International Immunology, Vol. 7, No. 3, pp. 481-491,March 1995
© 1995 Japanese Society for Immunology
Lymphocytes infiltrating the CNS during inflammation display a distinctive phenotype and bind to VCAM-1 but not to MAdCAM-1
1 Department of Pathology, Laboratory of Immunology and Vascular Biology and the Digestive Disease Center Stanford, CA 94305, USA
2Present address: Max-Planck-Institut für physiologische und klinische Forschung, W. G. Kerckhoff-Institut, Abteilung Molekulare Zellbiologie, Parkstrasse 1, 61231 Bad Nauheim, Germany
3 Department of Neurosurgery, Stanford University School of Medicine Stanford, CA 94305, USA
4 Department of Immunology, AFRC Babraham Institute Cambridge, UK
5 Center for Molecular Biology and Medicine, the Palo Alto Veterans Administration Medical Center Palo Alto, CA 94304, USA
Correspondence to: Correspondence to: B. Engelhardt
The nature of inflammatory lymphocytes recruited to the CNS has been studied in a model of chronic inflammation. Injection of killed Corynebacterlum parvum into the cortex of the mouse brain produces a circumscribed inflammatory cellular infiltrate around the injection site, and recruited mononuclear inflammatory cells (IC) can be isolated for flow cytometric analysis. The majority of IC were T cells. In comparison with the predominant naive population of mesenteric lymph node T cells, IC T cells express much higher levels of CD44, LFA-1 and ICAM-1, and lower levels of CD45RB, features commonly associated with memory (previously activated) cells. In addition, in contrast to the L-selectin+ 
6-integrinlow phenotype of naive lymph node T cells, IC T cells lacked L-selectin and were 6-integrin–. Mac-1, recently proposed as another marker of memory T cell differentation, was not displayed by IC T cells, suggesting that Mac-1 expression may be heterogeneous among memory T cell subsets. A subset of mesenteric lymph node (MLN) T cells, probably representing activated T cells undergoing the naive to memory transition, but not of IC T cells, expressed high levels of 6-, ß7- and E-integrin. IC and MLN naive T cells expressed comparable levels of 4-integrin, but IC T cells stain poorly with anti-ß7 mAbs and with mAb DATK 32, specific for the 4ß7 heterodimeric lymphocyte homing receptor for the mucosal addressin MAdCAM-1, suggesting that these inflammatory cells express more 4ß1 than 4ß7. Consistent with this, in in vitro adhesion assays, brain IC bound better than MLN cells to the 4ß1 integrin ligand VCAM-1 and the LFA-1 ligand ICAM-1 but adhered very poorly to the 4ß7 ligand MAdCAM-1. These findings are consistent with and extend previous immunohistological studies of T cells in murine experimental autoimmune encephalomyelitis, and demonstrate a distinctive phenotype for lymphocytes being present in the chronically inflamed brain.
Keywords: cell adhesion molecules, CNS, inflammation, T memory cells
Received 31 October 1994, accepted 5 December 1994.
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