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Neonatal complement depletion results in predominant expression of a myeloma M 104E private idiotope among anti-dextran antibodies.

作者信息

Weiler E, Lehle G

机构信息

Fakultät für Biologie, Universität Konstanz, FRG.

出版信息

Eur J Immunol. 1991 May;21(5):1207-12. doi: 10.1002/eji.1830210517.

Abstract

Myeloma M 104E (IgM, lambda 1) with specificity for the alpha(1----3) glucosidic linkage of dextran B 1355 S (Dex) carries two idiotopes (Id) as defined by isogenic anti-idiotype mAb. The public Id is not influenced by two amino acid replacements in CDR 2 nor by an alternative D region sequence. It is shared by all or nearly all humoral antibodies in the primary immune response against Dex of mice carrying haplotype Igha. The private Id-5' appears to depend on the integrity of the VH germ-line sequence and on the particular M 104E D region sequence. It is present on a highly fluctuating but usually small fraction of primary anti-Dex antibody. We report here that this situation is changed when mice are treated with Cobra venom anti-complement factor (CVF), after birth and thereby were deprived of complement for the first two weeks of life. When immunized with Dex as adults the majority of anti-Dex Ab carried the M 104E Id-5. Thus, humoral antibody in CVF-treated animals resembled the Ly-1+ anti-Dex precursor B cell population in the peritoneal cavity, while anti-Dex Ab in animals not treated with CVF more closely corresponded to the Ly-1- precursor B cell pool in spleen (H.-P. Lehmann and G. Lehle, Eur. J. Immunol. 1991. 21: 1201).

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