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Alternative versus classical macrophage activation during experimental African trypanosomosis
B Namangala1, P De Baetselier, W Noël
1Department of Immunology, Parasitology and Ultrastructure, Flemish Interuniversity Institute for Biotechnology, Free University Brussels (VUB), St-Genesius-Rode, Belgium.
Journal of Leukocyte Biology
|March 23, 2001
Summary
The balance of type I and type II cytokines shapes macrophage responses during Trypanosoma brucei brucei infection. Wild-type infections maintain type I responses, while PLC-deficient infections shift to type II, impacting T cell activation differently.
Area of Science:
- Immunology
- Parasitology
- Cell Biology
Background:
- The balance between type I and type II cytokines influences the differentiation of suppressive macrophages, specifically classically activated macrophages (caMphi, type I) and alternatively activated macrophages (aaMphi, type II).
- Previous research indicated that mice infected with wild-type (WT) Trypanosoma brucei brucei remain in a type I cytokine response, whereas mice infected with phospholipase C-deficient (PLC-/-) T. b. brucei show a shift towards type II cytokine production.
Purpose of the Study:
- To compare the phenotype and accessory cell function of macrophages during WT and PLC-/- T. b. brucei infection.
- To investigate the correlation between macrophage activation states, cytokine profiles, and T cell activation during different stages of infection.
Main Methods:
- Macrophage phenotype and function analysis in mice infected with WT and PLC-/- T. b. brucei.
- Assessment of T cell activation in response to mitogens, superantigens, and specific antigens.
Main Results:
- Classically activated macrophages (caMphi) develop in the early phase of both WT and PLC-/- infections, coinciding with inhibited T cell activation.
- In the late stage, only PLC-/- infected mice, which resist infection, develop type II cytokine-associated alternatively activated macrophages (aaMphi).
- aaMphi development in late-stage PLC-/- infection correlates with impaired antigen-specific T cell activation, but not mitogen- or superantigen-induced activation.
Conclusions:
- Macrophage polarization during T. b. brucei infection is influenced by the host's cytokine environment and parasite factors like PLC.
- The shift to type II cytokine-associated aaMphi in resistant infections correlates with selective impairment of antigen-specific T cell responses.
- Understanding these macrophage-cytokine-T cell interactions is crucial for developing strategies against parasitic infections.