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Effect of Bone Marrow Depletion on Prostaglandin E-Producing Suppressor Macrophages in Mouse Spleen

机译:骨髓耗竭对小鼠脾脏前列腺素E抑制巨噬细胞的影响

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The i.p. injection of Corynebacterium parvum (CP) into CBA/J mice effected increases in macrophage colony-forming cells (M-CFC) when spleen cells were cultured with L cell culture filtrate as a course of colony-stimulating factor. Significant increases in phagocytic macrophages with Fc receptors for IgG2a and Igc2b immune complexes were additionally noted among the spleen cells in these mice. These m0 effectively inhibited Con A-induced lymphocyte proliferation, probably reflecting a 10-fold increase above normal controls in prostaglandin E to 47 mg 3,000,000 spleen cells/ml. To determine whether the suppressor macrophages are immediate derivatives of splenic M-CFC, we tried to induce suppressor macrophages by the injection of CP by the earlier administration of the bone-seeking isotope, SR89. This procedure reduced M-CFC in the bone marrow to less than 1% or normal for more than 30 days. Monocytes in the blood fell to 5% of normal by day 10 and were 30% on day 30. Levels of resident pertioneal Macrophages showed relatively little change in this period. Splenic M-CFC increased to 20-fold higher than the SR88 controls. CP-induced suppressor macrophages activity, however, was sharply reduced in SR89 marrow-depleted mice on day 10. There was a threefold increase in the number of phagocytic M/binding IgG2a immune complexes. The kinetics of recovery of suppressor M0 activity showed that on days 20,30 and 50 after SR89 injection the activities reached 20%, 30%, and 70% of the cold control, respectively, and correlated with the recovery of significant levels of M-CFC in the bone marrow.

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