MHC class II molecules induction after infection of bovine brain endothetial cells by Cowdria ruminantium
DOI:
https://doi.org/10.19182/remvt.9362Keywords
Cattle, Major histocompatibility complex, cells, Experimental infection, BacteriosesAbstract
Major histocompatibility complex (MCH) class II molecules play a key role in inductions of immunity. In cattle, MCH class II molecules encoded by th DR and DQ loci are constituted by one α and one β protein chain which are associated to an invariant (I) chain during their intracellular transport. Bovine brain endothelial cells (BBEC) from microvessels can be cultured in vitro and do not express constitutively MCH class II molecules. However, after treatment with bovine γ interferon (γ INF), BBEC synthesize MHC class II proteins. In vitro infection with C. ruminantium of BBEC treated or not by γINF was performed. Expression of class II molecules was monitored at the RNA level by northern blot analysis. Forty eight hours after infection, transcripts corresponding to the I chain were detected on all infected cells. Two DQαmRNA of 1.3 and 1.5 kb were present on INF treated infected cells whereas a single 1.5 kb DQα transcript was observed on infected cells. In the other hand, treated but non-infected cells displayed a single 1.3 kb DQαmRNA. The nature and functionality of the 1.5 kb molecular specie remains unknown but it might represent a DQαmRNA polyadenylated at a second site downstream the first site of polyadendylation. In contrast, to the early expression of I and DQα chains, the DRαmRNA were detected 7 days after infection. It is important to note that total lysis of infected BBEC was obtained 13 days after infection while γINF treated and infected cells displayed an earlier and more market cytopathogenic effect. The results presented here show that MCH class II molecules can be induced in BBEC after C. ruminantium infection; leading to the hypothesis that brain endothelial cells can exert specific immune functions such as antigen presentation. Further work must be accomplished to assess whether or not these infected cells can specifically stimulate T-cells.
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© S.Bourdoulous et al., hosted by CIRAD 1993

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