Cytokine-Induced Inflammation in the Central Nervous System Revisited |
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Authors: | Martiney James A. Cuff Carolyn Litwak Mona Berman Joan Brosnan Celia F. |
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Affiliation: | (1) Laboratory of Microbial Pathogenesis, The Picower Institute for Medical Research, Manhasset, NY, 11030;(2) Department of Epidemiology & Public Health and Immunobiology, Yale University School of Medicine, New Haven, CT;(3) Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY, 10461;(4) Departments of Pathology, Microbiology and Immunology, Albert Einstein College of Medicine, Bronx, NY, 10461 |
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Abstract: | Cytokines play an essential role as mediators of the immune response. They usually function as part of a network of interactive signals that either activate, enhance, or inhibit the ensuing reaction. An important contribution of this cytokine cascade is the induction of an inflammatory response that recruits and activates subsets of leukocytes that function as effector cells in the response to the sensitizing antigen. Proinflammatory cytokines activate endothelial cells (EC) to express adhesion molecules and induce the release of members of the chemokine family, thus focusing and directing the inflammatory response to sites of antigen recognition. However, the vasculature of the central nervous system (CNS) is highly specialized and restricts the access of components of the immune system to the CNS compartment. In this review, we address the question as to whether endothelial cells in the CNS respond differently to specific cytokines known to induce either a proinflammatory effect or a regulatory effect in systemic vascular beds. |
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Keywords: | CNS inflammation neuroimmunology cytokines chemokines adhesion molecules review |
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