Cells comprising the blood brain barrier (BBB), including astrocytes and cerebrovascular endothelial cells (CVE's), contribute to a relatively inflammation-free environment during health, and also may play a role in the inflammation of the central nervous system (CNS) in response to infection or induced autoimmune disease. Previously, we have shown that IFNg activated SJL/J astrocytes upregulate MHC class II and B7-1 costimulatory molecules and are capable of processing and presenting antigen to both naïve and memory T cells. There is current controversy as to whether endothelial cells, including CVE's, express and upregulate MHC class II and B7 costimulatory molecules in response to an inflammatory stimulus, such as IFNg. We show that SJL/J CVE's upregulate MHC class II and B7-1 costimulatory molecules in response to IFNg. However, the addition of TNFa to SJL/J CVE's, but not astrocytes, decreased the IFNg induced MHC class II expression. The differential expression of MHC class II between CVE's and astrocytes is regulated at the level of the class II transactivator. Also, we have found that while CVE's constitutively express B7-1 on their surfaces, they are unable to function as antigen presenting cells (APC's) when MHC class II is upregulated by IFNg. In fact, they appear to induce antigen specific anergy.
|Original language||English (US)|
|State||Published - Mar 20 1998|
ASJC Scopus subject areas
- Molecular Biology