Adhesion molecule phenotype of T lymphocytes in inflamed CNS

Abstract

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.