EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK

Hypergammaglobulinemia in mink was produced by the injection of crude tissue suspensions from mink with spontaneous Aleutian disease. The initiating factor was found to be resistant to 0.3 per cent formalin for 2 weeks but not 40 weeks at 5°C. Foreign antigens as well as formalinized normal mink tis...

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Detalles Bibliográficos
Autores principales: Henson, James B., Gorham, John R., Leader, Robert W., Wagner, Bernard M.
Formato: Texto
Lenguaje:English
Publicado: The Rockefeller University Press 1962
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137549/
https://www.ncbi.nlm.nih.gov/pubmed/13906569
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author Henson, James B.
Gorham, John R.
Leader, Robert W.
Wagner, Bernard M.
author_facet Henson, James B.
Gorham, John R.
Leader, Robert W.
Wagner, Bernard M.
author_sort Henson, James B.
collection PubMed
description Hypergammaglobulinemia in mink was produced by the injection of crude tissue suspensions from mink with spontaneous Aleutian disease. The initiating factor was found to be resistant to 0.3 per cent formalin for 2 weeks but not 40 weeks at 5°C. Foreign antigens as well as formalinized normal mink tissue from homologous and heterologous genotypes did not cause a detectable change in the serum protein values. Mink homozygous recessive for the Aleutian gene were found to be significantly more susceptible to the experimental disease. Possible pathogenetic mechanisms as well as similarities between the mink disease and certain immunologic and connective tissue diseases of man are discussed.
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spelling pubmed-21375492008-04-17 EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK Henson, James B. Gorham, John R. Leader, Robert W. Wagner, Bernard M. J Exp Med Article Hypergammaglobulinemia in mink was produced by the injection of crude tissue suspensions from mink with spontaneous Aleutian disease. The initiating factor was found to be resistant to 0.3 per cent formalin for 2 weeks but not 40 weeks at 5°C. Foreign antigens as well as formalinized normal mink tissue from homologous and heterologous genotypes did not cause a detectable change in the serum protein values. Mink homozygous recessive for the Aleutian gene were found to be significantly more susceptible to the experimental disease. Possible pathogenetic mechanisms as well as similarities between the mink disease and certain immunologic and connective tissue diseases of man are discussed. The Rockefeller University Press 1962-09-01 /pmc/articles/PMC2137549/ /pubmed/13906569 Text en Copyright © Copyright, 1962, by The Rockefeller Institute This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).
spellingShingle Article
Henson, James B.
Gorham, John R.
Leader, Robert W.
Wagner, Bernard M.
EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK
title EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK
title_full EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK
title_fullStr EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK
title_full_unstemmed EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK
title_short EXPERIMENTAL HYPERGAMMAGLOBULINEMIA IN MINK
title_sort experimental hypergammaglobulinemia in mink
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2137549/
https://www.ncbi.nlm.nih.gov/pubmed/13906569
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AT gorhamjohnr experimentalhypergammaglobulinemiainmink
AT leaderrobertw experimentalhypergammaglobulinemiainmink
AT wagnerbernardm experimentalhypergammaglobulinemiainmink

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