Title of article :
Presence of dendritic cells in chicken spleen cell preparations and their functional interaction with the parasite Toxoplasma gondii
Author/Authors :
Quéré، نويسنده , , Pascale and Pierre، نويسنده , , Josette and Hoang، نويسنده , , My-Dung and Esnault، نويسنده , , Evelyne and Domenech، نويسنده , , Jorge and Sibille، نويسنده , , Pierre and Dimier-Poisson، نويسنده , , Isabelle، نويسنده ,
Issue Information :
سالنامه با شماره پیاپی سال 2013
Pages :
13
From page :
57
To page :
69
Abstract :
Toxoplasmosis is a worldwide epizootic disease of mammals. Chickens, albeit being less susceptible, can be contaminated in free-range flocks and may have an important role in parasite transmission. Plastic adherence selection of chicken spleen cells enriched 8F2+ (putative chicken CD11c) MHC II+ cells of the myeloid type; however, we did not succeed to separate dendritic cells from macrophages using their feature to become loosely adherent after culture as in mammals. Still we clearly identified dendritic-like cells being morphologically distinguishable from macrophages in the KUL01 (macrophage marker) negative fraction, exhibiting responsiveness to LPS and parasite extracts by developing characteristic cellular protrusions as well as a minor phagocytic incorporation of dead parasites. Live T. gondii tachyzoites were able to invade the two different types of myeloid adherent cells, to replicate, and to induce an overall decrease in the expression of MHC II and co-stimulatory molecules, CD80 and CD40. Our data indicate that dendritic cells in addition to macrophages may have a role in hiding viable replicating T. gondii tachyzoites from the immune system and in shuttling them to different organs in the chicken as previously described for different Apicomplexa infecting mammals.
Keywords :
chicken , Parasites , TOXOPLASMA GONDII , dendritic cells , macrophages
Journal title :
Veterinary Immunology and Immunopathology
Serial Year :
2013
Journal title :
Veterinary Immunology and Immunopathology
Record number :
2166730
Link To Document :
بازگشت