Expression of ICAM-1, VCAM-1, L-selectin, and leukosialin in the mouse central nervous system during the induction and remission stages of experimental allergic encephalomyelitis
- 31 October 1994
- journal article
- Published by Elsevier in Journal of Neuroimmunology
- Vol. 54 (1-2), 129-144
- https://doi.org/10.1016/0165-5728(94)90239-9
Abstract
No abstract availableKeywords
This publication has 35 references indexed in Scilit:
- Encephalitogenic Th1 cells are inhibited by Th2 cells with related peptide specificity: Relative roles of interleukin (IL)-4 and IL-10Journal of Neuroimmunology, 1993
- Inhibition of experimental autoimmune encephalomyelitis by an antibody to the intercellular adhesion molecule ICAM‐1Annals of Neurology, 1993
- ICAM-1-dependent pathway is not critically involved in the inflammatory process of autoimmune encephalomyelitis or in cytokine-induced inflammation of the central nervous systemJournal of Neuroimmunology, 1993
- Surface expression of alpha 4 integrin by CD4 T cells is required for their entry into brain parenchyma.The Journal of Experimental Medicine, 1993
- CD43, a molecule defective in Wiskott-Aldrich syndrome, binds ICAM-1Nature, 1991
- Enhancement of T-cell activation by the CD43 molecule whose expression is defective in Wiskott–Aldrich syndromeNature, 1991
- Adhesion receptors of the immune systemNature, 1990
- Lymphocyte migration into brain modelled in vitro: Control by lymphocyte activation, cytokines, and antigenCellular Immunology, 1990
- Neutrophil Mac-1 and MEL-14 Adhesion Proteins Inversely Regulated by Chemotactic FactorsScience, 1989
- Interleukin 1 of the central nervous system is produced by ameboid microglia.The Journal of Experimental Medicine, 1986