|Reference : Human Anti-Alpha-Galactosyl Igg Reduces the Lung Colonization by Murine Mo4 Cells|
|Scientific journals : Article|
|Human health sciences : Oncology|
Life sciences : Biochemistry, biophysics & molecular biology
|Human Anti-Alpha-Galactosyl Igg Reduces the Lung Colonization by Murine Mo4 Cells|
|Castronovo, Vincenzo [Université de Liège - ULg > Département des sciences biomédicales et précliniques > Biologie générale et cellulaire >]|
|Foidart, Jean-Michel [Université de Liège - ULg > Département des sciences cliniques > Gynécologie - Obstétrique >]|
|Li Vecchi, M. [> > > >]|
|Foidart, J. B. [> > > >]|
|Bracke, M. [> > > >]|
|Mareel, M. [> > > >]|
|Mahieu, P. [> > > >]|
|Invasion & Metastasis|
|[en] The lung colonization of MO4 cells, a highly malignant murine cell line, is strongly reduced in syngeneic C3H/He mice by a prior incubation with anti-alpha-galactosyl antibody (alpha-Gal Ab), a natural IgG antibody present in high titers in all normal human sera and specifically recognizing Gal alpha(1----3) structures (alpha-D-galactopyranosyl; alpha-D-Galp). The protective effect is due to a binding of alpha-Gal Ab to alpha-D-Galp end groups of MO4 cells, inducing both an increase in their sequestration into the liver and the spleen and a decrease in their sequestration into the lung. The F(ab')2 fragments of this antibody also exhibit a protective effect by inhibiting the homing of MO4 cells into the lung, without modifying their accumulation into the spleen and the liver. Since both the antibody and the alpha-galactosidase pretreatments of MO4 cells block their subsequent attachment to murine laminin in vitro, we suggest that, in this model, the lung colonization may be dependent on the alpha-D-Galp end groups exposed on the surface of MO4 cells.|
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