DESCRIPTION:

QTL associated with insulin dependent diabetes susceptibility 9. This interval was obtained by using a fixed interval width of 25 Mbp around the peak marker (124439115)

LABEL:

QTL-Idd9-Mouse-Chr 4

SCORE TYPE:

Binary

DATE ADDED:

2012-04-02

DATE UPDATED:

2024-04-25

SPECIES:

URI:

http://www.informatics.jax.org/searches/accession_report.cgi?id=MGI:96411

AUTHORS:

Cox SL, Stolp J, Hallahan NL, Counotte J, Zhang W, Serreze DV, Basten A, Silveira PA

TITLE:

Enhanced responsiveness to T-cell help causes loss of B-lymphocyte tolerance to a -cell neo-self-antigen in type 1 diabetes prone NOD mice.

JOURNAL:

European journal of immunology Dec 2010, Vol 40, pp. 3413-25

ABSTRACT:

Self-reactive B lymphocytes contribute to type 1 diabetes pathogenesis as APC and auto-Ab producers in NOD mice and humans. To shed light on the mechanisms responsible for the breakdown in B-lymphocyte self-tolerance to β-cell Ag, we utilised a model whereby hen-egg lysozyme (HEL)-specific Ig Tg (IgHEL-Tg)-Tg B lymphocytes were allowed to develop in or were transferred into mice expressing the HEL Tg under an insulin promoter (insHEL-Tg). IgHEL-Tg B lymphocytes enhanced type 1 diabetes susceptibility of insHEL-Tg NOD mice. A comparison of the tolerogenic activity of IgHEL-Tg B lymphocytes with NOD and non-autoimmune-prone C57BL/6 genetic backgrounds showed that both were rendered anergic in the presence of insHEL when competing with polyclonal B lymphocytes. Nevertheless, NOD IgHEL-Tg B lymphocytes transferred into insHEL-Tg mice were more readily susceptible to rescue from anergy than their C57BL/6 counterparts, following provision of in vivo T-cell help. The different tolerogenic outcomes were an intrinsic property of B lymphocytes rather than being related to the quality of T-cell help, with the defective response being at least partially controlled by genes mapping to insulin-dependent diabetes (Idd) susceptibility loci on Chromosome 1 (Idd5) and 4 (Idd9/11). PUBMED: 21108464
Find other GeneSets from this publication