Allotypic restriction of the expression of MOPC460 idiotope after immunization with either anti‐2,4‐dinitrophenyl (DNP) or anti‐idiotypic antibodies

Abstract

Restrictive idiotope expression 999The MOPC460 idiotype is expressed in mice with the IghC" allotypic haplotype after anti-2,4-dinitrophenyl (DNP) immunization. We have previously shown that two monoclonal syngeneic anti-idiotypic antibodies (IDM 92-13 and IDM 41-27) define two distinct idiotopes (the 460.92 and the 460.41) on the M460 idiotype. The current study demonstrates that only one idiotope (460.92) is recurrently expressed after antigen immunization in IghC" positive mice and also that, immunization against the monoclonal anti-idiotypic molecules induces the synthesis of 460.92 idiotope positive anti-DNP antibodies. However, the detection of such molecules is only possible when animals with the IghC" allotypic haplotype are immunized with the IDM 92-13 molecules. Immunization of mice with either of the two monoclonal anti-idiotypic antibodies never results in the synthesis 460.41 positive molecules. Therefore, whatever protocol of immunization used, the expression of 460.92 was allotypic restricted.

Differential Idiotype Utilization for the In Vivo Type 14 Capsular Polysaccharide-Specific Ig Responses to Intact Streptococcus pneumoniae versus a Pneumococcal Conjugate Vaccine

“…Thus, in addition to its dominant expression in BALB/c, but not C57BL/6 mice, minimal 44.1-Id usage is also observed in C.BKa mice, that express the Igh b allotype in an essentially BALB/c background. Although allotype-specific linkages have been described in other experimental systems using various PS antigens (20-23, 73), the 44.1-Id differs from these systems in several aspects. Firstly, 44.1-Id is prevalent in elicited PPS14-specific IgG, but not IgM, and it was undetectable in natural PPS14-specific Ig.…”

“…To further investigate whether the expression of the 44.1-Id was linked to the Igh -C allotype, as described for other antigenic systems (20-23), PPS14-specific responses to R6-14 in C.BKa mice were determined (Fig. 3).…”

“…Although the phenomenon of B cell dominance is poorly understood, dominant Id could be generated by random somatic mutation and selection of Ag-driven B cell clones, or reflect the use of germline-encoded Ig genes, conserved during evolution. The frequent linkage observed between the allotype of the heavy chain of Igs ( Igh-C ) and the individual expression of the dominant Id (20-23) suggest that they may be under the control of regulatory genes linked to the Igh-C allotype (21). Individual lack of expression of a particular dominant Id does not typically affect the quantity of the Ag-specific Ig response, with the exception of the murine response to α1-3 dextran (22).…”