Maintaining the Immunological Balance in Parasitic Infections: A Role for TGF-β?

Transforming growth factor β (TGF-β) is an important regulator of inflammation, being proinflammatory at low concentrations and anti-inflammatory at high concentrations. As such, TGF-β might be important in maintaining the balance between control and clearance of infectious organisms on the one hand...

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Bibliographic Details
Published in:Parasitology Today 2000-01, Vol.16 (1), p.18-23
Main Authors: Omer, F.M., Kurtzhals, J.A.L, Riley, E.M.
Format: Article
Language:English
Subjects:
Animals
Biological and medical sciences
Chagas Disease - immunology
Experimental protozoal diseases and models
Genetic Variation - genetics
Host-Parasite Interactions
Humans
Immunoregulation
Infectious diseases
Inflammation
Leishmaniasis - immunology
Malaria
Malaria - immunology
Medical sciences
Mice
Mice, Inbred BALB C
Mice, Inbred C57BL
Parasitic diseases
Plasmodium falciparum - immunology
Protozoal diseases
Schistosoma mansoni - immunology
Schistosomiasis mansoni - immunology
TGF-β
Transforming Growth Factor beta - immunology
Trypanosoma cruzi - immunology
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Summary:Transforming growth factor β (TGF-β) is an important regulator of inflammation, being proinflammatory at low concentrations and anti-inflammatory at high concentrations. As such, TGF-β might be important in maintaining the balance between control and clearance of infectious organisms on the one hand and prevention of immune-mediated pathology on the other. In this article, Fakhereldin Omer, Jørgen Kurtzhals and Eleanor Riley review the immunoregulatory properties of TGF-β in the context of parasitic infections. Data from murine malaria infections suggest that TGF-β modifies the severity of the disease, and a number of potential protective mechanisms are discussed. Evidence is accumulating that TGF-β is important for the regulation of other host–parasite interactions and that parasites might directly influence TGF-β-dependent pathways via the synthesis of TGF-β or TGF-β-receptor homologues.
ISSN:0169-4758
1873-1473
DOI:10.1016/S0169-4758(99)01562-8