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Antigen presentation at the blood–brain barrier amplifies neuroinflammation
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DOI：10.1016/j.it.2026.07.006.png)
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Abstract
En 中文
The migration of activated T cells into the central nervous system across the blood–brain barrier occurs under laminar flow conditions, is antigen-independent, and is guided by the sequential interaction of adhesion and signaling molecules with their receptors. Expression of major histocompatibility complex class I—and therefore, antigen presentation—at the blood–brain barrier is low under homeostatic conditions and emerges only during sustained neuroinflammation. Antigen presentation at the blood–brain barrier predominantly involves major histocompatibility complex class I–CD8 T-cell interactions under neuroinflammatory conditions, with few, if any, major histocompatibility complex class II–CD4 T-cell interactions. Antigen presentation at the blood–brain barrier sustains CD8 T-cell arrest and promotes vascular injury and barrier breakdown across different neuroinflammatory conditions. We propose that antigen presentation at the blood–brain barrier amplifies pathology rather than initiating and promoting T-cell entry across the blood–brain barrier in neuroinflammation.
Keywords:
brain barriers
T-cell migration
central nervous system
antigen presentation
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