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A role for alphabeta T cells in the resistant phase of the Brown Norway rat model of vasculitis.

https://arctichealth.org/en/permalink/ahliterature57380
Source
Clin Exp Immunol. 2005 Apr;140(1):32-40
Publication Type
Article
Date
Apr-2005
Author
C S Vinen
D R Turner
D B G Oliveira
Author Affiliation
Department of Renal Medicine, St George's Hospital Medical School, London, UK.
Source
Clin Exp Immunol. 2005 Apr;140(1):32-40
Date
Apr-2005
Language
English
Publication Type
Article
Keywords
Adoptive Transfer - methods
Animals
Anti-Infective Agents, Local - pharmacology
CD8-Positive T-Lymphocytes - immunology
Cecal Diseases - immunology
Cells, Cultured
Disease Models, Animal
Immune Tolerance - immunology
Killer Cells, Natural - immunology
Male
Mercuric Chloride - pharmacology
Rats
Rats, Inbred BN
Research Support, Non-U.S. Gov't
Spleen - immunology
T-Lymphocyte Subsets - immunology
T-Lymphocytes - drug effects - immunology
Vasculitis - immunology
Weight Loss - drug effects
Abstract
Administration of mercuric chloride (HgCl(2)) to Brown Norway rats causes Th2 dominated autoimmunity including a caecal vasculitis. Disease peaks 14 days after starting HgCl(2) after which animals immunoregulate spontaneously. In a third phase, if animals are rechallenged with HgCl(2) 6 weeks later they appear resistant, developing only attenuated disease. Previous studies suggested a role for CD8(+) cells as partial mediators of resistance but no groups had studied the role of alphabeta T cells, gammadelta T cells or natural killer (NK) cells in resistance. We used adoptive transfer and in vitro cell depletion to show that alphabeta T cells are also partially responsible for resistance. Donor animals were treated with HgCl(2) or saline and killed 21 days later. Cells from donor spleens were transferred into recipient animals which were challenged with HgCl(2) and killed 14 days later. Test recipients received spleen cells from HgCl(2)-treated donors after in vitro depletion of one subset of cells. Recipients receiving spleen cells from saline-treated donors remained susceptible to HgCl(2)-induced vasculitis; those receiving spleen cells from HgCl(2)-treated donors were resistant. Animals receiving alphabeta T-cell-depleted spleen cells from HgCl(2)-treated donors showed partial reversal of resistance. Our results suggest a role for alphabeta T cells in the resistant phase of the Brown Norway rat model of vasculitis.
PubMed ID
15762872 View in PubMed
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