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 Hansen, D. S.
Right arrow Articles by Schofield, L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Hansen, D. S.
Right arrow Articles by Schofield, L.
Right arrowPubmed/NCBI databases
*Gene*GEO Profiles
*HomoloGene*UniGene
*Substance via MeSH
Medline Plus Health Information
*Malaria

 Previous Article  |  Next Article 

Infection and Immunity, April 2005, p. 2288-2297, Vol. 73, No. 4
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.4.2288-2297.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

The Natural Killer Complex Regulates Severe Malarial Pathogenesis and Influences Acquired Immune Responses to Plasmodium berghei ANKA

Diana S. Hansen,1* Krystal J. Evans,1 Marthe C. D'Ombrain,1 Nicholas J. Bernard,1 Adrienne C. Sexton,1 Lynn Buckingham,1 Anthony A. Scalzo,2 and Louis Schofield1

The Walter and Eliza Hall Institute of Medical Research, Parkville, Victoria,1 Immunology and Virology Program, Centre for Ophthalmology and Visual Science, University of Western Australia, and Centre for Experimental Immunology, Lions Eye Institute, Nedlands, Western Australia, Australia2

Received 20 August 2004/ Returned for modification 29 September 2004/ Accepted 22 November 2004

The natural killer complex (NKC) is a genetic region of highly linked genes encoding several receptors involved in the control of NK cell function. The NKC is highly polymorphic, and allelic variability of various NKC loci has been demonstrated in inbred mice. Making use of BALB.B6-Cmv1r congenic mice, in which the NKC from disease-susceptible C57BL/6 mice has been introduced into the disease-resistant BALB/c background, we show here that during murine malaria infection, the NKC regulates a range of pathophysiological syndromes such as cerebral malaria, pulmonary edema, and severe anemia, which contribute to morbidity and mortality in human malaria. Parasitemia levels were not affected by the NKC genotype, indicating that control of malarial fatalities by the NKC cells does not operate through effects on parasite growth rate. Parasite-specific antibody responses and the proinflammatory gene transcription profile, as well as the TH1/TH2 balance, also appeared to be influenced by NKC genotype, providing evidence that this region, known to control innate immune responses via NK and/or NK T-cell activation, can also significantly regulate acquired immunity to infection. To date, NKC-encoded innate system receptors have been shown mainly to regulate viral infections. Our data provide evidence for critical NKC involvement in the broad immunological responses to a protozoan parasite.

* Corresponding author. Mailing address: The Walter and Eliza Hall Institute of Medical Research, 1G Royal Parade, Parkville, Victoria 3050, Australia. Phone: 61 3 93452644. Fax: 61 3 93470852. E-mail: hansen{at}wehi.edu.au.

Editor: W. A. Petri, Jr.

Infection and Immunity, April 2005, p. 2288-2297, Vol. 73, No. 4
0019-9567/05/$08.00+0     doi:10.1128/IAI.73.4.2288-2297.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Fodil-Cornu, N., Lee, S.-H., Belanger, S., Makrigiannis, A. P., Biron, C. A., Buller, R. M., Vidal, S. M. (2008). Ly49h-Deficient C57BL/6 Mice: A New Mouse Cytomegalovirus-Susceptible Model Remains Resistant to Unrelated Pathogens Controlled by the NK Gene Complex. J. Immunol. 181: 6394-6405 [Abstract] [Full Text]  
  • Patel, S. N., Berghout, J., Lovegrove, F. E., Ayi, K., Conroy, A., Serghides, L., Min-oo, G., Gowda, D. C., Sarma, J. V., Rittirsch, D., Ward, P. A., Liles, W. C., Gros, P., Kain, K. C. (2008). C5 deficiency and C5a or C5aR blockade protects against cerebral malaria. JEM 205: 1133-1143 [Abstract] [Full Text]  
  • Lovegrove, F. E., Gharib, S. A., Patel, S. N., Hawkes, C. A., Kain, K. C., Liles, W. C. (2007). Expression Microarray Analysis Implicates Apoptosis and Interferon-Responsive Mechanisms in Susceptibility to Experimental Cerebral Malaria. Am. J. Pathol. 171: 1894-1903 [Abstract] [Full Text]  
  • Hansen, D. S., Bernard, N. J., Nie, C. Q., Schofield, L. (2007). NK Cells Stimulate Recruitment of CXCR3+ T Cells to the Brain during Plasmodium berghei-Mediated Cerebral Malaria. J. Immunol. 178: 5779-5788 [Abstract] [Full Text]  
  • Baratin, M., Roetynck, S., Lepolard, C., Falk, C., Sawadogo, S., Uematsu, S., Akira, S., Ryffel, B., Tiraby, J.-G., Alexopoulou, L., Kirschning, C. J., Gysin, J., Vivier, E., Ugolini, S. (2005). Natural killer cell and macrophage cooperation in MyD88-dependent innate responses to Plasmodium falciparum. Proc. Natl. Acad. Sci. USA 102: 14747-14752 [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»