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Biological Expressions of Lymphocyte Activation

III. Suppression of Plaque-Forming Cell Responses in Vitro by Supernatant Fluids from Concanavalin a-Activated Spleen Cell Cultures¹

From the Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115

Abstract

Mouse spleen lymphocytes activated by a mitogenic concentration of concanavalin A (Con A) secrete a factor(s), termed soluble immune response suppressor (SIRS), which is a potent, non-cytotoxic inhibitor of primary plaque-forming cell (PFC) responses by mouse spleen cells to heterologous erythrocytes in vitro. SIRS activity was detected in supernatant fluids of spleen cell cultures within 6 hr of stimulation with Con A and was maximal from 12 to 24 hr after stimulation. SIRS profoundly suppressed 5-day PFC responses when added to antigen-stimulated spleen cell cultures at initiation, was less effective when added 24 hr after initiation, and had no significant effect when added 48 or more hours after initiation. SIRS had to be present in antigen-stimulated spleen cell cultures only during the initial 24 hr of incubation to cause suppression of PFC responses which by kinetic analysis was not manifest until 120 hr of incubation. Background and antigen-stimulated IgM and IgG PFC responses were suppressed by SIRS.

Exposure to SIRS did not render spleen cells totally incapable of developing PFC responses to heterologous erythrocytes. Instead, antigen-stimulated PFC responses in control cultures and cultures containing SIRS had the same kinetics and were of comparable magnitude during the first 96 hr of incubation. Thereafter, however, PFC responses in cultures containing SIRS abruptly aborted and the SIRS-induced suppression of PFC responses became evident at 120 and 144 hr of incubation. Although the precise mechanism(s) of action of SIRS is unknown, it appears to function during the early, antigen-dependent phase of the immune response in vitro to abort full expression of the PFC response during the later exponential expansion of the clones of antibody-synthesizing cells.

Footnotes

¹ This investigation was supported by United States Public Health Service Grant AI-09897 from the National Institute of Allergy and Infectious Diseases and by a grant from the Anna Fuller Fund.

² Recipient of United States Public Health Service Special Fellowship 5-F03-AI-50,602 from the National Institute of Allergy and Infectious Diseases. Present address: Department of Microbiology and Immunology, Baylor College of Medicine, Houston, Texas 77025.

³ Recipient of United States Public Health Service Research Career Development Award 5K4-AI-70,173 from the National Institute of Allergy and Infectious Diseases.

Address correspondence and reprint requests to: Carl W. Pierce, Department of Pathology, Harvard Medical School, 25 Shattuck Street, Boston, Massachusetts 02115.

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