Interaction between the immune and central nervous systems.
Much of the understanding of tolerance has focused on the requirements for antigen-specific lymphocyte activation and function. However, there is increasing evidence for anatomic regulation of effector access to self antigens. Recently, a number of studies have provided evidence for tissue-specific "addressins" in chemokine/chemokine receptor pairs. The central nervous system (CNS) provides special anatomic barriers to the movement of cells from the vascular compartment to the parenchyma. Herein I raise the possibility that antigen, perhaps through specialized antigen-presenting cells, may play a role in regulating access of activated lymphocytes into the CNS parenchyma. The results suggest that a reexamination of the widely held dogma that all activated lymphocytes have access to the CNS parenchyma is necessary to understand the relationship between the immune and central nervous systems.
Russell
John H
JH
Program in Immunology, Department of Molecular Biology and Pharmacology, Washington University School of Medicine, St. Louis, MO 63110, USA. jrussell@wustl.edu
D000818:Animals; D017951:Antigen Presentation; D001324:Autoantigens; D002465:Cell Movement / Q000276:immunology; D002490:Central Nervous System / Q000276:immunology*; D004681:Encephalomyelitis, Autoimmune, Experimental / Q000276:immunology; D006801:Humans; D007249:Inflammation / Q000209:etiology / Q000276:immunology; D007962:Leukocytes / Q000276:immunology; D008213:Lymphocyte Activation; D051379:Mice; D015213:Neuroimmunomodulation; D047888:Receptors, Tumor Necrosis Factor, Type I / Q000276:immunology; D019014:fas Receptor / Q000276:immunology
D001324:Autoantigens; D047888:Receptors, Tumor Necrosis Factor, Type I; D019014:fas Receptor