Studies of immune responses in mice prone to autoimmune disorders. II. Decreased down-regulation by auto-anti-idiotype antibody in autoimmune-prone mice

Edmond A. Goidl, Robert A. Good, Gregory W. Siskind, Marc E. Weksler, Gabriel Fernandes

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

Three lines of evidence are presented which suggest that autoimmune-prone mice are deficient in the production of auto-anti-idiotype antibody during their immune response to trinitrophenylated Ficoll (TNP-F). (1) NZB, MRL lpr/lpr and older BXSB male mice have no hapten-augmentable plaque-forming cells (PFC). Hapten-augmentable PFC have been previously shown to be cells whose secretion of antibody has been inhibited by the binding of auto-anti-idiotype antibody to cell surface idiotype. (2) Sera from TNP-F immunized NZB mice lack PFC inhibiting activity (anti-idiotype antibody). (3) Spleen cells from TNP-F immune NZB mice fail to transfer antiidiotype antibody-mediated suppression to naive mice as do spleen cells from immune nonautoimmune-prone mice. Taken together these data suggest that autoimmune-prone mice are deficient in auto-anti-idiotype antibody-mediated downward regulation of their immune responses. It was further shown that the immune response of NZB mice to TNP-F shows a slower decline in splenic PFC and a greater heterogeneity of PFC affinity than do the responses of non-autoimmune-prone strains. Since athymic (nude) mice, which were previously shown to be defective in the production of auto-anti-idiotype antibody, also show a slower decline in splenic PFC and an increased heterogeneity of PFC affinity, it is suggested that these peculiarities of the immune responses of autoimmune-prone and athymic mice are also the consequences of the lack of autoanti-idiotype antibody-mediated down-regulation.

Original languageEnglish (US)
Pages (from-to)281-289
Number of pages9
JournalCellular Immunology
Volume101
Issue number2
DOIs
StatePublished - Sep 1986

ASJC Scopus subject areas

  • Immunology

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