Studies of Structure and Immunosuppression of a Cross‐Reactive Idiotype in Strain A Mice

Nisonoff, Alfred; Ju, Shyr‐Te; Owen, Frances L.

doi:10.1111/j.1600-065x.1977.tb00369.x

Cited by 124 publications

(57 citation statements)

References 49 publications

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“…In previous studies, Nisonoff and colleagues have found that A/J mice hyperimmunized with antigen and suppressed with anti-idiotypic antibodies develop "Is with putative antiidiotypic structures (19). That is, these T~ bind idiotype-coupled erythrocytes.…”

Section: Antigen-and Receptor-driven Regulatory Mechanismsmentioning

confidence: 99%

“…We have studied DTH reactivity to p-azobenzenearsonate (ABA) in mice and its regulation. Extensive information is available concerning the humoral immune response to ABA (19). In our earlier studies, we have demonstrated that anti-idiotypic antibodies to the major cross-reactive idiotype (CRI) associated with anti-ABA antibodies in A/J mice, when injected intravenously into normal A/J mice will stimulate ABA-specific suppressor T-cell responses (20).…”

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confidence: 99%

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Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.

Sy¹,

Brown²,

Benacerraf³

et al. 1980

The Journal of Experimental Medicine

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Delayed-type hypersensitivity (DTH) to p-azobenzenearsonate (ABA) can be induced in A/J mice with intravenous injection of minute amounts of anti-cross-reactive idiotypic (CRI) antibodies, providing that the animals have been pretreated 2 d earlier with low doses of cyclophosphamide (50 mg/kg). However intravenous injection of the F(ab')2 fragments of the anti-CRI antibodies or subcutaneous administration with anti-CRI antibodies induces comparable immunity in both cyclophosphamide-pretreated and normal nontreated animals. Furthermore adoptive transfer experiments indicate that lymph node cells taken from animals sensitized with anti-CRI 4 d earlier can adoptively transfer immunity to naive recipients. Transfer of immunity is mediated by a population of thymus-dependent (T) cells, which express idiotypic structures on their surface. Treatment of effector cells with either anti-theta serum or anti-idiotypic antibodies plus complement completely abrogated their ability to transfer immunity. In addition idiotype-bearing suppressor T cells induced with ABA-coupled spleen cells inhibit the development of ABA-specific DTH induced with anti-CRI antibodies. Genetic analysis revealed that the ability of anti-CRI antibodies to induce ABA-specific DTH was linked to Igh-1 heavy-chain allotype. Anti-idiotypic antibodies to the major CRI associated with anti-ABA antibodies in A/J mice failed to induce significant immunity in BALB/c mice (H-2d, Igh-1a). Nevertheless, they were able to induce significant immunity in C.AL20 mice (H-2d, Igh-1d) which possess a heavy-chain allotype similar to that of A/J mice.

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Section: Antigen-and Receptor-driven Regulatory Mechanismsmentioning

confidence: 99%

mentioning

confidence: 99%

Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.

Sy¹,

Brown²,

Benacerraf³

et al. 1980

The Journal of Experimental Medicine

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“…We specifically have chosen the hapten ABA, because A/J mice, when immunized with ABA-KLH, produce a restricted spectrum of anti-ABA antibodies, 20-70% of which bear a specific CRI (13,18,(25)(26)(27). Because the cross-reactive idiotype may be reflective of a germ-line gene product, an analysis of ABA-specific T cells (suppressor, helper, or effector) or the ABA-specific SF might allow structural comparisons to CRI bearing Ig as has been done in other systems (28)(29)(30).…”

Section: Aba-celt Induced Suppressor T-cells-derived-suppressor Factomentioning

confidence: 99%

Mechanisms of regulation of cell-mediated immunity. III. The characterization of azobenzenearsonate-specific suppressor T-cell-derived-suppressor factors.

Greene¹,

Bach²,

Benacerraf³

1979

The Journal of Experimental Medicine

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Delayed type hypersensitivity to the hapten azobenzenearsonate (ABA) can be induced and suppressed by the administration of hapten-coupled syngeneic spleen cells by the appropriate route. Suppressor T cells stimulated by the intravenous administration of ABA-coupled spleen cells have been shown to produce a discrete subcellular factor(s) which is capable of suppressing delayed type hypersensitivity to azobenzenearsonate in the mouse. Such suppressor factors may be produced by the mechanical disruption of suppressor cells or by placing such suppressor cells in culture for 24 h. The suppressor factor(s) (SF) derived from ABA-specific suppressor cells exhibit biological specificity for the suppression of ABA delayed type hypersensitivity (DTH), but not trinitro-phenyl DTH, as well as the capacity to bind to ABA immunoadsorbents. Passage of suppressor factor(s) over reverse immunoadsorbents utilizing a rabbit anti-mouse F(ab')2 antiserum demonstrated that the antigen-specific T-cell derived SF does not bear conventional immunoglobulin markers. The suppressor factor(s) are not immunoglobulin molecules was further demonstrated by the inability of anti-ABA antibodies to suppress ABA DTH. Gel filtration of ABA suppressor factor(s) showed that the majority of the suppressive activity was present in a fraction with molecular weight ranging between 6.8 x 10(4) and 3.3 x 10(4) daltons. We also analyzed for the presence of determinants encoded by the H-2 major histocompatibility complex (MHC) and found that immunoadsorbents prepared utilizing antisera capable of interacting with gene products of the whole or selected gene regions of H-2 MHC, i.e., B10.D2 anti-B10.A and B10 anti-B10.A immunoadsorbents, retained the suppressive activity of ABA-SF. Elution of such columns with glycine HCl buffers (pH 2.8) permitted recovery of specific suppressive activity. Taken collectively such data supports the notion that suppressor T-cell-derived ABA suppressor factors have antigen-binding specificity as well as determinants controlled by the K end of the H-2 MHC. The distribution of strains capable of making SF has also been analyzed. The relationship of the antigen-binding specificity to VH gene products is discussed in this and the companion paper.

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“…Furthermore, anti-Id antibodies are able to suppress the synthesis by normal B cells of antibodlies carrying the relevant idiotypes. This suppression can be the result of either a direct effect of anti-Id antibodies on the precursors of antibody-forming cells, as shown in the inulin and phosphorylcholine systems (5,6), or by generation of suppressor T cells that can inhibit helper functions in the arsonate and streptococcal systems (7,8).…”

Section: Introductionmentioning

confidence: 99%

In vitro idiotypic suppression of chronic lymphocytic leukemia lymphocytes secreting monoclonal immunoglobulin M anti-sheep erythrocyte antibody.

Bona¹,

Fauci²

1980

J. Clin. Invest.

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Studies of Structure and Immunosuppression of a Cross‐Reactive Idiotype in Strain A Mice

Cited by 124 publications

References 49 publications

Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.

Antigen- and receptor-driven regulatory mechanisms. III. Induction of delayed type hypersensitivity to azobenzenearsonate with anti-cross-reactive idiotypic antibodies.

Mechanisms of regulation of cell-mediated immunity. III. The characterization of azobenzenearsonate-specific suppressor T-cell-derived-suppressor factors.

In vitro idiotypic suppression of chronic lymphocytic leukemia lymphocytes secreting monoclonal immunoglobulin M anti-sheep erythrocyte antibody.

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