| Background. Th17 is identified as a lineage of T helper cells that plays an important role in the adaptive immunity against bacterial infection and pathognensis of some diseases. Galectin-3 is a molecule found both intra- and extracellularly, and has been demonstrated to contribute to a variety of immunological responses.;Objective. First, to examine whether galectin-3 can affect the Th17 polarization from naive T cells to a Th17 phenotype. Second, to determine whether extracellular or intracellular galectin-3 is responsible for this polarization. Third, to utilize a collagen-induced arthritis (CIA) mouse model and an atopic dermatitis (AD) mouse model induced by epicutaneous sensitization with ovalbumin to test Th17 polarization efficacy in both gal3 +/+ and gal3-/- mice. Fourth, to investigate whether gal3-/- or gal3+/+ Th17 cells can induce more severe atopic dermatitis.;Methods. IL-17 levels secreted from gal3-/- or gal3+/+ cells were determined by ELISA. In the CIA model, we compared clinical severity of arthritis between gal3+/+ and gal3-/- mice. In the AD model, we transferred activated CD4 OT-II T cells into B6 mice to compare severity of allergic inflammatory response and IL-17 levels from the lymph nodes. Furthermore, we transferred either gal3-/- or gal3+/+ Th17 cells into mice and compare the severity of allergic inflammatory response in the recipient.;Results. Th17 cells polarized from gal3-/- mice produced more IL-17 in vitro. Galectin-3 affected IL-17 production through intracellular pathways. Gal3+/+ cells expressed more TGF-betaII receptors compared to gal3-/- cells which may have contributed to lower Th17 polarization efficacy. In the CIA mouse model, no obvious arthritis was established in C57BL/6 mice and thus we did not detect any difference between gal3+/+ and gal3-/- mice. In contrast, using the AD mouse model, we found higher IL-17 secretion by lymph node cells in gal3-/- mice. |
