Regulating immunity to malaria

E M Riley, S Wahl, D J Perkins, L Schofield

Research output: Contribution to journalReview articlepeer-review

Abstract / Description of output

The optimal outcome of a malaria infection is that parasitized cells are killed and degraded without inducing significant pathology. Since much of the pathology of malaria infection can be immune-mediated, this implies that immune responses have to be carefully regulated. The mechanisms by which anti-malarial immune responses are believed to be regulated were discussed at the recent Malaria Immunology Workshop (Bloomberg School of Public Health, Johns Hopkins University, Baltimore, Maryland, USA; February 2005). Potential regulatory mechanisms include regulatory T cells, which have been shown to significantly modify cellular immune responses to various protozoan infections, including leishmania and malaria; neutralising antibodies to pro-inflammatory malarial toxins such as glycosylphosphatidylinositol and haemozoin; and self-regulating networks of effector molecules. Innate and adaptive immune responses are further moderated by the broader immunological environment, which is influenced by both the genetic background of the host and by co-infection with other pathogens. A detailed understanding of the interplay between these different immunoregulatory processes may facilitate the rationale design of vaccines and novel therapeutics.

Original languageEnglish
Pages (from-to)35-49
Number of pages15
JournalParasite Immunology
Issue number1-2
Publication statusPublished - 28 Jan 2006

Keywords / Materials (for Non-textual outputs)

  • Animals
  • Cytokines/immunology
  • Genetic Predisposition to Disease
  • Glycosylphosphatidylinositols/immunology
  • Humans
  • Immune Tolerance
  • Malaria/genetics
  • Nitric Oxide/immunology
  • Plasmodium/immunology
  • T-Lymphocytes, Regulatory/immunology


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