Antigen induced modulation by shed lymphocyte membrane gangliosides.

A unique regulatory mechanism has been proposed for ganglioside which functions to immune responses to temporarily restrain B lymphocytes of all specificities and at various levels of differentiation. Utilizing antigen competition protocols, experiments was designed to exploit and extend the antigen induction properties of this modulation. Spleen cell cultures were prepared from TNP-BGG primed mice. In vitro stimulation of the cultures with ovalbumin (OVA) followed 24 hours later by addition of TNP-BGG resulted in only one weak TNP hemolytic plaque responses when compared to control cultures which did not receive OVA. OVA induced competitive effects were absorbed by anti-Thy-1 or anti-ganglioside. Glycolipids could be extracted from the culture media supernatants of experimental and control groups as a ganglioside fraction containing Thy-1 determinants. These molecules, when formulated into liposomes, produced the same modulatory effect as that of media from the competitive culture group. These results support and extend the proposal that glycolipids released by antigen stimulated T cells provide unrestricted modulation of B cells to prevent overload during T cell maturation. This regulatory mechanism prevents direct antigen binding and prepares B cell receptivity for further stimuli which orchestrate their terminal differentiation into plasma cells.