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Pathophysiology of Immune Hemolytic Anemia
- MICHAEL M. FRANK, M.D.;
- ALAN D. SCHREIBER, M.D.;
- JOHN P. ATKINSON, M.D.; and
- CHARLES J. JAFFE, M.D., Ph.D.
Abstract
Studies of the pathophysiology of autoimmune hemolytic anemia emphasize the important role of cell membrane receptors for various immunologically active proteins in the clearance of foreign or damaged particulate materials from the blood stream. Receptors for the Fc fragment of immunoglobulin G (IgG) antibodies and for opsonically active fragments of the third component of complement on cells of the reticuloendothelial system function to clear from the circulation erythrocytes coated with these proteins. Our studies show the key role that complement plays in the biologic function of immunoglobulin M (IgM) antibodies like many cold agglutinins and isoagglutinins. They show how complement may contribute to IgG-mediated cell destruction. The IgG and IgM antibodies have dramatically different effects on erythrocyte survival, and these effects explain many of the clinical differences between IgG- and IgM-mediated hemolytic diseases. These studies also show that many of the factors that influence the course of autoimmune hemolytic anemia act by altering the level of immunologic sensitization required to mediate clearance.
Article and Author Information
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▸An edited transcription of a Combined Clinical Staff Conference at the Clinical Center, Bethesda, Maryland, 25 March 1976, by the National Institute of Allergy and Infectious Diseases, National Institutes of Health, U.S. Department of Health, Education, and Welfare.
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▸Authors who wish to cite a section of this conference and specifically indicate its author can use this example for the form of reference:
SCHREIBER AD: An experimental model of immune hemolytic anemia, pp. 211-213 in FRANK MM (moderator): Pathophysiology of immune hemolytic anemia. Ann Intern Med 87:210-222, 1977
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▸Requests for reprints should be addressed to Michael M. Frank, M. D.; Chief, Laboratory of Clinical Investigation, and Clinical Direction, National Institute of Allergy and Infectious Diseases, Building 10, Room 11B-12, National Institutes of Health; Bethesda, MD 20014.
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- Received May 17, 1977.
- Accepted May 23, 1977.
