期刊
PARASITE IMMUNOLOGY
卷 28, 期 1-2, 页码 35-49出版社
WILEY
DOI: 10.1111/j.1365-3024.2006.00775.x
关键词
anti-toxic immunity; glycosylphosphatidylinositol; IL-10; nitric oxide; regulatory T cell; TGF-beta
资金
- FIC NIH HHS [D43 TW005884] Funding Source: Medline
- NIAID NIH HHS [R01 AI051305] Funding Source: Medline
- FOGARTY INTERNATIONAL CENTER [D43TW005884] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI051305] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DENTAL &CRANIOFACIAL RESEARCH [Z01DE000513, Z01DE000691, Z01DE000046] Funding Source: NIH RePORTER
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 antimalarial 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.
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