Expression of MHC class II and costimulatory molecules by endothelial cells of the blood brain barrier: Effect on antigen presentation

Girvin, Ann M.; Gordon, Kenneth B.; Tan, Lee K.; Welsh, Jane; Miller, S D

doi:10.1016/s0165-5728(98)91306-6

Cited by 1 publication

(2 citation statements)

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“…This suggests that brain ECs, in the presence of a pro‐inflammatory microenvironment (with IFN‐γ) could present an antigen to a T cell. Risau and co‐workers (Risau et al, 1990) and Girvin (1998) both found that rodent brain ECs did not, however, support primary antigen‐induced T‐cell proliferation, even if the ECs expressed MHC class II and B7 molecules. McCarron and colleagues (McCarron, 1992) proposed that this paradox could be attributed to the production of the prostaglandin 6‐KPGF1α (a metabolite of PGI 2 ) by mouse brain ECs.…”

Section: Endothelial Cell Regulation Of Immune Cell Migration and Reamentioning

confidence: 99%

“…ECs, unlike perivascular microglia, do not constitutively express MHC class II molecules in vivo or in vitro. They can however be induced to do so (Jemison et al, 1993; Prat et al, 1998; Girvin et al, 1998; Etienne et al, 1999; McCarron et al, 1991; Washington et al, 1994). Induction of MHC molecules on brain endothelium by IFN‐γ has been linked to the activation of a non‐DNA‐binding molecule and seems to correlate with EAE susceptibility (Nikcevich et al, 1998).…”

Section: Endothelial Cell Regulation Of Immune Cell Migration and Rea...mentioning

confidence: 99%

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Glial cell influence on the human blood‐brain barrier

Prat

Biernacki

Wosik

et al. 2001

Glia

295

216

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The blood-brain barrier (BBB) is a specialized structure of the central nervous system (CNS) that restricts immune cell migration and soluble molecule diffusion from the systemic compartment into the CNS. Astrocytes and microglia are resident cells of the CNS that contribute to the formation of the BBB. In this article, we consider the influence of these glial cells on the immune regulatory functions of the microvascular endothelium, with special emphasis on the human BBB. A series of in vitro studies demonstrate that soluble factors produced by glial cells, under basal culture conditions, help restrict development of inflammation within the CNS. These soluble factor effects include upregulating expression of molecules including HT7, UEA-1 lectin-binding sites, and angiotensin receptors that help define the phenotype of endothelial cells. These factors also induce tight junction formation between brain endothelial cells, contributing to the restricted permeability of the BBB. In contrast, these factors have little effect on expression of molecules by ECs that either promote lymphocyte migration, such as chemokines and adhesion molecules or molecules that are required for competent antigen presentation, such as MHC and co-stimulatory molecules. Glial cells that become activated in response to signals derived from the immune system or generated within the CNS, produce an array of inflammatory molecules that increase permeability and promote lymphocyte trafficking and persistence. These observations emphasize the bidirectional nature of neural-immune interactions; this dynamic system should be amenable to therapeutic interventions.

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Section: Endothelial Cell Regulation Of Immune Cell Migration and Reamentioning

confidence: 99%