ArticleImmunology1994
Anaemia and resistance to malaria in transgenic mice expressing human tumour necrosis factor.
Article in Immunology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 70 citations in OpenAlex.
- The Role of IL-10 in Malaria: A Double Edged Sword.Frontiers in immunology · 2019Review
- Hemozoin inhibition and control of clinical malaria.Advances in pharmacological sciences · 2014Review
- Allicin enhances host pro-inflammatory immune responses and protects against acute murine malaria infection.Malaria journal · 2012Article
- Malaria-related anaemia: a Latin American perspective.Memorias do Instituto Oswaldo Cruz · 2011Review
- The severity of malarial anaemia in Plasmodium chabaudi infections of BALB/c mice is determined independently of the number of circulating parasites.Malaria journal · 2008Article
- Human malarial disease: a consequence of inflammatory cytokine release.Malaria journal · 2006Review
- TNF as a malaria candidate gene: polymorphism-screening and family-based association analysis of mild malaria attack and parasitemia in Burkina Faso.Genes and immunity · 2005Article
- Serum levels of the proinflammatory cytokines interleukin-1 beta (IL-1beta), IL-6, IL-8, IL-10, tumor necrosis factor alpha, and IL-12(p70) in Malian children with severe Plasmodium falciparum malaria and matched uncomplicated malaria or healthy controls.Infection and immunity · 2004Article
- Tumor necrosis factor alpha p55 receptor is important for development of memory responses to blood-stage malaria infection.Infection and immunity · 2000Article
- Central role of endogenous gamma interferon in protective immunity against blood-stage Plasmodium chabaudi AS infection.Infection and immunity · 2000Article
- A defect in interleukin-10 leads to enhanced malarial disease in Plasmodium chabaudi chabaudi infection in mice.Infection and immunity · 1999Article
- Macrophages expressing heat-shock protein 65 play an essential role in protection of mice infected with Plasmodium yoelii.Immunology · 1999Article
- Thiolated recombinant human tumor necrosis factor-alpha protects against Plasmodium berghei K173-induced experimental cerebral malaria in mice.Antimicrobial agents and chemotherapy · 1999Article
- Plasmodium falciparum produces prostaglandins that are pyrogenic, somnogenic, and immunosuppressive substances in humans.The Journal of experimental medicine · 1998Article
- Early gamma interferon responses in lethal and nonlethal murine blood-stage malaria.Infection and immunity · 1997Article
- Structural similarities among malaria toxins insulin second messengers, and bacterial endotoxin.Infection and immunity · 1996Article
- A Th1-associated increase in tumor necrosis factor alpha expression in the spleen correlates with resistance to blood-stage malaria in mice.Infection and immunity · 1996Article
- Chimeric tumor necrosis factor receptors with constitutive signaling activity.Proceedings of the National Academy of Sciences of the United States of America · 1995Article
- Blood-stage malaria infection in diabetic mice.Clinical and experimental immunology · 1995Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transgenic mice carrying a modified human tumour necrosis factor (huTNF)/beta-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 macrophage 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.
Indexed as
Identifiers
7959874PMC1414872W161852282What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.