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P025. Distinct effect of galectins on the mononuclear phagocyte system

D. Paclik, A. Sturm

Charité, Berlin, Germany

Aim: Monocytes and macrophages represent the link between the innate and adaptive immune systems and protect the host from the outside world. In inflammatory disorders, however, their activation leads to tissue damage. Galectins have emerged as central regulators of the immune system. Galectins are expressed by intestinal epithelial cells and bind to mucosal T cells but if and how they interfere with immune homeostasis by regulating monocyte/macrophage physiology is still unknown. For this we analysed the effect of different galectins on monocytes/macrophages.

Material and Methods: Monocytes and macrophages were isolated from peripheral blood and mucosa and FACS analysis was used to determine Gal-1, Gal-2, Gal-3 and Gal-4 binding. Activation, cytokine secretion and apoptosis were determined by flow cytometric analysis, migration by transwell system, and phagocytosis by phagotest. Using supernatants from macrophages co-cultured with galectins we revealed their influence on T cell function.

Results: In our study Gal-1, Gal-2, Gal-4, and partly Gal-3 bound to and activated monocytes and macrophages. Galectins prevented Salmonella-induced MHCII upregulation. Cytokine release was distinctly induced by different galectins. We revealed that T-cell activation is significantly restricted by supernatants of macrophages co-cultured in the presence of Gal-1, Gal-2 or Gal-4, but not Gal-3. Furthermore, we showed that all galectins tested potently inhibit monocyte migration. Finally, we showed for the first time that galectins induce monocyte, but not macrophage apoptosis.

Conclusion: Our study provides evidence that galectins distinctively modulate central monocyte and macrophage function. By inhibiting T cell function via macrophage priming, we also show that galectins link the innate and adaptive immune systems and provide new insights into the action of sugar-binding proteins.