A monoclonal anti‐idiotypic antibody against anti‐receptor antibodies from myasthenic sera

Lefvert, Ann‐Kari; James, Richard; Alliod, Christine; Fulpius, Bernard W.

doi:10.1002/eji.1830120917

Cited by 55 publications

(7 citation statements)

References 5 publications

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“…The potential usefulness of anti-id for antigenspecific immunosuppression is limited by the need to produce specific, anti-id antisera for each patient. Our results demonstrating crossreactivity remove this limitation, and are in concordance with findings in such diverse antigen systems as Hepatitis B (42), rheumatoid factor (43), p-azophenylarsonate (44), and more recent studies with acetylcholine receptor (45). The findings of crossreactivity and an anti-id that conformationally appears to be the "internal image" of antigen places this anti-id in the second class of a recently proposed system for categorizing anti-ids (46,47), and implies a common, antigenic determinant for the Rbabs binding site.…”

Section: Discussionsupporting

confidence: 91%

Production, isolation, and characterization of rabbit anti-idiotypic antibodies directed against human antithyrotrophin receptor antibodies.

Baker¹,

Lukes²,

Burman³

1984

J. Clin. Invest.

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A s bstract. Previous studies have shown that antiidiotypic antibodies can be developed in vivo through animal immunization with idiotype, and that these antibodies can be isolated from other anti-immunoglobulin antibodies by affinity purification. These techniques have relied on large amounts ofidiotype, which were produced either by hyperimmunization or by monoclonal antibodies, to serve as the affinity adsorbent. In the present study, we produced anti-idiotypic antibodies to human anti-thyroid-stimulating hormone (TSH) receptor antibodies by first injecting rabbits with (TSH receptor purified) IgG from Graves' patients. The resulting antiserum was then adsorbed with Sepharose-coupled TSH in an attempt to specifically bind and isolate the anti-idiotype. The antibody obtained from this process was shown to bind specifically to TSH receptor-binding antibodies from Graves' patients, and this binding could be inhibited by 56% with the addition of 10-4 M TSH but not by HCG (10-2 M). The anti-idiotype also bound to TSH, and this binding could be specifically inhibited by receptor-purified Graves' IgG (60% inhibition at 10 Ag/ml IgG), but not by IgG from normal subjects (no inhibition at 50 ,g/ml IgG). In a TSH receptor binding assay, the anti-idiotype could inhibit TSH receptor binding in Graves' sera at a 1,000-fold lower concentration than could anti-kappa/

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Section: Discussionsupporting

confidence: 91%

Production, isolation, and characterization of rabbit anti-idiotypic antibodies directed against human antithyrotrophin receptor antibodies.

Baker¹,

Lukes²,

Burman³

1984

J. Clin. Invest.

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“…The similarities between the behavior in cross-idiotype sys- (15). Therefore, the idiotypic network to which TH9 belongs may be distinct from the network(s) that gave rise to the other antibodies in this study.…”

Section: Resultsmentioning

confidence: 80%

“…The seven monoclonal antibodies were derived from three patients of different racial origin and they have different ligand binding properties (Table I). Five of them are autoantibodies against DNA or mitochondria; one binds to a monoclonal antibody bearing an internal image of the acetylcholine receptor (15), and may therefore also be an autoantibody; the binding specificity of the seventh is unknown. Of the six autoantibodies, 4G7, derived from a patient with lepromatous leprosy is of considerable in- terest.…”

Section: Resultsmentioning

confidence: 99%

Idiotypic markers of polyclonal B cell activation. Public idiotypes shared by monoclonal antibodies derived from patients with systemic lupus erythematosus or leprosy.

Mackworth‐Young¹,

Sabbaga²,

Schwartz³

1987

J. Clin. Invest.

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We investigated idiotypic markers of monoclonal antibodies derived from patients with polyclonal B-cell activation. Four monoclonal antibodies with different ligand binding specificities derived from a patient with lepromatous leprosy and three monoclonal anti-DNA antibodies from two patients with SLE were studied. Three new public idiotopes, which were common to monoclonal antibodies from all three patients, were defined by five polyclonal rabbit antiidiotypes, two monoclonal mouse antiidiotopes, and a monoclonal mouse antibody against a synthetic peptide that contains residues of the heavy chain CDR-1 of a monoclonal lupus anti-DNA antibody. The antibody against the synthetic idiotype was found to react with native immunoglobulins in solution. One idiotope was found to be consistently immunogenic in all animals tested. Since the three patients are of different ethnic origins, these shared idiotypes are probably encoded by germline V genes. These genes may be recurrently expressed in states of polyclonal B-cell activation, regardless of etiology. The results suggest that some autoantibodies arise by expansion of a pool of precursors in the normal antibody repertoire.

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“…There is much accumulated evidence for the role of anti-idiotypic antibodies in regulating immune responses to exogenous and endogenous antibodies (139,. For example, myasthenia gravis patients have endogenously formed anti-idiotypic antibodies directed against their acetylcholine receptor antibodies (250,270). Rheumatoid arthritis (268) and lupus erythematosis (255) are examples of two other diseases in which both idiotypic and anti-idiotypic antibodies are produced endogenously.…”

Section: Specificity Of Tsh Receptor Antibodies For Graves' Diseasementioning

confidence: 99%

Immune Mechanisms In Graves' Disease

1985

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A monoclonal anti‐idiotypic antibody against anti‐receptor antibodies from myasthenic sera

Cited by 55 publications

References 5 publications

Production, isolation, and characterization of rabbit anti-idiotypic antibodies directed against human antithyrotrophin receptor antibodies.

Production, isolation, and characterization of rabbit anti-idiotypic antibodies directed against human antithyrotrophin receptor antibodies.

Idiotypic markers of polyclonal B cell activation. Public idiotypes shared by monoclonal antibodies derived from patients with systemic lupus erythematosus or leprosy.

Immune Mechanisms In Graves' Disease

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