title: Studies on the capacity of intact cells and purified Ia from different B cell sources to function in antigen presentation to T cells.
abstract: In this study we have evaluated some of the potential mechanisms that may be responsible for the inefficiency with which resting B cells function as antigen-presenting cells (APC) and the mechanism by which that function is enhanced following treatment of B cells with neuraminidase. One mechanism that has been previously suggested is that glycosylation differences in Ia associated with different APC accounts for the different functional capacities of resting and activated B cells. It has been postulated that removal of sialic acid from resting B cell Ia results in a correction of its antigen-presenting defect. To study this possibility, we have used purified I-Ad from different B cell sources in a planar membrane system to present an immunogenic peptide of chicken ovalbumin (Ova) to an I-Ad-restricted Ova-specific T cell hybridoma. It was found that I-Ad isolated from resting B cells, B cell stimulatory factor 1 (BSF-1) or lipopolysaccharide and dextran sulfate-stimulated B cells, or A20 B lymphoma cells were all equivalent in their antigen-presenting capacity. Furthermore, removal of sialic acid from Ia did not enhance its capacity to serve as a restriction element. The mechanism by which neuraminidase treatment enhances B cell APC function was further investigated by studying the effect of sialic acid removal on a primary mixed leukocyte reaction (MLR). When allogeneic fixed B cells were used as stimulator cells it was found that neither resting nor BSF-1-stimulated B cells could induce a MLR. Following neuraminidase treatment, BSF-1-treated B cells, but not resting B cells, were capable of stimulating a MLR. However, a MLR was also stimulated by allogeneic BSF-1-treated B cells when the responder T cells, rather than the stimulator cells, were treated with neuraminidase. An enhancing effect similar to that obtained by neuraminidase treatment could be obtained by the addition of 2% polyethylene glycol to the MLR culture. These data suggest that the inability of BSF-1-stimulated cells to function efficiently as accessory cells in stimulating a primary MLR is due to their relative inability to interact physically with T cells, a deficiency that is overcome by neuraminidase treatment of either T or B cell populations or by the addition of polyethylene glycol to the culture. Although the reason for the failure of these same treatments to restore the accessory cell function of resting B cells is not known, some possible mechanisms are discussed.
mesh_terms: D000818:Animals; D000938:Antigen-Presenting Cells / Q000187:drug effects / Q000276:immunology*; D001402:B-Lymphocytes / Q000187:drug effects / Q000276:immunology*; D002448:Cell Adhesion / Q000187:drug effects; D000949:Histocompatibility Antigens Class II / Q000276:immunology*; D008213:Lymphocyte Activation / Q000187:drug effects; D007959:Lymphocyte Culture Test, Mixed; D051379:Mice; D008807:Mice, Inbred BALB C; D008808:Mice, Inbred CBA; D009439:Neuraminidase / Q000494:pharmacology; D011092:Polyethylene Glycols / Q000494:pharmacology; D013601:T-Lymphocytes / Q000187:drug effects / Q000276:immunology*
chemical_list: D000949:Histocompatibility Antigens Class II; D011092:Polyethylene Glycols; D009439:Neuraminidase