer BiologyT-cell and B-cell ImmunologyImmune Response and Inflammation

Galectin-3 Modulates Th17 Responses by Regulating Dendritic Cell Cytokines

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Fermin Lee, Agnes, Chen, Huan-Yuan, Wan, Lei, Wu, Sheng-Yang, Yu, Jhang-Sian, Huang, Annie C., Miaw, Shi-Chuen, Hsu, Daniel K. +2 more·2013·The American Journal of Pathology

Abstract

Galectin-3 is a β-galactoside-binding animal lectin with diverse functions, including regulation of T helper (Th) 1 and Th2 responses. Current data indicate that galectin-3 expressed in dendritic cells (DCs) may be contributory. Th17 cells have emerged as critical inducers of tissue inflammation in autoimmune disease and important mediators of host defense against fungal pathogens, although little is known about galectin-3 involvement in Th17 development. We investigated the role of galectin-3 in the induction of Th17 immunity in galectin-3-deficient (gal3(-/-)) and gal3(+/+) mouse bone marrow-derived DCs. We demonstrate that intracellular galectin-3 negatively regulates Th17 polarization in response to the dectin-1 agonist curdlan (a β-glucan present on the cell wall of fungal species) and lipopolysaccharide, agents that prime DCs for Th17 differentiation. On activation of dectin-1, gal3(-/-) DCs secreted higher levels of the Th17-axis cytokine IL-23 compared with gal3(+/+) DCs and contained higher levels of activated c-Rel, an NF-κB subunit that promotes IL-23 expression. Levels of active Raf-1, a kinase that participates in downstream inhibition of c-Rel binding to the IL23A promoter, were impaired in gal3(-/-) DCs. Modulation of Th17 by galectin-3 in DCs also occurred in vivo because adoptive transfer of gal3(-/-) DCs exposed to Candida albicans conferred higher Th17 responses and protection against fungal infection. We conclude that galectin-3 suppresses Th17 responses by regulating DC cytokine production.

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Crossref · 10.1016/j.ajpath.2013.06.017

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  • The expression of Rel, a nuclear factor κB subunit, in DC cluster 3 promoted Il-23 expression to regulate the Th17 response.

    “The expression of Rel , a nuclear factorκ B subunit, in DC cluster 3 promoted Il-23 expression to regulate the Th17 response. 25”

    From Single-Cell RNA Sequencing to Dissect the Immunological Network of Autoimmune Myocarditis. (2020) · cites this paper as [25]

    The section “Galectin-3 Negatively Regulates Activation of c-Rel in DCs after Curdlan Stimulation” identifies c-Rel as an NF-κB subunit that promotes IL-23 p19 transcription. “Differential IL-23 Production Accounts for Enhanced Th17 Induction by gal3−/− DCs” shows that blocking IL-23 p19 decreased DC-induced Th17 differentiation. The paper does not identify a “DC cluster 3” or establish that this mechanism occurs specifically in that cluster; page numbers were unavailable in our copy. (LLM, conf=0.88)

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  1. Fermin Lee et al 1220 ajp.amjpathol.org -The American Journal of Pathology

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Authors
Fermin Lee, A., Chen, H.-Y., Wan, L., Wu, S.-Y., Yu, J.-S., Huang, A. C., Miaw, S.-C., Hsu, D. K., Wu-Hsieh, B. A., & Liu, F.-T.
Affiliations
  • Institute of Biomedical Sciences, Academia Sinica (TW)
  • China Medical University Hospital (TW)
  • National Taiwan University (TW)
Corresponding author
Liu, Fu-Tong
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2013-10
Volume
183
Issue
4
Pages
1209-1222
ISSN
0002-9440 (ISSN-L)
OpenAlex
W2110432110
Cited by
63
References
51
Citations by year
2026: 5 · 2025: 4 · 2024: 3 · 2023: 5 · 2022: 1 · 2021: 9 · 2020: 6 · 2019: 5 · 2018: 4 · 2017: 2 · 2016: 5 · 2015: 11 · 2014: 3
FWCI
3.51
Type
journal article
Language
en
Open access
Locations
  • American Journal Of Pathology (publishedVersion, cc-by-nc-nd)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • Academia Sinica
  • Institute of Biomedical Sciences, Academia Sinica
  • National Heart, Lung, and Blood Institute (T32-HL-07013, T32HL007013)
  • National Cancer Institute (P30CA093373)
  • National Institute of Arthritis and Musculoskeletal and Skin Diseases (R01AR056343, AR056343)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Galectins and Cancer Biology
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
galectin-3, Th17 cells, dendritic cells, IL-23, c-Rel, Raf-1, Dectin-1, curdlan, lipopolysaccharide, Candida albicans, fungal infection, Th17 polarization, cytokine production, beta-galactoside-binding lectin
MeSH terms
Dectin-1, Animals, Candida albicans, Candidiasis, Chickens, Dendritic Cells, Enzyme Activation, Immunity, Lipopolysaccharides, Mice, Inbred C57BL, Models, Biological, Signal Transduction, Cytokines, Cell Polarity, Adoptive Transfer, Proto-Oncogene Proteins c-raf, Proto-Oncogene Proteins c-rel, Lectins, C-Type, Galectin 3, beta-Glucans, Extracellular Signal-Regulated MAP Kinases, Mice, Interleukin-23, Th17 Cells

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