Tolerogenic and inflammatory stimuli differentially regulate galectin-1 expression on dendritic cells

DERGAN DYLON LS; ILARREGUI JM; CROCI DO; SALATINO M; TOSCANO MA; RABINOVICH GA

Viña del Mar, Chile

Congreso; 9th Latinamerican Congress of Immunology; 2009

Asociación Latinoamericana de Inmunología

621 Tolerogenic and inflammatory stimuli differentially regulate galectin-1 expression on dendritic cells Leonardo Sebastián Dergan Dylon, Juan Martín Ilarregui, Diego Omar Croci, Mariana Salatina, Marta Alicia Toscano, Gabriel Adrián Rabinovich Laboratorio de Inmunopatología, Instituto de Biología y Medicina Experimental, CONICET. Buenos Aires We have recently demonstrated that galectin-1, an endogenous glycan-binding protein, plays an essential role in the generation of tolerogenic dendritic cells (DCs). However, the regulation of galectin-1 expression on immune cells, particularly on DCs, is largely unexplored. Here, we evaluated the expression of galectin-1 on DCs expose to inflammatory and tolerogenic stimuli. Bone marrow-derived immature DCs synthesized and secreted more galectin-1 than DCs matured with LPS. Given this differential profile, we first differentiated DCs in the presence of a panel of tolerogenic stimuli which induced a substantial increase in galectin-1 transcript and protein expression (p<0.05). When we first differentiated DCs and subsequently exposed immature DCs to tolerogenic stimuli this effect was even more pronounced (p<0.05). On the other hand, exposure of DCs to pro-inflammatory stimuli resulted in substantially reduced galectin-1 expression (p<0.05). However, exposure of immature DCs to Schistosoma mansoni egg antigen (SEA), a typical Th2 stimulus, resulted in a dose-dependent increase in galectin-1 synthesis (p<0.001). Inhibition of the ERK1-2 or JNK pathway abrogated SEA-induced up-regulation of galectin-1. Thus, tolerogenic and inflammatory stimuli can selectively regulate galectin-1 expression on mouse DCs. These contrasting effects might offer an alternative explanation for the plasticity of DCs to drive divergent T helper responses.