Multiple sclerosis: Immune cell invasion enabled by blood-brain barrier breakdown MultipleSclerosis Research BloodBrainBarrier ImmuneCellInfiltration CNS CD8TCells Neuroinflammation Brain EndothelialCells NatureComms
By Bhavana KunkalikarJun 4 2023Reviewed by Benedette Cuffari, M.Sc. In a recent study published in the journal Nature Communications, researcher discovered that CD8+ T-cells are detained at the blood-brain barrier , wherein they contribute to its breakdown and subsequent infiltration of inflammatory cells into the brain.
New findings suggest that CD8+ T-cells have unique ways of crossing the BBB that differ from CD4+ T-cells. CD4+ T-cell migration across the BBB does not require Ag-specific mechanisms; however, the transfer of CNS autoantigen-specific CD8+ T-cells across the BBB appears to be dependent on the luminal expression of major histocompatibility complex class I.
The researchers also explored whether pMBMECs could uptake and process exogenous antigens from their abluminal side and present these antigens on their luminal surface to naïve CD8+ T-cells. This was performed by growing pMBMECs on filter inserts, stimulating these cells with luminal TNF-α/IFN-γ, and subsequently subjecting pMBMECs to increasing proportions of OVA or SIINFEKL from the abluminal compartment and naïve OT-I cells on the luminal surface.
Exposure of abluminal pMBMECs to SIINFEKL or OVA protein resulted in the activation of naïve OT-I cells, as demonstrated by the increased expression of CD25, CD69, and CD44, and shedding of CD62L. Comparatively, OT-I cells that were cocultured with pMBMECs without added abluminal Ag remained in a naïve state.
Effector OT-I cells crossed the WT or B2M–/– pMBMEC monolayer in the absence of SIINFEKL after probing or crawling. However, OT-I cells exhibited decreased crawling and increased probing behavior without diapedesis when exposed to SIINFEKL-pulsed WT pMBMECs, as opposed to the control group.
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