SCID Mouse as a Model of Systemic Lupus Erythematosus

Proven Lupus Treatment By Dr Gary Levin

Proven Lupus Treatment System by Dr. Gary Levin

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The SCID mouse is a mutant of the mouse strain C.B-17, an IgHb congenic partner of the BALB/c (H-2d) mouse. The mutation in the SCID mouse is autosomal recessive and is mapped to the centromeric region of chromosomes (Vladutiu 1993). The effect of the SCID mutation is manifested in lymphoid cells. Myeloid, erythroid, antigen-presenting cells, splenic colony stem cells, and NK cell development and function are not influenced by the SCID mutation. There is a defect in a DNA break repair enzyme; this V(D)J recombinase-associated defect affects somatic rearrangement of TCR genes and immunoglobulin genes in B lymphocytes. The development of T lymphocytes is stopped at the CD4-, CD8 immature thymocyte stage, and the maturation of B lymphocytes is arrested at the pro-B lymphocytes (from the review of Vladutiu 1993).

Because the SCID mouse is deficient in active T and B lymphocytes, this mutant can be reconstituted with different allogeneic as well as xenogeneic hematopoietic and lymphoid cells. Indeed, studies using SCID mice as the recipients of peripheral blood lymphocytes from patients with SLE or experimental SLE mice have been reported (Duchosal et al. 1990, Reininger et al. 1992, Segal et al. 1992,Vladutiu 1993). Dixon and associates reported that SCID mice reconstituted with peripheral blood lymphocytes from patients with SLE showed the long-term presence of donor-type autoantibodies in their sera, as well as human immunoglobulin deposits in their renal glomeruli (Duchosal et al. 1990). The development of autoimmune disease can also be induced in SCID mice populated with long-term in vitro proliferating B/W F1 pre-B cells (Reininger et al. 1992). This SCID model for SLE allows us to directly evaluate the effects of cellular and humoral function in the progression of SLE and enables us to compare various potential therapies (e. g., the use of antisense oligonucleotides, anti-TCR antibodies) simultaneously on the disease-producing cells of a single human patient.

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