Modulation of Spleen and Thymus Lymphoid Subsets by In Vivo Administration of di-M-PGE2 in Normal and Tumor-Bearing Mice
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Prostaglandin E2 (PGE2) have been implicated both in experimental tumor growth and in the modulation of immune response (reviewed in 1, 2). Regarding to their immunomodulating action, PGE2 are known to exert a suppressive activity after in vitro and in vivo treatment. However, in some conditions, they are also able to cause enhancing effects on the immune system (3,4,5). We have previously demonstrated that the in vivo administration of 16,16 dimethyl-PGE2-methyl ester (di-M-PGE2), a long-acting synthetic analog of PGE2, causes differential effects on the immune response in normal or tumor-bearing mice and that these effects could be related to the inhibition of tumor growth (reviewed in 6). Thus di-M-PGE2 has been clearly shown to inhibit in normal mice a variety of immune functions as the number of plaque forming cells from spleen, the seric hemagglutinin titers or the delayed hypersensitivity reaction to sheep erythrocytes, as well as natural killer (NK) activity or mitogen induced IL-2 production. On the other hand, PGE2 has been able to enhance the same functions in B-16 melanoma tumor-bearing mice (7,8,9).
KeywordsSpleen Cell Lymphocyte Subset Tumor Inoculation Sheep Erythrocyte Tumor Bearing Mouse
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