Literature DB >> 8405065

The effect of bone marrow and thymus chimerism between non-obese diabetic (NOD) and NOD-E transgenic mice, on the expression and prevention of diabetes.

N M Parish1, P Chandler, R Quartey-Papafio, E Simpson, A Cooke.   

Abstract

The non-obese diabetic (NOD) mouse is an established animal model of the autoimmune disease, insulin-dependent diabetes mellitus (IDDM). The NOD-E mouse is a transgenic mouse which expresses the I-E molecule (absent in NOD mice). Expression of I-E protects these mice from both insulitis and IDDM. We have investigated the possible mechanisms of this protection by constructing bone marrow, and combined bone marrow and thymus chimeras between NOD and NOD-E mice. Our data suggest that thymic epithelium may play no direct role in either protection against, or promotion of, IDDM. Protection from diabetes is provided either by NOD-E donor bone marrow or NOD-E recipient non-thymic radioresistant cells. The means by which protection may be achieved in this system are discussed.

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Year:  1993        PMID: 8405065     DOI: 10.1002/eji.1830231042

Source DB:  PubMed          Journal:  Eur J Immunol        ISSN: 0014-2980            Impact factor:   5.532


  12 in total

Review 1.  Facilitating physiologic self-regeneration: a step beyond islet cell replacement.

Authors:  Pleunie P M Rood; Rita Bottino; A N Balamurugan; Yong Fan; David K C Cooper; Massimo Trucco
Journal:  Pharm Res       Date:  2006-01-01       Impact factor: 4.200

2.  Alleviation of insulitis in NOD mice is associated with expression of transgenic MHC E molecules on primary antigen-presenting cells.

Authors:  B Pilström; J Böhme
Journal:  Immunology       Date:  1997-04       Impact factor: 7.397

3.  Protective major histocompatibility complex allele prevents type 1 diabetes by shaping the intestinal microbiota early in ontogeny.

Authors:  Michael Silverman; Lindsay Kua; Alessandro Tanca; Mauro Pala; Antonio Palomba; Ceylan Tanes; Kyle Bittinger; Sergio Uzzau; Christophe Benoist; Diane Mathis
Journal:  Proc Natl Acad Sci U S A       Date:  2017-08-22       Impact factor: 11.205

4.  H2-A polymorphism contributes to H2-Ebeta-mediated protection in collagen-induced arthritis.

Authors:  M A Gonzalez-Gay; E Zanelli; S D Khare; C J Krco; M M Griffiths; H S Luthra; C S David
Journal:  Immunogenetics       Date:  1996       Impact factor: 2.846

5.  A role of Hsp60 in autoimmune diabetes: analysis in a transgenic model.

Authors:  O S Birk; D C Douek; D Elias; K Takacs; H Dewchand; S L Gur; M D Walker; R van der Zee; I R Cohen; D M Altmann
Journal:  Proc Natl Acad Sci U S A       Date:  1996-02-06       Impact factor: 11.205

6.  Antidiabetogenic MHC class II promotes the differentiation of MHC-promiscuous autoreactive T cells into FOXP3+ regulatory T cells.

Authors:  Sue Tsai; Pau Serra; Xavier Clemente-Casares; Jun Yamanouchi; Shari Thiessen; Robyn M Slattery; John F Elliott; Pere Santamaria
Journal:  Proc Natl Acad Sci U S A       Date:  2013-02-11       Impact factor: 11.205

Review 7.  Dissecting autoimmune diabetes through genetic manipulation of non-obese diabetic mice.

Authors:  Y Yang; P Santamaria
Journal:  Diabetologia       Date:  2003-10-28       Impact factor: 10.122

8.  Studies on the thymus of non-obese diabetic (NOD) mice: effect of transgene expression.

Authors:  L A O'Reilly; D Healey; E Simpson; P Chandler; T Lund; M A Ritter; A Cooke
Journal:  Immunology       Date:  1994-06       Impact factor: 7.397

9.  Major histocompatibility complex class II molecules can protect from diabetes by positively selecting T cells with additional specificities.

Authors:  F Lühder; J Katz; C Benoist; D Mathis
Journal:  J Exp Med       Date:  1998-02-02       Impact factor: 14.307

10.  A mechanism for the major histocompatibility complex-linked resistance to autoimmunity.

Authors:  D Schmidt; J Verdaguer; N Averill; P Santamaria
Journal:  J Exp Med       Date:  1997-10-06       Impact factor: 14.307

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