Autoimmunity. Insights provided by the SCID mouse model.
CB17 SCID mice have severe combined immunodeficiency as a result of a mutation on chromosome 16 responsible for deficient activity of an enzyme involved in DNA repair. Because VDJ rearrangement does not occur, the humoral and cellular immune systems fail to mature. SCID mice do not reject human cells. They have been used to study the development of human tumors, human hematopoiesis and humoral responses in antibody-dependent organ-specific autoimmune diseases and in systemic lupus erythematosus. Studies involving grafting of synovial membrane under the renal capsule or in the subcutaneous tissue of SCID mice have provided information on the cells involved in the pathogenesis of rheumatoid arthritis. SCID mice have also been used to study adhesion molecules that play a role in the recruitment of lymphocytes in rheumatoid synovial tissue. The SCID mouse model provides new means of investigating immunologic treatments for rheumatoid arthritis.
Jorgensen
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Department of Immuno-Rheumatology, Gui de Chauliac Hospital, Montpellier, France.
Bologna
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Sany
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D000818:Animals; D001172:Arthritis, Rheumatoid / Q000276:immunology* / Q000473:pathology; D015551:Autoimmunity / Q000276:immunology*; D004195:Disease Models, Animal; D006801:Humans; D051379:Mice; D016513:Mice, SCID; D016511:Severe Combined Immunodeficiency / Q000276:immunology* / Q000473:pathology