Title of article :
The ontogeny of MHC class I expression in rainbow trout (Oncorhynchus mykiss)
Author/Authors :
Fischer، نويسنده , , Uwe and Dijkstra، نويسنده , , Johannes Martinus and Kِllner، نويسنده , , Bernd and Kiryu، نويسنده , , Ikunari and Koppang، نويسنده , , Erling Olav and Hordvik، نويسنده , , Ivar and Sawamoto، نويسنده , , Yoshihiro and Ototake، نويسنده , , Mitsuru، نويسنده ,
Issue Information :
روزنامه با شماره پیاپی سال 2005
Pages :
12
From page :
49
To page :
60
Abstract :
In the present study, clonal rainbow trout (Oncorhynchus mykiss) embryos and larvae were assayed for the expression of key molecules involved in specific cell-mediated cytotoxicity using an anti-MHC class I monoclonal Ab and by RT-PCR using specific primers derived from classical MHC class I (class Ia), TCR and CD8. Whereas RT-PCR revealed that MHC class Ia and CD8 were expressed from at least 1 week after fertilisation (p.f.) on, TCR expression was detectable from 2 weeks p.f. Immunohistochemistry indicated an early and distinct expression of MHC class I protein in the thymus. Positive lymphoid, epithelial and endothelial cells were found in the pronephros, in the spleen and in the inner and outer epithelia at later stages. Whereas in older rainbow trout the intestine is counted among the organs of the highest class I expression, during ontogeny it was the last site (39 days after hatching) where such expression was detectable. Knowledge on the appearance of the assayed key molecules during fish development is relevant for the pathogenesis of infections as well as for early vaccine delivery. Besides such information regarding the development of the adaptive immune system, immunohistochemistry revealed that in early larvae MHC class I was expressed in neurons whereas in older rainbow trout this was not observed.
Keywords :
CD8 , Rainbow trout (Oncorhynchus mykiss) , MHC , ontogeny , T Cell Receptor
Journal title :
Fish and Shellfish Immunology
Serial Year :
2005
Journal title :
Fish and Shellfish Immunology
Record number :
2106980
Link To Document :
بازگشت