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Centenary Institute of Cancer Medicine and Cell Biology, Royal Prince Alfred Hospital, Camperdown, Sydney, Australia
Central nervous system (CNS)-resident macrophages (microglia)
normally express negligible or low level MHC class II, but this is
up-regulated in graft-vs-host disease (GvHD), in which a sparse CNS T
cell infiltrate is observed. Relative to microglia from the normal CNS,
those from the GvHD-affected CNS exhibited a 5-fold up-regulation of
characteristically low CD45, MHC class II expression was increased 10-
to 20-fold, and microglial cell recoveries were enhanced substantially.
Immunohistologic analysis revealed
CD4+
ßTCR+CD2+ T cells
scattered infrequently throughout the CNS parenchyme, 90% of which
were blast cells of donor origin. An unusual clustering of activated
microglia expressing strongly enhanced levels of CD11b/c and MHC class
II was a feature of the GvHD-affected CNS, and despite the paucity of T
lymphocytes present, activated microglial cell clusters were invariably
intimately associated with these T cells. Moreover, 70% of T cells in
the CNS were associated with single or clustered MHC class
II+ microglia, and interacting cells were predominantly
deep within the tissue parenchyme. Approximately 3.7% of the microglia
that were freshly isolated from the GvHD-affected CNS were cycling, and
proliferating cell nuclear Ag-positive microglia were detected in situ.
Microglia from GvHD-affected animals sorted to purity by flow cytometry
and cultured, extended long complex processes, exhibited spineous
processes, and were phagocytic and highly motile. These outcomes are
consistent with direct tissue macrophage-T cell interactions in situ
that lead to activation, proliferation, and expansion of the responding
tissue-resident cell.
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