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Galectin-3 in autoimmunity and autoimmune diseases
Felipe L de Oliveira1, Mariele Gatto2, Nicola Bassi2
1Coimbra Group Fellowship for Latin American Professors, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Rio de Janeiro, RJ CEP 21941-902, Brazil Rheumatology Unit, Department of Medicine, University of Padova, Padova 35128, Italy.
Experimental Biology and Medicine (Maywood, N.J.)
|July 5, 2015
Summary
Galectin-3 (gal-3) influences immune cell function and inflammation, potentially contributing to autoimmune diseases. Further research is needed to clarify gal-3
Area of Science:
- Immunology
- Cell Biology
- Pathophysiology
Background:
- Galectin-3 (gal-3) is a lectin regulating cell interactions, inflammation, and immune responses.
- Gal-3's functions vary based on its location within or outside cells.
- It impacts monocyte-macrophage differentiation, dendritic cell fate, T lymphocyte apoptosis, and B lymphocyte differentiation.
Purpose of the Study:
- To review the role of galectin-3 in cellular and tissue events in autoimmune and immune-mediated inflammatory diseases.
- To explore gal-3's potential therapeutic applications in autoimmune disorders.
Main Methods:
- Literature review focusing on galectin-3's involvement in autoimmune disease pathogenesis.
- Analysis of studies investigating gal-3's effects on immune cell populations.
Main Results:
- Gal-3 influences key immune cells implicated in autoimmune disease development.
- Its precise role in driving inflammation in these conditions requires further elucidation.
- Exogenous gal-3 may not fully replicate endogenous gal-3 functions.
Conclusions:
- Galectin-3 plays a significant role in immune cell regulation and inflammatory processes.
- Understanding gal-3's function is crucial for developing therapeutic strategies for autoimmune diseases.
- Further investigation is warranted to clarify gal-3's exact contribution to autoimmunity.
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