Journal
JOURNAL OF IMMUNOLOGY
Volume 178, Issue 11, Pages 6695-6699Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.178.11.6695
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Funding
- NINDS NIH HHS [R01 NS047687, R01 NS047687-03, R01 NS047687-04, NS047687-01A1] Funding Source: Medline
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CD11c(+) dendritic cells (DCs) are a prominent component of CNS infiltrates in mice with experimental autoimmune encephalomyelitis. However, their role in immunopathogenesis is controversial. In this study, we report that they originate from peripheral hemopoietic cells and exhibit diverse functions that change during the course of acute disease. CNS DCs stimulate naive T cells to proliferate and polarize Th-17 responses when harvested shortly following disease onset but are relatively inefficient APC by the time of peak disability. Conversely, they can support CD4(+) CD25(+) T cell-mediated immunosuppression early during experimental autoimmune encephalomyelitis. Such paradoxical functions might reflect dual roles of CNS DO in promoting local inflammation while setting the stage for remission.
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