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From The Department of Pathology, Harvard Medical School, Boston, Massachusetts 02115
Abstract
The cellular requirements for the development of primary trinitrophenyl (TNP)-specific plaque-forming cell (PFC) responses to TNP-
X in cultures of spleen cells from normal mice and from mice immunized 7 days earlier with
X were compared. Significant enhancement of the primary anti-TNP PFC responses of both the
G and
M immunoglobulin classes was demonstrated in cultures of
X-primed spleen cells stimulated with TNP-
X at a concentration suboptimal for normal spleen cells. After separation of normal and
X-primed spleen cells into macrophage and lymphoid cell populations on the basis of the ability of macrophages to adhere to plastic, it was demonstrated that primary TNP-specific PFC responses of normal spleen cells were strictly dependent on the presence of the macrophages, while the responses of
X-primed spleen cells were much less dependent on their presence.
The depletion of
-bearing cells from cultures of normal spleen cells by treatment with anti-
serum and complement minimized primary TNP-specific PFC responses to TNP-
X. Depletion of the
-bearing cells from cultures of spleen cells from
X-primed mice reduced primary TNP-specific PFC responses only 10% to 50%, while the primary anti-horse red cell PFC responses in the same cell preparations were reduced over 90%.
Footnotes
1 This investigation was supported by United States Public Health Service Research Grants AI-09897 and AI-09920 from the National Institute of Allergy and Infectious Diseases.
2 Present address: Department of Medicine, University Hospital, University of California, San Diego, La Jolla, California 92037.
3 Recipient of United States Public Health Service Research Career Development Award 1K4-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, Boston, Massachusetts 02115.
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