Abstract
We have demonstrated previously that spleen cells from mice bearing M-1 fibrosarcomas release low molecular weight factors capable of activating suppressor cells from unprimed normal spleen cells. Using Markbrook vessels to separate inducer and precursor populations, we found in the previous paper that cyclooxygenase inhibitors blocked the activation of suppressor cells and that this activation could be restored by exogenous PGE 1. In this paper we have examined the site of action of the prostaglandins in the activation of suppressor cells. To do so, we tested cell-free supernatants from cultured spleen cells of tumor-bearing mice (inducer cells) for the ability to activate suppressor cells from unprimed normal spleen cells (precursor cells). Supernatants from acetyl salicyclic acid (ASA) treated inducer cells did not activate suppressor cells and exogenous PGE 1 could not restore the activity of this supernatant. In contrast, if inducer cells were treated with ASA and then incubated with PGE 1, the supernatant was capable of activating suppressor cells. No role for prostaglandins at the level of the precursor cells or the effector suppressor cells was seen. These data suggest that the inducer cells in tumor-bearer spleens require prostaglandins for the release of an inducer factor but that prostaglandins are not required for the action of this factor on the precursor cells or for the effector function of the activated suppressor cells.
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