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Immunosuppressive Effects of Anti-lymphocyte Serum in Complement Deficient Mice. II. Evidence That Activity Is Mediated by C3 Independent Antibodies¹

From the Department of Pathology and Oncology, University of Kansas Medical Center, Kansas City, Kansas 66103 and the Department of Pathology, University of Connecticut, Farmington, Connecticut 06032

Abstract

The immunosuppressive effects of anti-lymphocyte serum (ALS) have been studied in both normal and C5-deficient mice which were depleted of the third component of complement (C3) by treatment with an inactivator isolated from cobra venom. BALB/c and treated B10·D2 old and new line mice which had been treated with C3 inactivator and either ALS or ALG had a marked reduction in both splenic plaque-forming cells and serum hemagglutinin and hemolysin titers 4 days after immunization with sheep erythrocytes compared to normal serumtreated C3 deficient controls. The effectiveness of ALG was particularly significant since this was devoid of C3. The mean survival time of C57BL/6 skin allografts was significantly prolonged on ALS treated, C3-depleted BALB/c mice compared to controls. These findings indicate that antibody-mediated immune adherence, cytolysis, and phagocytosis that require the participation of C3 are not essential for ALS activity. They support the hypothesis that cytophilic antibodies, which are capable of promoting phagocytosis independent of the complement system, are primarily responsible for the immunosuppressive activity of ALS.

Footnotes

¹ This investigation was supported in part by Public Health General Research Grant 1 SO 4 RRO 06147 and Grant AI-09947, National Institute of Allergy and Infectious Diseases.