Prolonged infection by Fonsecaea pedrosoi after antigenic co-stimulation at different sites in experimental XXXX @entity8711 .

@entity738 @entity19 @entity8711 @entity73097 @entity75 @entity1618 @entity281 @entity364
In the present study, we examined prolonged @entity281 after antigenic co-stimulation by inoculation of the fungus Fonsecaea pedrosoi at two different sites in three @entity19 strains (BALB/c, Swiss, and C57BL/6). Using this @entity19 model of @entity281 , we showed that antigen induction of @entity281 at more than one site led to a local suppression of active lesions, which increased the time course of experimental @entity8711 ( @entity8711 ). @entity281 with a simultaneous @entity281 of the peritoneum or a mucosal site appeared to cause prolonged @entity364 . Using knockout (KO) @entity19 , we observed that antigenic co-stimulation caused progressive illness in CD8-KO animals and an effective immune response in the absence of @entity1618 . In @entity73097 @entity19 , co-stimulation provoked @entity281 (not prolonged), suggesting that B1 B cells play an important role in the control of @entity364 . The tissue response to @entity281 was similar in all co-stimulated @entity19 groups, as anatomopathologic sections revealed @entity75 ( @entity738 -like). In general, these @entity19 had acute responses at primary antigenic sites with an intense migration of polymorphonuclear leukocytes (PMNs), whereas the distant @entity281 sites (footpad) showed signs of @entity281 . The migration of PMNs to the secondary site (footpad) increased in the later periods of @entity281 , especially after the disappearance of the primary antigenic focus. PMN migration was associated with lesion-dormancy breakage and fungal elimination. Our findings suggest that the host inflammatory/suppression mechanisms induced by antigenic co-stimulation to systemically fight the same pathogen act coordinately through responses that differ at the sites of @entity281 between acute and chronic integrated healing processes that are more prolonged than an acute @entity281 at a single site. However, the long persistence of fungal cells in the host may be linked to microbial adaptation to a @entity281 as observed in co-stimulated @entity73097 @entity19 .
