J Autoimmun 2001 Dec;17(4):261-71
Gao YL, Rajan AJ, Raine CS, Brosnan
CF.
Department of Pathology (Neuropathology),
Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, New
York, 10461, USA
In this study, we assessed the expression of activation markers on gammadelta T cells in central nervous system (CNS) lesions of SJL mice adoptively sensitized to develop experimental autoimmune encephalomyelitis (EAE) using myelin basic protein-reactive T cells.
Although disease expression is known to be dependent upon T cells that express the alphabeta T cell receptor (TCR), a role for gammadelta T cells has been implicated in some studies but not in others.
Using three-color flow cytometric analysis of both total and gammadelta T cells in spleen and CNS, the data showed that expression of CD69 (early activation marker), CD62L (lymphocyte homing receptor), CD25 (IL-2Ralpha), CD122 (IL-2Rbeta) and CD95/CD95L (Fas/FasL), fluctuated on gammadelta T cells in EAE lesions in a disease-related fashion.
Furthermore, the pattern of expression for these markers on gammadelta T cells was distinct from that found on the total lymphocyte population.
Cytokine analysis of gammadelta T cells in the CNS demonstrated a bias towards a Th1-like cytokine profile.
From these data, we conclude that
gammadelta T cells in EAE lesions display an activated phenotype and form
a dynamic component of the total lymphocyte population in the CNS, supporting
a contributory role for these cells.
Copyright 2001 Academic Press.