Antigen-specific control of CD4+ T cell trans-migration by brain endothelial cells via presentation of CNS-derived antigens in MHC-II molecules.

Sepsis-induced numerical loss of naive autoantigen-specific CD4 T cells reduces host capacity to develop autoimmune immune disease, thereby demonstrating an intriguing relationship between infection and autoimmune disease.

Reactive endothelial venules are a new vessel subtype characterized by consistent expression of cell adhesion molecules, preferential leukocyte transmigration, association with perivascular macrophages, and the initiation of CNS immune responses.

Peptide immunotherapy in mice depends upon sustained expression of co-inhibitory protein PD-1 in T cells.

Cell biology and animal model analysis in mice shows that molecules involved in glycolytic metabolism could potentially serve as therapeutic targets for the treatment of neurological diseases.