Search

Normal lymphocytes labelled with 51Crk were injected into mice at various stages of lethal and non-lethal malaria infections. Marked alterations were seen in the uptake into spleen and liver, which correlated with the outcome of the infection. Non-lethal infections and lethal infections in mice protected by vaccination caused increased uptakes, especially in the liver. In lethal infections, particularly Plasmodium berghei, uptakes were below normal values at certain times: this was apparently due to destruction of lymphocytes, probably caused by autoantibody. [ABSTRACT FROM AUTHOR]

Investigates the differences in effectiveness against Plasmodium yoelii and P. Berghei in the protection of mice against malaria by a killed vaccine. Observation that the protection was specific and at least partly mediated by a serum factor; Consideration of possible reasons for the difference and discussion of the mechanisms by which vaccination works against P. yoelii.

Examines the response of mouse helper T cells to plasmodial and babesial parasites. Capability of helper T cells to recognize all the parasites but was unable to distinguish between them; Role of vaccination with formalin-fixed parasites in augmenting helper T cell responses; Helper T cell response in mice resistant to infection because of prior recovery from a homologous or heterologous infection; Role of T cells and helper T cell subpopulation on the ability of a mouse to resist plasmodial and babesial infection.

Transgenic mice carrying a modified human tumour necrosis factor (huTNF)/β-globin gene construct linked to the T-cell-specific locus control region of the human CD2 gene express huTNF in their T cells which is released into the circulation and causes the development of a wasting syndrome. We now report that the mice develop anaemia, probably through enhanced erythrophagocytosis rather than inhibition of reticulocyte production. Thus autologous erythrocytes, as well as sheep erythrocytes, were cleared more rapidly from the circulation of transgenic mice than from littermate controls. By contrast, peritoneal macrophages from transgenic mice were less phagocytic in vitro than cells from controls. They also secreted less murine (mu)TNF when stimulated by either bacterial lipopolysaccharide or toxic malarial antigens. The yields of muTNF approached normal levels, however, when these refractory cells from the transgenic mice were stimulated in the presence of a high concentration of indomethacin, suggesting that the production of muTNF was inhibited by enhanced synthesis of prostaglandins. The parasitaemia of transgenic mice infected with Plasmodium yoelii was about 10-fold less at its peak than in controls, although it followed the same time-course, and the multiplication of P. chabaudi was inhibited to an even greater degree. This control of parasitaemia may also be explained by enhancement of macrophnge activity, mediated by huTNF acting on the murine p55 receptor, presumably by increasing the removal of parasites by phagocytosis or their killing by toxic products released by the activated macrophages. These observations suggest that a factor in the anaemia of human malaria may be macrophage activation caused by the secretion of TNF that occurs in this disease. [ABSTRACT FROM AUTHOR]

Presents a letter to the editor on endotoxin induced tumor-necrosis serum.

Presents a letter to the editor about anti-lymphocyte autoantibodies in lethal mouse malaria and their absence in an irradiation-induced non-lethal variant.