Heterologous immunity in the absence of variant-specific antibodies after exposure to subpatent infection with blood-stage malaria

Elliott, Salenna R., Kuns, Rachel D. and Good, Michael F. (2005) Heterologous immunity in the absence of variant-specific antibodies after exposure to subpatent infection with blood-stage malaria. Infection and Immunity, 73 4: 2478-2485. doi:10.1128/IAI.73.4.2478-2485.2005

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Author Elliott, Salenna R.
Kuns, Rachel D.
Good, Michael F.
Title Heterologous immunity in the absence of variant-specific antibodies after exposure to subpatent infection with blood-stage malaria
Journal name Infection and Immunity   Check publisher's open access policy
ISSN 1098-5522
1070-6313
Publication date 2005-04-01
Sub-type Article (original research)
DOI 10.1128/IAI.73.4.2478-2485.2005
Open Access Status File (Publisher version)
Volume 73
Issue 4
Start page 2478
End page 2485
Total pages 8
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Formatted abstract
We examined immunity induced by subpatent blood-stage malaria (undetectable by microscopy) using the rodent malaria parasite, Plasmodium chabaudi chabaudi, postulating that limited infection may allow expansion of antigen-specific T cells that are normally deleted by apoptosis. After three infections drug cured at 48 h, mice were protected against high-dose challenge with homologous or heterologous parasites (different strain or variant). Immunity differed from that generated by three untreated, patent infections. Subpatently infected mice lacked immunoglobulin G (IgG) to variant surface antigens, despite producing similar titers of total malaria-specific IgG to those produced by patently infected mice, including antibodies specific for merozoite surface antigens conserved between heterologous strains. Antigen-specific proliferation of splenocytes harvested prechallenge was significantly higher in subpatently infected mice than in patently infected or naive mice. In subpatently infected mice, lymphoproliferation was similar in response to homologous and heterologous parasites, suggesting that antigenic targets of cell-mediated immunity were conserved. A Th1 cytokine response was evident during challenge. Apoptosis of CD4+ and CD8+ splenic lymphocytes occurred during patent but not subpatent infection, suggesting a reason for the relative prominence of cell-mediated immunity after subpatent infection. In conclusion, subpatent infection with blood stage malaria parasites induced protective immunity, which differed from that induced by patent infection and targeted conserved antigens. These findings suggest that alternative vaccine strategies based on delivery of multiple parasite antigens at low dose may induce effective immunity targeting conserved determinants.
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Institutional Status Non-UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: ERA 2012 Admin Only
School of Public Health Publications
 
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Created: Wed, 26 Oct 2011, 00:16:51 EST by Geraldine Fitzgerald on behalf of School of Public Health