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Thymus-independent B-cell activation: passively incorporated membrane antibodies serve to focus the antigen but
1Department of Immunology, University of Stockholm, Sweden.
We have activated B cells with membrane-incorporated monoclonal antibodies against the hapten trinitrophenyl (TNP) using various concentrations of the polyclonal activator lipopolysaccharide (LPS) haptenated with TNP. We found that anti-TNP-decorated B cells were polyclonally activated by 1000-fold lower concentrations of TNP-LPS than untreated B cells or B cells decorated with antibodies of other specificities. In order to test whether the passively incorporated anti-TNP monoclonals could mediate activation signals or only served to focus the polyclonal activator TNP-LPS to the B cells, we compared the response of anti-TNP-decorated B cells from normal C3H/He mice and from the LPS-unresponsive strain C3H/HeJ. We found that B cells from C3H/HeJ mice could not be activated to polyclonal antibody synthesis, in contrast to B cells from the LPS-responsive strain C3H/He. Thus, contrary to what was previously suggested, the incorporated anti-TNP antibodies could not mediate activation signals, but only served to passively bind and concentrate TNP-LPS to the membrane of the B cells, thereby increasing the concentration of the polyclonal B-cell activator LPS to the B cells.
We have activated B cells with membrane-incorporated monoclonal antibodies against the hapten trinitrophenyl (TNP) using various concentrations of the polyclonal activator lipopolysaccharide (LPS) haptenated with TNP. We found that anti-TNP-decorated B cells were polyclonally activated by 1000-fold lower concentrations of TNP-LPS than untreated B cells or B cells decorated with antibodies of other specificities. In order to test whether the passively incorporated anti-TNP monoclonals could mediate activation signals or only served to focus the polyclonal activator TNP-LPS to the B cells, we compared the response of anti-TNP-decorated B cells from normal C3H/He mice and from the LPS-unresponsive strain C3H/HeJ. We found that B cells from C3H/HeJ mice could not be activated to polyclonal antibody synthesis, in contrast to B cells from the LPS-responsive strain C3H/He. Thus, contrary to what was previously suggested, the incorporated anti-TNP antibodies could not mediate activation signals, but only served to passively bind and concentrate TNP-LPS to the membrane of the B cells, thereby increasing the concentration of the polyclonal B-cell activator LPS to the B cells.
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