Clinical immunity to malaria
- Author(s)
- Schofield, L; Mueller, I;
- Details
- Publication Year 2006-03,Volume 6,Issue #2,Page 205-221
- Journal Title
- CURRENT MOLECULAR MEDICINE
- Publication Type
- Journal Article
- Abstract
- Under appropriate conditions of transmission intensity, functional immunity to malaria appears to be acquired in distinct stages. The first phase reduces the likelihood of severe or fatal disease; the second phase limits the clinical impact of 'mild' malaria; and the third provides partial but incomplete protection against pathogen burden [1, 2]. These findings suggest clinical immunity to mortality and morbidity is acquired earlier, with greater ease, and via distinct mechanisms as compared to anti-parasite immunity, which is more difficult to achieve, takes longer and is only ever partially efficacious. The implications of this view are significant in that current vaccination strategies aim predominantly to achieve. anti-parasite immunity, although imparting clinical immunity is the public health objective. Despite enormous relevance for global public health, the mechanisms governing these processes remain obscure. Four candidate mechanisms might mediate clinical immunity, namely immunity to cytoadherence determinants, tolerance to toxins, acquired immunity to toxins, and immunoregulation. This review addresses the targets and determinants of clinical immunity, and considers the implications for vaccine development.
- Publisher
- BENTHAM SCIENCE PUBL LTD
- Keywords
- TUMOR-NECROSIS-FACTOR; PLASMODIUM-FALCIPARUM MALARIA; MURINE CEREBRAL MALARIA; PLACEBO-CONTROLLED TRIAL; CD1D-RESTRICTED NKT CELLS; NITRIC-OXIDE SYNTHASE; ENHANCED VASCULAR-PERMEABILITY; NATURALLY ACQUIRED-IMMUNITY; NATURAL-KILLER COMPLEX; PROTEIN-KINASE-C
- Publisher's Version
- https://doi.org/10.2174/156652406776055221
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2006-03-01 12:00:00