ENHANCEMENT OF THE MIXED LYMPHOCYTE-REACTION BY INVIVO TREATMENT OF STIMULATOR SPLEEN-CELLS WITH ANTI-IGD ANTIBODY

Abstract

The injection of anti-IgD antibody into mice increases the expression of Ia antigens on splenic B cells. These antigens are the most potent lymphocyte-activating determinants (LAD) that trigger proliferation in an H-2-defined mixed lymphocyte reaction (MLR) and may play a role in the recognition of minor lymphocyte-stimulating (Mls) determinants. A study was made to investigate a possible correlation between apparent quantitative alterations in B cell Ia expression after anti-IgD activation with changes in the functional capacity to present allogeneic major histocompatibility complex (MHC) and Mls antigens to responsive T cells. The capacity of splenocytes removed 24 h after the in vivo injection of anti-IgD to stimulate T cell proliferation across an H-2 barrier was most frequently enhanced 2- to 4-fold when a suboptimal concentration of stimulator cells was used or an early time point in the MLR was examined. The capacity of splenocytes to stimulate across an Mlsa,d difference after exposure to heterologous or hybridoma anti-IgD antibody often was increased 10-fold or more. Optimal MLR stimulatory capacity was induced by injection of 100-200 .mu.g of heterologous anti-IgD. Augmented Mls stimulatory capacity of spleen cells peaked 24 h after such treatment and continued to decline from this value at day 3 and at day 7 after injection. The H-2 stimulatory capacity increased 1 day after injection of anti-IgD and remained at that elevated level 3 and 7 days after injection. The spleen cells from B cell-defective (CBA/N .times. DBA/2)F1 male mice were unaffected in their capacity to stimulate across an Mls1 barrier after in vivo anti-IgD treatment. Spleen cells from phenotypically normal (DBA/2 .times. CBA/N)F1 male mice after exposure to anti-IgD did evidence a considerably enhanced ability to stimulate in an Mlsa-defined MLR. Because anti-IgD antibodies presumably have their major initial effect on surface IgD-bearing cells, these studies suggest that anti-Ig-activated B cells may have a role (direct or indirect via interaction with accessory cells) in the presentation of allogeneic MHC and Mls antigens to responsive T cells.