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5. In vivo immunosuppression by targeting a novel protease receptor

Author

Duchosal, Michel A., Rothermel, Annette L., McConahey, Patricia J., Dixon, Frank J., and Altieri, Dario C.

Subjects
Immunosuppression -- Analysis, Proteases -- Analysis, Environmental issues, Science and technology, Zoology and wildlife conservation
Abstract

Membrane receptors for blood proteinases control clotting and fibrinolytic cascades, signal transduction and the growth of mesenchymal cells. It is not clear whether the mechanisms in developing vascular injury take part in the production of an immune response. A new role for protease receptors in regulating immune response is derived. A potential target for therapeutic immunosuppression in humans is also identified.

Published
1996

21. Increased survival times of New Zealand hybrid mice immunosuppressed by graft-versus-host reactions.

Author

Lehman, David H., Wilson, Curtis B., and Dixon, Frank J.

Subjects
IMMUNOREGULATION, IMMUNOLOGIC diseases, AUTOIMMUNE diseases, LYMPHOID tissue, MOUSE diseases
Abstract

New Zealand mice develop autoimmune disease usually accompanied by glomerulonephritis. A graft-versus-host reaction was induced in New Zealand Black × New Zealand White F1 hybrid mice by administration of New Zealand White spleen cells. The mice so treated had diminished antibody responses to both an exogenous antigen (sheep red blood cells) and an endogenous antigen (native DNA). They had much less glomerulonephritis and increased survival times compared to unmanipulated controls, apparently due to immunosuppression. Similar hybrid mice treated with high doses of cyclophosphamide (70 mg/kg/week) were more immunosuppressed than mice with graft-versus-host reactions and had even greater survival times. [ABSTRACT FROM AUTHOR]

Published
1976
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43. IMMUNE COMPLEX DISEASES.

Author

Dixon, Frank J.

Subjects
*IMMUNE complex diseases, *IMMUNOLOGIC diseases, *IMMUNOGLOBULINS, *EXTRACELLULAR fluid, *BODY fluids, *RETICULOENDOTHELIAL granulomas, *PHAGOCYTES, *LEUCOCYTES
Abstract

The essential feature of immune complex diseases is that they are caused by antigen-antibody complexes formed in the circulation or in interstitial fluids. Complexes so formed are for the most part taken up and catabolized to harmless end products by reticuloendothelial phagocytes and blood leukocytes, but a small fraction eludes these cells and tends to accumulate in filtering structures throughout the body such as glomeruli and blood vessels where they can cause injury. This accumulation is apparently determined by anatomic and physiologic, not immunologic, factors so that the sites of injury or disease need have no immunologic relationship to the causative antigen or antibody.

Published
1972
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