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Publication Detail
Transgenic models of tolerance and autoimmunity: with special reference to systemic lupus erythematosus
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Ravirajan CT, Isenberg DA
  • Publication date:
    2002
  • Pagination:
    843, 849
  • Journal:
    Lupus
  • Volume:
    11
  • Issue:
    12
  • Print ISSN:
    0961-2033
  • Keywords:
    ACTIVATION, anergy, antigen receptor, As, autoimmune, Autoimmune Diseases, AUTOIMMUNE-DISEASES, Autoimmunity, B CELL, B-cell, cell, Cell Lineage, CELLS, CHALLENGE, DELETION, development, disease, Diseases, DISTINCT, EVENTS, EXAMPLE, FATE, GENE, Genes, IM, IMMUNOGLOBULIN, Immunoglobulin Gene, IMMUNOGLOBULIN GENES, in vivo, in-vivo, knockout, LA, Lupus, LYMPHOCYTE, Lymphocytes, MECHANISM, mechanisms, model, MODELS, Molecular, mouse, process, processes, SYSTEMIC, SYSTEMIC LUPUS ERYTHEMATOSUS, SYSTEMIC-LUPUS-ERYTHEMATOSUS, T cell, T CELLS, T-CELL, T-CELLS, tolerance, transgenic, understanding, vivo
  • Notes:
    UI - 22416390 DA - 20030116 IS - 0961-2033 LA - eng PT - Journal Article SB - IM
Abstract
Transgenic and knockout mouse carrying rearranged antigen-receptor genes have been invaluable for the elucidation of basic mechanisms in autoimmunity and have contributed new models of human autoimmune diseases. Several examples of transgenic models expressing rearranged immunoglobulin genes have been described. These models have provided a window into the events involved in this process, allowing the development and fate of self-reactive lymphocytes to be followed in vivo. In the B cell lineage, as in T cells, self-reactive cells have been found to undergo several distinct fates in vivo: they can be physically eliminated, functionally inactivated, or they can persist unchanged or become activated. Nevertheless the precise understanding of the molecular events leading to lymphocyte deletion, anergy or activation remains a challenge
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