Animal models substantially contribute to the understanding of the pathogenesis of various human diseases, including those associated with genetic defects. Our study investigated the characteristics of antibody responses elicited by T-dependent and T-independent antigens in mice rendered k-deficterrt by targeted deletion of the JkCk gene segments. It is known that in normal murine species the k repertoire dominates the antibody repertoire (k/λratio = 95:5). Our results indicate that the k gene deletion causes the alternative usage of λ1 (93%) and λ2 (7%) light chains, confirming previous studies demonstrating that in k-deficlent mice all B cells express IGλ receptors. The anti-trinitrophenylbenzene (TUP) response in K-/- mice was compensated for by α1 and α2 bearing Igs. However, isoelectric focusing analysis of anti-TNP antibodies showed a considerably more restricted pattern of α anti-TNP antibodies in K-/- as compared with κ antibodies in normal mice. No major differences were observed in the affinity for the hapten of κ orα1 or α2 mAbs obtained from 129/Sv and K-/- mice. Furthermore, κ1 and κ2 chains can reconstitute the expression of an Idiotype (460ld) borne on κ anti-TNP antibodies. The 460ld was detected both in polyclonal and monoclonal anti-TNP antibodies obtained from K-/- mice. Our results clearly showed that the κ anti-TNP repertoire is compensated by the α repertoire even though the latter is clonally restricted in K-/- mice.
- Antibody response
- K-deficient mice