The Role of Galectin-3 in Th17 Differentiation
Date Issued
2009
Date
2009
Author(s)
Chu, An-Hsiang
Abstract
T helper 17, a recently discovered subset in the effector arm of T helper cells and also a major contributor to autoimmune diseases, has been the subject of intense research. To date, a great amount of information on the lineage differentiation and functions of Th17 has been generated. In contrast, only few molecules that are involved in the negative control of Th17 cells have been identified and therefore the negative regulatory mechanisms on Th17 lineage development remain largely elusive. In this study, we found that Galectin-3-deficient Th cells differentiated more efficiently to the Th17 lineage than wild type Th cells. The gene expression level of major cytokine products such as IL-17 and IL-21 along with several lineage-associated markers, including RORγt, RORα and IL-23R, was correspondingly enhanced in Galectin-3 KO Th17 cells. Overexpression of retroviral Galectin-3 in differentiating Th17 cells slightly decreased the IL-17 production in Galectin-3-deficient cells, demonstrating its negative regulatory role in the Th17 differentiation. In addition, in vitro promoter luciferase assay revealed a potential role of Galectin-3 to suppress the transcription of Il21, the major self-amplifying cytokines during the early differentiation of Th17 cell lineage, thus providing a reasonable mechanism underlying the negative regulation by Galectin-3. Based on above observations, we conclude that Galectin-3 play a negative role in the differentiation of Th17 cells.
Subjects
Galectin
Th17
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