par Cnops, Jennifer;Kauffmann, Florence;De Trez, Carl 
;Baltz, Théo;Keirsse, Jiri;Radwanska, Magdalena ;Muraille, Eric ;Magez, Stefan
Référence Parasite immunology, 38, 10, page (642-647)
Publication Publié, 2016-10
;Baltz, Théo;Keirsse, Jiri;Radwanska, Magdalena ;Muraille, Eric ;Magez, StefanRéférence Parasite immunology, 38, 10, page (642-647)
Publication Publié, 2016-10
Article révisé par les pairs
| Résumé : | African trypanosomosis is a debilitating parasitic disease occurring in large parts of sub-Saharan Africa. Trypanosoma brucei gambiense accounts for 98% of the reported HAT infections and causes a chronic, gradually progressing disease. Multiple experimental murine models for trypanosomosis have demonstrated inflammation-dependent apoptosis of splenic follicular B (FoB) cells and the destruction of B-cell memory against previously encountered pathogens. Here, we report that during murine infection with a chronic T. b. gambiense field isolate, FoB cells are retained. This coincided with reduced levels of IFN-γ and TNF-α during the acute phase of the infection. This result suggests that in chronic infections with low virulent parasites, less inflammation is elicited and consequently no FoB cell destruction occurs. |
