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Projection of an immunological self shadow within the thymus by the aire protein.

Science (New York, N.Y.) | Nov 15, 2002

http://www.ncbi.nlm.nih.gov/pubmed/12376594

Humans expressing a defective form of the transcription factor AIRE (autoimmune regulator) develop multiorgan autoimmune disease. We used aire- deficient mice to test the hypothesis that this transcription factor regulates autoimmunity by promoting the ectopic expression of peripheral tissue- restricted antigens in medullary epithelial cells of the thymus. This hypothesis proved correct. The mutant animals exhibited a defined profile of autoimmune diseases that depended on the absence of aire in stromal cells of the thymus. Aire-deficient thymic medullary epithelial cells showed a specific reduction in ectopic transcription of genes encoding peripheral antigens. These findings highlight the importance of thymically imposed "central" tolerance in controlling autoimmunity.

Pubmed ID: 12376594 RIS Download

Mesh terms: Aging | Animals | Autoantibodies | Autoantigens | Autoimmune Diseases | Autoimmunity | Epithelial Cells | Female | Gene Expression Profiling | Gene Expression Regulation | Gene Targeting | Humans | Lymphocytes | Male | Mice | Mice, Inbred C57BL | Mice, Knockout | Polyendocrinopathies, Autoimmune | Radiation Chimera | Reverse Transcriptase Polymerase Chain Reaction | Self Tolerance | Stromal Cells | T-Lymphocytes | Thymus Gland | Transcription Factors

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Associated grants

  • Agency: NIDDK NIH HHS, Id: 2 P30 DK36836-16
  • Agency: NIDDK NIH HHS, Id: 2T32 DK07260-26
  • Agency: NIDDK NIH HHS, Id: KO8-DK59958-01A1
  • Agency: NIDDK NIH HHS, Id: R01 DK60027-01
  • Agency: NCI NIH HHS, Id: T32CA70083-05

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