Dual role of macrophages in the suppression of interleukin 2 production and interleukin 2 receptor expression in trypanosome‐infected mice

Abstract

Lymph node cells derived from T. brucei‐infected mice fail to produce interleukin 2 (IL 2) subsequent to a potent mitogenic trigger and actively suppress the capacity of normal cells to produce IL 2 in co‐culture experiments. The depletion of Thy‐1⁺ cells does not decrease but rather increases the suppressive potential of the LNC derived from infected mice. A T cell‐enriched nylon wool‐nonadherent fraction, on the other hand, is not suppressive. The suppression of IL 2 production is promptly restored by the addition of prostaglandin synthesis inhibitors suggesting a key role of the prostaglandin‐producing macrophages. Our data indicate that such macrophages do not act indirectly through the induction of suppressor T cells, but rather directly interfere with the normal lymph node cells. In contrast to the essential role of prostaglandins in the impairment of IL 2 production, these mediators are not involved in the suppression of IL 2 receptor expression. Lymph node cells derived from Trypanosoma brucei‐infected mice fail to produce interleukin 2 (IL 2) subsequent to a potent mitogenic trigger and actively suppress the capacity of normal cells to produce IL 2 in co‐culture experiments. The depletion of Thy‐1⁺ cells does not decrease but rather increases the suppressive potential of the LNC derived from infected mice. A T cell‐enriched nylon wool‐nonadherent fraction, on the other hand, is not suppressive. The suppression of IL 2 production is promptly restored by the addition of prostaglandin synthesis inhibitors suggesting a key role of the prostaglandin‐producing macrophages. Our data indicate that such macrophages do not act indirectly through the induction of suppressor T cells, but rather interfere directly with the normal lymph node cells.