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Induction of diabetes in NOD‹–›C57BL/6 embryo aggregation chimeras by cyclophosphamide through preferential depletion of C57BL/6 lymphocytes
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department for Cell and Molecular Biology, University of Umeå, Umeå, Sweden)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department of Cell and Molecular Biology. University of Umeå)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). Department of Paediatrics, University of Rome ‘La Sapienza’ Rome, Italy. (Department for Cell and Molecular Biology, University of Umeå, Umeå, Sweden)
Umeå University, Faculty of Medicine, Department of Molecular Biology (Faculty of Medicine). (Department for Cell and Molecular Biology, University of Umeå, Umeå, Sweden)
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1996 (English)In: Journal of Autoimmunity, ISSN 0896-8411, E-ISSN 1095-9157, Vol. 9, no 4, 493-499 p.Article in journal (Refereed) Published
Abstract [en]

The majority of embryo aggregation (EA) mouse chimeras between non-obese diabetic (NOD) mice and C57BL/6 (B6) mice show clear signs of insulitis frequently accompanied by beta-cell destruction. Less than 5% of these chimeras, however, spontaneously progress to autoimmune diabetes, an incidence far lower than observed in NOD mice. The resistance in chimeras can be accounted for by the target organ chimerism and/or the immune system chimerism. To investigate the mechanism(s) controlling diabetes resistance in these mice, we studied a total of 92 NOD<-->B6 EA chimeras that showed overt lymphoid chimerism and treated 34 chimeras with cyclophosphamide (CY), a compound known to precipitate an acute form of insulin-dependent diabetes mellitus (IDDM) in pre-diabetic NOD mice, by interfering with regulatory mechanisms. We found that CY-treated EA chimeras displayed an increase in the NOD:B6 lymphocyte ratio and 32% of them developed diabetes that could be adoptively transferred to irradiated NOD or NOD-rag-2-/- mice. These findings suggest that lymphocyte chimerism rather than beta-cell chimerism accounts for diabetes resistance in NOD<-->B6 EA chimeras and that the susceptibility to CY-induced diabetes may be related to the proportion of NOD versus B6 lymphoid cells.

Place, publisher, year, edition, pages
Elsevier, 1996. Vol. 9, no 4, 493-499 p.
Keyword [en]
immunoregulation, organ-specific autoimmunity, IDDM, NOD mouse
National Category
Basic Medicine
Research subject
Immunology
Identifiers
URN: urn:nbn:se:umu:diva-87684DOI: 10.1006/jaut.1996.0066PubMedID: 8864824OAI: oai:DiVA.org:umu-87684DiVA: diva2:710387
Available from: 2014-04-07 Created: 2014-04-07 Last updated: 2017-12-05Bibliographically approved
In thesis
1. Cellular and genetic components in the development of IDDM in NOD mice.
Open this publication in new window or tab >>Cellular and genetic components in the development of IDDM in NOD mice.
1996 (English)Doctoral thesis, comprehensive summary (Other academic)
Place, publisher, year, edition, pages
Umeå: Umeå universitet, 1996. 80 p.
Series
Umeå University medical dissertations, ISSN 0346-6612 ; 464
Keyword
non-obese diabetic, IgVh gene utilisation, immunoregulation, programmed cell death, genetic linkage analysis
National Category
Basic Medicine
Research subject
Immunology
Identifiers
urn:nbn:se:umu:diva-87787 (URN)91-7191-150-2 (ISBN)
Public defence
1996-03-22, Institutionen för Mikrobiologi, föreläsningssalen, Umeå universitet, Umeå, 09:30
Supervisors
Available from: 2014-04-11 Created: 2014-04-09 Last updated: 2014-04-11Bibliographically approved

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Colucci, FrancescoLejon, KristinaCilio, Corrado M.Bergqvist, IngelaHolmberg, Dan
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