The Tohoku Journal of Experimental Medicine
Online ISSN : 1349-3329
Print ISSN : 0040-8727
Molecular Analysis of the Pathogenesis of Autoimmune Insulitis in NOD Mice
YUKIO KOIDETOSHIO KAIDOHMORITAKA NAKAMURATAKATO O. YOSHIDA
Author information
JOURNALS FREE ACCESS

Volume 173 (1994) Issue 1 Pages 157-170

Details
Download PDF (1720K) Contact us
Abstract

KOIDE, Y., KAIDOH, T., NAKAMURA, M. and YOSHIDA, T.O. Molecular Analysis of the Pathogenesis of Autoimmune Insulitis in NOD Mice. Tohoku J. Exp. Med., 1994, 173 (1), 157-170-Among diabetes-susceptibility genes in NOD mice, only Idd-1 has been clearly assigned: Idd-1 could be a gene complex composed of class II major histocompatibility complex (MHC) genes, I-Aβ and I -E. Employing restriction fragment length polymorphism (RFLP) analysis and nucleotide sequencing, we revealed that ILI and CTS mice, which are nondiabetic but are derived from the same Jcl-ICR mice as NOD mice, share the same class II MHC genes with NOD mice, suggesting that both ILI and CTS mice also possess susceptible Idd-1 genotype. This was supported by a breeding study. To compare the usage of T cell receptor (TCR) Vβ genes in NOD mice with that in ILI mice, we employed quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) which revealed that TCR Vβ usages of these mice were indistinguishable. RT-PCR method also revealed that the Vβ transcript of T cells infiltrating into pancreas of NOD mice was not restricted but was rather diverse. Since NOD and ILI mice share the same class I and II MHC antigens, we performed lymphocyte transfer experiments between these mice to examine the mechanism by which ILI mice do not develop insulitis. The results of reciprocal transfer of lymphocytes from NOD to ILI-nu/nu mice or from ILI to young NOD mice suggest that ILI mice exhibit autoantigens responsible for the development of insulitis but do not possess T cells reacting with islets. Of the diabetes-susceptibility genes, only in the case of Idd-1 is there any evidence for the identity of the gene products. ILI mice should provide more information on the products of the other diabetes-susceptibility genes of NOD mice.

Information related to the author
© Tohoku University Medical Press
Previous article Next article

Recently visited articles
  • About this Journal
    The Tohoku Journal of Experimental Medicine (TJEM) was founded in 1920 by professors of Tohoku Imperial University, Medical School. The TJEM has been published continuously, except for the year of 1946 just after the World War II. The TJEM is open to original articles in all branches of medical sciences. The TJEM also covers the fields of disaster-prevention science, including earthquake archeology.

  • Submitted manuscripts will be screened for plagiarism with Similarity Check (https://www.crossref.org/services/similarity-check/).
Journal news & Announcements
  • Subscriptions
    Inland subscriptions should be sent to Tohoku University Medical Press, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, JAPAN.

    Subscriptions from abroad should be addressed to MARUZEN CO., LTD., EXPORT DEPARTMENT, Postal address: P.O.Box 75, Shinagawa, Tokyo 140-8799, JAPAN. 
    e-mail: export@maruzen.co.jp

feedback
Top