Glycobiology, 2000, Vol. 10, No. 3 237-242
© 2000 Oxford University Press
Interaction between galectin-3 and Fc
RII induces down-regulation of IL-5 gene: implication of the promoter sequence IL-5REIII
Immunology Department, Fundación Jiménez Díaz, 28040 Madrid, Spain, 2Department of Experimental Immunology, Institute of Development, Aging and Cancer (IDAC), Tohoku University, Sendai 9808575, Japan, 3Department of Immunology, University of Utrecht, The Netherlands, and 4Division of Allergy, La Jolla Institute for Allergy and Immunology, San Diego CA 92121, USA
Our previous work demonstrated the capacity of galectin-3 (a ß-galactoside binding animal lectin) to inhibit IL-5 gene expression in different cell types, but the interaction of lectin with the cells and the pathways for the inhibition process are unknown. One of the purposes of this work was to study the cellular ligand for galectin-3. We have demonstrated that galectin-3 can bind to the low affinity IgG receptor (Fc
RII or CD32) by using different experimental approaches, such as flow cytometry, fusion protein GST technology, and with a model of Fc
RII-deficient mice. To further analyze the interaction between Fc
RII and galectin-3, and its implication in IL-5 gene down-regulation we used Fc
RII-deficient mice. When PBMC from these mice were incubated with galectin-3, the expression of the IL-5 gene was unchanged. However, when PBMC from wild type mice and Fc
RIII-deficient mice were incubated with galectin-3, IL-5 gene expression was down-regulated. Finally, we studied the implication of the negative regulatory sequence in the IL-5 gene promoter. In the presence of galectin-3, a DNA-protein complex was formed with the IL-5REIII region. This complex was not observed when unrelated oligonucleotide was used. So, galectin-3 induces a pathway, which activates a transcription factor that binds to IL-5REIII. This interaction is capable of inhibiting IL-5 gene transcription.
1 To whom correspondence should be addressed
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