ArticleInfection and immunity2000
Tumor necrosis factor alpha p55 receptor is important for development of memory responses to blood-stage malaria infection.
Article in Infection and immunity, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 34 citations in OpenAlex.
- Antibody-dependent immune responses elicited by blood stage-malaria infection contribute to protective immunity to the pre-erythrocytic stages.Current research in immunology · 2023Article
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- 11β-hydroxysteroid dehydrogenase type 1 has no effect on survival during experimental malaria but affects parasitemia in a parasite strain-specific manner.Scientific reports · 2017Article
- Adjuvant-like effect of vaccinia virus 14K protein: a case study with malaria vaccine based on the circumsporozoite protein.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Article
- Decreased influenza-specific B cell responses in rheumatoid arthritis patients treated with anti-tumor necrosis factor.Arthritis research & therapy · 2011Article
- Nitric oxide is involved in the upregulation of IFN-γ and IL-10 mRNA expression by CD8⁺ T cells during the blood stages of P. chabaudi AS infection in CBA/Ca mice.International journal of biological sciences · 2011Article
- A defunctioning polymorphism in FCGR2B is associated with protection against malaria but susceptibility to systemic lupus erythematosus.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Germinal centre and marginal zone B cells expand quickly in a second Plasmodium chabaudi malaria infection producing mature plasma cells.Parasite immunology · 2009Article
- Systemic lupus erythematosus-associated defects in the inhibitory receptor FcgammaRIIb reduce susceptibility to malaria.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Suppression of Plasmodium chabaudi parasitemia is independent of the action of reactive oxygen intermediates and/or nitric oxide.Infection and immunity · 2004Article
- CD28 costimulation is required for the expression of T-cell-dependent cell-mediated immunity against blood-stage Plasmodium chabaudi malaria parasites.Infection and immunity · 2004Article
- Pathogenesis of malaria and clinically similar conditions.Clinical microbiology reviews · 2004Review
- Small variant STEVOR antigen is uniquely located within Maurer's clefts in Plasmodium falciparum-infected red blood cells.Eukaryotic cell · 2002Article
- Cytokines in the pathogenesis of and protection against malaria.Clinical and diagnostic laboratory immunology · 2002Review
- Different regions of the malaria merozoite surface protein 1 of Plasmodium chabaudi elicit distinct T-cell and antibody isotype responses.Infection and immunity · 2001Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Tumor necrosis factor alpha (TNF-alpha) is associated with malarial pathology in both humans and mice. In Plasmodium chabaudi chabaudi (AS) infections, the production of TNF-alpha and reactive metabolites from macrophages are also thought to play a role in controlling acute parasitemia. Since many of the biological functions of TNF-alpha are effected through the p55 receptor (p55R), mice made defective in this receptor via a targeted gene disruption (p55R(-/-)) have been used to study its involvement in the immune response against P. chabaudi chabaudi and in the pathology associated with this infection. In the absence of the p55R, mice could overcome their primary infection, although higher acute-blood-stage parasitemias and more significant recrudescences were observed. Hypoglycemia, hypothermia, loss of erythrocytes, and loss of body weight, which occur transiently in this infection, were exacerbated by the lack of the p55R, but the differences were small, suggesting that other factors affect these symptoms. In contrast to wild-type (WT) mice, a second challenge infection in p55R(-/-) mice resulted in a course of infection similar to a primary infection. The malaria-specific immunoglobulin G antibody response of p55R(-/-) mice was lower than that of WT mice and was not increased by the second challenge infection. These data suggest that p55R(-/-) mice do not develop an efficient memory B-cell response against malarial infection and that this antibody response is important in immunity to reinfection.
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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.