Title of article :
Active suppression of D. melanogaster immune response by long gland products of the parasitic wasp Leptopilina boulardi
Author/Authors :
Labrosse، نويسنده , , C and Carton، نويسنده , , Y and Dubuffet، نويسنده , , A and Drezen، نويسنده , , J.M and Poirie، نويسنده , , M، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2003
Pages :
10
From page :
513
To page :
522
Abstract :
To develop inside their insect hosts, endoparasitoid wasps must either evade or overcome the host’s immune system. Several ichneumonid and braconid wasps inject polydnaviruses that display well-studied immune suppressive effects. However, little is known about the strategies of immunoevasion used by other parasitoid families, such as figitid wasps. The present study provides experimental evidence, based on superparasitism and injection experiments, that the figitid species Leptopilina boulardi uses an active mechanism to suppress the Drosophila melanogaster host immune response, i.e. the encapsulation of the parasitoid eggs. The immune suppressive factors are localised in the long gland and reservoir of the female genital tractus, where virus-like particles (VLPs) have been observed. Parasitism experiments using a host tumorous strain indicate that these factors do not destroy host lamellocytes but that they impair the melanisation pathway. Interestingly, they are not susceptible to heating and are not depleted with prolonged oviposition experience, in contrast to observations reported for L. heterotoma, another figitid species. The mechanisms that prevent encapsulation of eggs from L. boulardi and L. heterotoma differ in several respects, suggesting that different physiological strategies of immunosuppression might be used by specialised and generalist parasitoids.
Keywords :
Drosophila melanogaster , Parasitoid wasps , Encapsulation , Injection experiments , Immune suppressive factors
Journal title :
Journal of Insect Physiology
Serial Year :
2003
Journal title :
Journal of Insect Physiology
Record number :
1412594
Link To Document :
بازگشت