Abstract
When peripheral blood lymphocytes (PBL) were stimulated in vitro with the rough form of type 2 S. pneumoniae R36a, the resulting plaque-forming cells (PFC) did not produce antibodies directed against phosphorylcholine, a major antigenic determinant of the cell wall C-polysaccharide. Instead, R36a stimulated polyclonal PFC in PBL and splenic lymphocytes. The polyclonal responses stimulated by R36a were compared with those induced by 2 well-characterized polyclonal activators (PA), Staphylococcus aureus Cowan I and pokeweed mitogen (PWM). R36a was a poor mitogen for PBL, whereas the other 2 PA were potent mitogens. The predominant isotype produced in response to all 3 PA was IgM. Adherent cells strongly inhibited the polyclonal PFC response to both R36a and S. aureus but not PWM. T cells were necessary for induction of polyclonal antibody-secreting cells by all 3 stimuli.

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