@article{4e07a0a43023478c853e2cb0d5d86de5,
title = "Co-expression of adhesion molecules during GNS inflammation in murine EAE",
author = "Barbara Cannella and Cross, \{Anne H.\} and Raine, \{Cedric S.\}",
note = "Funding Information: CO-EXPRESSION OF ADHESION MOLECULES DURING GNS INFLAMMATION IN MURINE EAE Barbara Cannella, Anne H. Cross and Cedric S. Raine Albert Einstein College of Medicine, Bronx, NY, USA The expression of molecules implicated in lymphocyte adhesion and trafficking has been examined within the CNS of mice with adoptively-transferred EAE where increases in vascular permeability and horn; Ig of T cells to the CNS have been shown. An immunocytochemical/ultrastructural analysis was performed on spinal cord tissue from animals sampled during the pro-clinical, acute, remitting and relapsing stages of EAE. MAb to a high endothelial vanule (HEV) differentiation antigen, MECA-325; to MALA-2, the murine homolog of human intcrcellular adhesion molecule-1 (ICAM-I); to lymphocyte function-associated antigen, LFA-I (the receptor for ICAM-I); to MHC clas\textasciitilde{} I and H molecules, a\_\textasciitilde{}d \textasciitilde{}o t\textbackslash{}]ieir\textasciitilde{} eptors, CD8 and CD4, were applied. These antibodies revealen consistently high levels of expression during periods of inOemmation (acute onset and relapses) and downregulation during remissions. MECA-79, which defines a peripheral lymph node HEV addressin, was uniformly negative within the CNS throughout all stages of EAE. MECA-367 and MECA-89, which both define distinct epitopes on the same mucosal addrc.\textasciitilde{}sin, stained endothelium of inflamed vessels within lesions as\textasciitilde{}-\textasciitilde{}ciated with relapses. Ultrastructurally, at the height of disease and adhesion molecule expression, blood vessels showed lymphocyte attachment and transmigration which involved unique membrane specializations. Thus, the upregulated simultaneous expression of lymphoid adhesion molecules in the GNS might support a role for receptor-mediated inflammatory cell invasion of relevance to the initiation and perpetuation of inflammation in multiple sclerosis. (Supported by NMSS RG 1001-G-7 and JF 2042-A-2; and NIH NS 08952 and NS 11920).",
year = "1991",
doi = "10.1016/0165-5728(91)90505-2",
language = "English",
volume = "1991",
pages = "152",
journal = "Journal of Neuroimmunology",
issn = "0165-5728",
number = "SUPPL. 1",
}