Ganglioside expression in tissues of mice lacking β2-microglobulin

This study presents a comparative analysis of gangliosides from lymphoid (spleen and thymus) and other (brain, liver, lungs and muscle) tissues of C57BL/6 mice lacking the gene for B-2-microglobulin (beta(2)M), a constitutive component of the MHC class I molecule. Ganglioside fractions in the tissues of mice homozygous (B2M-/-) and heterozygous (B2M-/+) for the gene deletion were determined by high performance thin-layer chromatography (HPTLC), followed by immunostaining with specific polyclonal antibodies. Ubiquitous gangliosides G(M3)(Neu5Ac) and G(M3)(Neu5Gc) were the dominant gangliosides in the lungs of the control B2M-/+ mice, whereas the homozygous knockout mice had substantially decreased expression of these structures. The lungs of the B2M-/- mice also had reduced expression of T-lymphocyte-specific G(M1b)-type gangliosides (G(M1b) and GalNAc-G(M1b)). beta(2)M-deficient mice also had more G(M1a) and G(D1a) gangliosides in the liver, and several neolacto-series gangliosides were increased in the brain and lungs. This study provides in vivo evidence that the beta(2)M molecule can influence the acquisition of a distinct ganglioside assembly in different mouse organs, implicating its non-immunological functions.