Antigens apparently nonimmunogenic forxid/Y mice cause the development of specific splenic plasmablasts and of fusion partners for SP2 cells giving hybridomas that secrete antibodies

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Abstract
Although xid/Y mice fail to make a detectable primary antibody response to a variety of antigens such as Type III pneumococcal capsular polysaccharide (SIII), 2,4,6-trinitrophenyl (TNP)-Ficoll, pneumococcal C carbohydrate, group A streptococcal vaccine and several kinds of related antigenic determinants such as phosphorylcholine (PC) and N-acetyl-glucosaminyl (GlcNAc), even when the latter are coupled to hemocyanin (Hy), they do show: (a) an antigen-dependent development of splenic B cells which can act as successful, productive fusion partners for SP2 cells giving hybridomas making monoclonal anti-SIII, anti-PC, anti-GlcNAc, anti-TNP, etc., and (b) an antigen-dependent appearance of antigen-binding plasmablasts in their spleens. The frequencies of specific B cells arising in xid/Y males with either of these properties are of the same order of magnitude as those found in immunocompetent xid/Y female littermates. Further, both PC-Hy and GlcNAc-Hy prime xid/Y and xid/X mice for quantitatively and qualitatively similar secondary responses. All three of these expressions of a specific, primary response occur in xid/Y mice in the absence of any rise in circulating antibodies. The properties of successful, productive normal fusion partners leading to secretory hybridoma lines are unknown. Thus we cannot decide whether the antigen-binding plasmablasts that arise in xid/Y mice can also play the role of productive fusion partners. Neither do we know whether the development of specific IgM and IgG3 plasmablasts in xid/Y mice after antigen stimulation is an abnormality reflecting the xid mutation. It cannot be excluded that the development of productive fusion partners, of nonsecretory plasmablasts and of memory cells are all interrelated and reflect a process that also normally occurs in xid/Y, X/X and X/Y mice following similar immunization regimens. It is tempting to speculate that such cells initially responding may lag in the development of normal secretory mechanisms and that the “transformed” fusion partner may complement this deficiency.

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