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Adhesion molecule phenotype of T lymphocytes in inflamed CNS
The phenotype of T cells in the central nervous system (CNS) in two models of chronic inflammation (experimental allergic encephalomyelitis and Corynebacterium parvum-induced inflammation) was compared to that of T cells in gut and chronically inflamed subcutaneous tissue and lung. CNS T cells displ...
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Published in: | Journal of neuroimmunology 1998-04, Vol.84 (1), p.92-104 |
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Main Authors: | , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The phenotype of T cells in the central nervous system (CNS) in two models of chronic inflammation (experimental allergic encephalomyelitis and
Corynebacterium parvum-induced inflammation) was compared to that of T cells in gut and chronically inflamed subcutaneous tissue and lung. CNS T cells display a similar phenotype in both inflammatory models, and are phenotypically unique compared to T cells from the other inflamed tissues. T cells from inflamed CNS are mainly CD4
+ and are the only population examined that express a typical activated/memory phenotype: CD44
high/LFA-1
high/ICAM-1
high/CD45RB
low. The CNS T cells are
α
4
β
7-integrin
negative, but express
α
4-integrin and activated
β
1 integrin, suggesting expression of the
α
4
β
1-heterodimer in an activated state. In contrast, most T cells in gut express low levels of activated
β
1 integrin. The CNS T cells lack expression of
α
6 and
α
E integrin chains and L-selectin. In inflamed CNS and inflamed subcutaneous tissue, approximately 50% of T cells express high affinity ligands for P-selectin while fewer than 10% express high affinity ligands for E-selectin. In summary, our data show that, independent of the inflammatory stimulus, T cells recruited into the inflamed CNS are phenotypically distinct from T cells in other inflamed tissues. This finding leads us to hypothesize the existence of a phenotypically distinct `CNS-seeking' T lymphocyte population. |
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ISSN: | 0165-5728 1872-8421 |
DOI: | 10.1016/S0165-5728(97)00237-3 |