CD62L(high) Treg cells with superior immunosuppressive properties accumulate within the CNS during remissions of EAE

The role of regulatory T cell populations within the CNS in the regulation of CNS-autoimmunity is controversial. We show that during recovery from relapsing remitting experimental autoimmune encephalomyelitis, regulatory T cells accumulate within the CNS that express high levels of CD62L. These CD62...

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Bibliographic Details
Published in:Brain, behavior, and immunity behavior, and immunity, 2011-01, Vol.25 (1), p.120-126
Main Authors: Lange, Christian, Scholl, Matthias, Melms, Arthur, Bischof, Felix
Format: Article
Language:English
Subjects:
Animals
Annexin A5 - metabolism
Antigens, CD - biosynthesis
Apoptosis - drug effects
Caspase 3 - metabolism
Central Nervous System - cytology
Central Nervous System - immunology
CTLA-4 Antigen
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - pathology
Female
Flow Cytometry
Immunization
Immunosuppression
Inducible T-Cell Co-Stimulator Ligand
L-Selectin - metabolism
Mice
Myelin Proteolipid Protein - immunology
Peptide Fragments - immunology
Proteins - genetics
Proteins - metabolism
T-Lymphocytes, Regulatory - immunology
T-Lymphocytes, Regulatory - metabolism
Transforming Growth Factor beta - biosynthesis
Transforming Growth Factor beta - genetics
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Summary:The role of regulatory T cell populations within the CNS in the regulation of CNS-autoimmunity is controversial. We show that during recovery from relapsing remitting experimental autoimmune encephalomyelitis, regulatory T cells accumulate within the CNS that express high levels of CD62L. These CD62L(high) Treg cells express increased amounts of CTLA-4, ICOS and TGF-β and are more potent than CD62L(low) Treg cells in suppressing proliferation and inducing apoptosis in effector T cells. CD62L(high) Treg cells thus represent a population of Treg cells that display superior immunosuppressive properties and accumulate in the CNS during recovery from CNS-autoimmunity.
ISSN:1090-2139
DOI:10.1016/j.bbi.2010.09.004