       Document 0252
 DOCN  M9640252
 TI    Autoimmune diabetes-prone NOD mice express the Lyt2 alpha (Lyt2.1) and
       Lyt3 alpha (Lyt3.1) alleles of CD8.
 DT    9604
 AU    Johnson-Tardieu JM; Walworth EW; Cornelius JG; Ye X; Schuster SM; Peck
       AB; Department of Pathology & Laboratory Medicine, University of;
       Florida College of Medicine, Gainesville 32610, USA.
 SO    Immunogenetics. 1996;43(1-2):6-12. Unique Identifier : AIDSLINE
       GENBANK/U34882
 AB    Predisposition to Type I insulin-dependent diabetes (IDD) has a strong
       underlying genetic basis involving class II major histocompatibility
       complex (MHC) genes as well as several non-MHC genetic systems. In the
       non-obese diabetic (NOD) mouse, a model for human IDD, genes associated
       with the appearance of immune cell infiltrates in the pancreatic islets
       (insulitis) and/or overt IDD have been mapped to chromosomes 1, 3, 6,
       11, and 17. A recent report has suggested that CD8+ lymphocytes of the
       NOD mouse might be deficient in the expression of the CD8 beta molecule,
       a protein encoded by a gene on chromosome 6. The CD8 beta molecule is a
       T-cell surface marker, the lack of which could affect selection in the
       thymus, possibly permitting auto-reactive T-cell clones to populate the
       peripheral lymphoid tissues. For this reason, we examined the expression
       of the CD8 molecule by lymphocytes in the NOD mouse. Results indicate
       that the NOD mouse is not deficient in its transcription of detectable
       mRNA encoding either the CD8 alpha or beta subunits. However, the NOD
       mouse expresses the Lyt2 alpha and Lyt3 alpha alleles, suggesting that a
       portion of chromosome 6 centromeric to the diabetes-susceptibility
       genetic region is derived from an ancestry common to AKR and, like AKR,
       the CD8 alpha and CD8 beta 3.1 (but not CD8 beta 3.2) subunits are
       detected on the cell surface of T lymphocytes of the NOD mouse.
       Interestingly, though, the CD8 beta 3.1 molecule may not be expressed in
       the NOD mouse to the same extent as it is expressed in the AKR/J mouse,
       suggesting the possibility that the NOD mouse possesses a defect
       somewhere between transcription and cell surface expression of the CD8
       beta molecule.
 DE    Alleles  Amino Acid Sequence  Animal  Antigens, Ly/*GENETICS  Autoimmune
       Diseases/*GENETICS/IMMUNOLOGY  Base Sequence  Comparative Study
       Complement/IMMUNOLOGY  Cytotoxicity, Immunologic  CD8-Positive
       T-Lymphocytes  Diabetes Mellitus, Insulin-Dependent/*GENETICS/IMMUNOLOGY
       Disease Models, Animal  Disease Susceptibility/GENETICS/IMMUNOLOGY
       Female  Gene Expression  Male  Mice  Mice, Inbred AKR/GENETICS  Mice,
       Inbred NOD/*GENETICS/IMMUNOLOGY  Mice, Inbred Strains  Molecular
       Sequence Data  Sequence Alignment  Sequence Homology, Nucleic Acid
       Support, Non-U.S. Gov't  T-Lymphocyte Subsets/*IMMUNOLOGY  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).

