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Prevention and induction of occlusive coronary vascular disease in
autoimmune (W/B)F1 mice by haploidentical bone marrow transplantation:
possible role for anticardiolipin autoantibodies
H Mizutani, RW Engelman, K Kinjoh, Y Kurata, S Ikehara and RA Good
Department of Pediatrics, University of South Florida, All Children's
Hospital, St Petersburg 33701.
Male (NZW x BXSB)F1 (W/BF1) mice develop systemic autoimmunity involving
autoantibodies, thrombocytopenia, lupus nephritis, and coronary vascular
disease with myocardial infarction (CVD). To determine whether this murine
lupus-associated CVD could be transferred to otherwise autoimmune-resistant
(C57BL/6 x C3H/He)F1 (B6C3F1) mice via W/BF1 T-cell-depleted marrow (TCDM)
transplants, or conversely whether the CVD of W/BF1 mice could be prevented
by the reciprocal transplant, reciprocal haploidentical transplants of TCDM
were performed. CVD developed only in mice with systemic autoimmunity. Mice
that developed lupus had glomerulonephritis and thrombocytopenia and also
had elevated titres of autoantibodies to double-strand DNA, cardiolipin,
and platelets and elevated levels of circulating immune complexes. Of
control W/BF1 mice, 80% developed lupus, and of these, 81% developed CVD
with a mean grade of 2.5 +/- 0.8. Engraftment of W/BF1 mice with B6C3F1
marrow protected 90% of the recipients from the development of lupus, and
none developed CVD. Engraftment of B6C3F1 mice with W/BF1 marrow induced
lupus in 60% of the recipients, and of those, 33% developed CVD with a mean
grade of 1.3 +/- 0.3. The B6C3F1 recipients of W/BF1 marrow which developed
CVD had significantly higher titres of autoantibodies to cardiolipin (aCL;
P < .01). These findings show that genetic abnormalities present in the
W/BF1 hematopoietic stem cells contribute to autoantibody development,
including aCL, and suggest that thrombogenic mechanisms induced by aCL may
contribute to the development of CVD in this form of murine lupus
erythematosus.
Volume 82,
Issue 10,
pp. 3091-3097,
11/15/1993
Copyright © 1993 by The American Society of Hematology
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