Reaginic antibody formation in the mouse. VII. Depression of the ongoing IgE antibody formation by suppressor T cells.

The ongoing IgE antibody formation against ovalbumin (OA) in high responder mice was depressed by i.v. injections of either native or urea-denatured ovalbumin (UD-OA). Adoptive transfer experiments to determine the helper function of spleen cells from the treated animals showed that helper function for both IgE and IgG antibody responses diminished after treatment. Evidence was obtained that treatment suppressed the expansion of IgE-G memory cells. When the same treatment with OA or UD-OA was given to OA-primed mice before the appearance of IgE antibody in their serum, OA-specific splenic suppressor T cells were demonstrable. Thus, the transfer of splenic T cells from treated mice into normal mice suppressed the primary IgE and IgG antibody responses of the recipeints to DNP-OA. It was also found that the transfer of the splenic T cells from UD-OA-treated mice into OA-primed mice depressed ongoing IgE antibody formation in the recipients. The results suggested strongly that the decrease of helper function and the depression of ongoing IgE antibody formation by repeated injections of UD-OA was caused by generation of antigen (OA)-specific suppressor T cells.     

Stimulation of antibody formation by bacterial lipopolysaccharide. The influence of repeated doses of lipopolysaccharide on antibody formation

1. (1)
   Липополисахарид стимулирует образование антител даже при 8-кратном введении в сочетании с частично очищенным дифтерийным анатоксином.     
   
   

Induction of booster antibody formation without specific antigenic drive.

Injection of antigen into the rabbit eye leads to the development of an immunogenic uveitis and local immunologic memory, with extensive intraocular formation of immunoglobulins. During both primary and booster responses within the eye, only a small proportion of Ig-forming cells contain antibody specific for the inciting antigen. Preliminary evidence suggests that most of the antibody formed is specific for antigens within the prior extraocular experience of the host. It is postulated that the inflammatory reaction is accompanied by the local release of lymphokines capable of attracting a representative sample of B cells from the blood, and of nonspecifically activating them to booster antibody formation without specific antigenic drive.