Immune-suppressive factors (ISFs) introduced into larvae of Drosophila melanogaster during infection by virulent endoparasitic wasps effectively block the innate immune response mediated by blood cells (hemocytes) but have little influenceon the autoimmune response made by a tumor strain in which the blood cells manifest a similar response but instead target anddestroy endogenous tissues. Quantitative hemocyte analyses indicate that ISFs interfere with the immune effector responsesdownstream of nonself recognition, hemocyte activation and differentiation, because these responses were manifested by tumorhosts, in which the parasitoids developed. The data suggest that once activated to encapsulate aberrant tissues, the target specificityof the autoimmune-activated hemocytes, and the genetic program underlying tumor formation, cannot be blocked by parasitoidderivedISFs, which effectively inhibit identical hemocyte-mediated responses during parasitization.
The effects of parasite-derived immune-suppressive factors on the cellular innate immune and autoimmune responses of Drosophila melanogaster / Nappi, A. J.; Vass, E.; Malagoli, Davide; D., Carton. - In: THE JOURNAL OF PARASITOLOGY. - ISSN 0022-3395. - STAMPA. - 90:5(2004), pp. 1139-1149. [10.1645/GE-266R]
The effects of parasite-derived immune-suppressive factors on the cellular innate immune and autoimmune responses of Drosophila melanogaster
MALAGOLI, Davide;
2004
Abstract
Immune-suppressive factors (ISFs) introduced into larvae of Drosophila melanogaster during infection by virulent endoparasitic wasps effectively block the innate immune response mediated by blood cells (hemocytes) but have little influenceon the autoimmune response made by a tumor strain in which the blood cells manifest a similar response but instead target anddestroy endogenous tissues. Quantitative hemocyte analyses indicate that ISFs interfere with the immune effector responsesdownstream of nonself recognition, hemocyte activation and differentiation, because these responses were manifested by tumorhosts, in which the parasitoids developed. The data suggest that once activated to encapsulate aberrant tissues, the target specificityof the autoimmune-activated hemocytes, and the genetic program underlying tumor formation, cannot be blocked by parasitoidderivedISFs, which effectively inhibit identical hemocyte-mediated responses during parasitization.
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