This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Li, C.
Right arrow Articles by Langhorne, J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Li, C.
Right arrow Articles by Langhorne, J.

 Previous Article  |  Next Article 

Infection and Immunity, October 2000, p. 5724-5730, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.

Tumor Necrosis Factor Alpha p55 Receptor Is Important for Development of Memory Responses to Blood-Stage Malaria Infection

Ching Li and Jean Langhorne*

Division of Parasitology, National Institute for Medical Research, London NW7 1AA, United Kingdom

Received 8 May 2000/Accepted 12 July 2000

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.

* Corresponding author. Mailing address: Division of Parasitology, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, United Kingdom. Phone: 44-208-959-3666, ext. 2588. Fax: 44-0208-913-8605. E-mail: jlangho{at}nimr.mrc.ac.uk.

Infection and Immunity, October 2000, p. 5724-5730, Vol. 68, No. 10
0019-9567/00/$04.00+0
Copyright © 2000, American Society for Microbiology. All rights reserved.


This article has been cited by other articles:

  • Clatworthy, M. R., Willcocks, L., Urban, B., Langhorne, J., Williams, T. N., Peshu, N., Watkins, N. A., Floto, R. A., Smith, K. G. C. (2007). Systemic lupus erythematosus-associated defects in the inhibitory receptor Fc{gamma}RIIb reduce susceptibility to malaria. Proc. Natl. Acad. Sci. USA 104: 7169-7174 [Abstract] [Full Text]  
  • Gillman, B. M., Batchelder, J., Flaherty, P., Weidanz, W. P. (2004). Suppression of Plasmodium chabaudi Parasitemia Is Independent of the Action of Reactive Oxygen Intermediates and/or Nitric Oxide. Infect. Immun. 72: 6359-6366 [Abstract] [Full Text]  
  • Rummel, T., Batchelder, J., Flaherty, P., LaFleur, G., Nanavati, P., Burns, J. M., Weidanz, W. P. (2004). CD28 Costimulation Is Required for the Expression of T-Cell-Dependent Cell-Mediated Immunity against Blood-Stage Plasmodium chabaudi Malaria Parasites. Infect. Immun. 72: 5768-5774 [Abstract] [Full Text]  
  • Clark, I. A., Alleva, L. M., Mills, A. C., Cowden, W. B. (2004). Pathogenesis of Malaria and Clinically Similar Conditions. Clin. Microbiol. Rev. 17: 509-539 [Abstract] [Full Text]  
  • Kaviratne, M., Khan, S. M., Jarra, W., Preiser, P. R. (2002). Small Variant STEVOR Antigen Is Uniquely Located within Maurer's Clefts in Plasmodium falciparum-Infected Red Blood Cells. Eukaryot Cell 1: 926-935 [Abstract] [Full Text]  
  • Angulo, I., Fresno, M. (2002). Cytokines in the Pathogenesis of and Protection against Malaria. CVI 9: 1145-1152 [Full Text]  
  • Quin, S. J., Langhorne, J. (2001). Different Regions of the Malaria Merozoite Surface Protein 1 of Plasmodium chabaudi Elicit Distinct T-Cell and Antibody Isotype Responses. Infect. Immun. 69: 2245-2251 [Abstract] [Full Text]  


Copyright © 2009 by the American Society for Microbiology.   For an alternate route to Journals.ASM.org, visit: http://intl-journals.asm.org | More Info»