Epitopes described in "Breaking self-tolerance in nonobese diabetic mice."

Reference
Article Authors:W M Ridgway; M Fassò; A Lanctot; C Garvey; C G Fathman
Article Title:Breaking self-tolerance in nonobese diabetic mice.
Reference Detail
Reference ID:1014522
Abstract:Unresponsiveness to self is maintained through two mechanisms of immune regulation: thymic-negative selection and peripheral tolerance. Although thymic-negative selection is a major mechanism to eliminate self-reactive T cells, normal mice have readily detectable populations of T cells reactive to self-proteins but do not exhibit autoimmune responses. It has been postulated that autoimmune disease results from breakdown or loss of peripheral tolerance. We present data that demonstrate that peripheral tolerance or unresponsiveness to self can be broken in nonobese diabetic (NOD) mice. Immunization of NOD mice (but not of conventional mice) with self-peptides caused an immune response to self-peptide with resultant autoproliferation of peripheral lymphocytes. Autoproliferation of self-reactive T cells in NOD mice resulted from the recognition and proliferation of the activated T cells to endogenously processed and presented self-antigens. This loss of self-tolerance demonstrated in vitro may well be the basis of NOD autoimmune disease in vivo.
Date:1996
Reference Type:Literature
PubMed ID:8666923
Journal:J Exp Med
Journal Volume:183
Article Pages:1657-62
Journal ISSN:1540-9538
Article Chemical List:Histocompatibility Antigens Class II;Myoglobin;Peptide Fragments
Article MeSH List:Amino Acid Sequence; Animals; Autoimmune Diseases(etiology); CD4-Positive T-Lymphocytes(immunology); Histocompatibility Antigens Class II(immunology); Immunization; Lymphocyte Activation; Mice; Mice, Inbred DBA; Mice, Inbred NOD(immunology); Molecular Sequence Data; Myoglobin(immunology); Peptide Fragments(immunology); Self Tolerance(immunology); Species Specificity
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