Changes in the capacity of macrophages and T cells to produce interleukins during murine malaria infection.

Interleukin 1 (I1-1) produced by activated macrophages and interleukin 2 (I1-2) released by a subset of T lymphocytes upon antigen or mitogen stimulation are the soluble mediators involved in the mechanism of T-cell activation, proliferation, and differentiation. Since these T-cell responses are depressed during malaria infection, the capacity of macrophages to produce I1-1 following lipopolysaccharide (LPS) stimulation and that of lymphocytes to release I1-2 upon stimulation with concanavalin A (Con-A) in mice infected with either nonlethal Plasmodium yoelii (NLPY) or lethal Plasmodium berghei (PB) malaria parasites was analyzed. The results show that while adherent cells from spleen or peritoneal exudates of infected mice were able to produce I1-1, although to a different extent in the two infections, splenic lymphocytes were unable to produce I1-2, but capable of responding to it. This suggests that the diminished T-cell responses in malaria might be due to a defect of I1-2 synthesis.