T-cell trafficking in the central nervous system.
To perform their distinct effector functions, pathogen-specific T cells have to migrate to target tissue where they recognize antigens and produce cytokines that elicit appropriate types of protective responses. Similarly, migration of pathogenic self-reactive T cells to target organs is an essential step required for tissue-specific autoimmunity. In this article, we review data from our laboratory as well as other laboratories that have established that effector function and migratory capacity are coordinately regulated in different T-cell subsets. We then describe how pathogenic T cells can enter into intact or inflamed central nervous system (CNS) to cause experimental autoimmune encephalomyelitis or multiple sclerosis. In particular, we elaborate on the role of CCR6/CCL20 axis in migration through the choroid plexus and the involvement of this pathway in immune surveillance of and autoimmunity in the CNS.
Institute for Research in Biomedicine, Bellinzona, Switzerland. federica.sallusto@irb.usi.ch
Federica
F
Sallusto
Daniela
D
Impellizzieri
Camilla
C
Basso
Alice
A
Laroni
Antonio
A
Uccelli
Antonio
A
Lanzavecchia
Britta
B
Engelhardt
D000818:Animals; D015551:Autoimmunity; D001812:Blood-Brain Barrier / Q000276:immunology / Q000473:pathology; D002465:Cell Movement / Q000276:immunology*; D002490:Central Nervous System / Q000276:immunology* / Q000473:pathology; D002831:Choroid Plexus / Q000276:immunology / Q000473:pathology; D006801:Humans; D007157:Immunologic Surveillance; D007249:Inflammation / Q000276:immunology / Q000473:pathology; D009103:Multiple Sclerosis / Q000276:immunology / Q000473:pathology / Q000628:therapy; D016176:T-Lymphocyte Subsets / Q000276:immunology* / Q000378:metabolism