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      Overview of Traumatic Brain Injury: An Immunological Context

      1 , 2 , 1 , 2 , *

      Brain Sciences

      MDPI

      traumatic brain injury, neuroimmunity, neuroinflammation

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          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Traumatic brain injury (TBI) afflicts people of all ages and genders, and the severity of injury ranges from concussion/mild TBI to severe TBI. Across all spectrums, TBI has wide-ranging, and variable symptomology and outcomes. Treatment options are lacking for the early neuropathology associated with TBIs and for the chronic neuropathological and neurobehavioral deficits. Inflammation and neuroinflammation appear to be major mediators of TBI outcomes. These systems are being intensively studies using animal models and human translational studies, in the hopes of understanding the mechanisms of TBI, and developing therapeutic strategies to improve the outcomes of the millions of people impacted by TBIs each year. This manuscript provides an overview of the epidemiology and outcomes of TBI, and presents data obtained from animal and human studies focusing on an inflammatory and immunological context. Such a context is timely, as recent studies blur the traditional understanding of an “immune-privileged” central nervous system. In presenting the evidence for specific, adaptive immune response after TBI, it is hoped that future studies will be interpreted using a broader perspective that includes the contributions of the peripheral immune system, to central nervous system disorders, notably TBI and post-traumatic syndromes.

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          Most cited references 143

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          Naturally arising Foxp3-expressing CD25+CD4+ regulatory T cells in immunological tolerance to self and non-self.

          Naturally arising CD25(+)CD4(+) regulatory T cells actively maintain immunological self-tolerance. Deficiency in or dysfunction of these cells can be a cause of autoimmune disease. A reduction in their number or function can also elicit tumor immunity, whereas their antigen-specific population expansion can establish transplantation tolerance. They are therefore a good target for designing ways to induce or abrogate immunological tolerance to self and non-self antigens.
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            ASSESSMENT OF OUTCOME AFTER SEVERE BRAIN DAMAGE A Practical Scale

             B Jennett (1975)
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              The IL-1 family: regulators of immunity.

              Over recent years it has become increasingly clear that innate immune responses can shape the adaptive immune response. Among the most potent molecules of the innate immune system are the interleukin-1 (IL-1) family members. These evolutionarily ancient cytokines are made by and act on innate immune cells to influence their survival and function. In addition, they act directly on lymphocytes to reinforce certain adaptive immune responses. This Review provides an overview of both the long-established and more recently characterized members of the IL-1 family. In addition to their effects on immune cells, their involvement in human disease and disease models is discussed.
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                Author and article information

                Contributors
                Role: Academic Editor
                Journal
                Brain Sci
                Brain Sci
                brainsci
                Brain Sciences
                MDPI
                2076-3425
                23 January 2017
                January 2017
                : 7
                : 1
                Affiliations
                [1 ]Department of Surgery, Texas A & M University Health Science Center, College of Medicine, Temple, TX 76504, USA; dnizamutdinov@ 123456medicine.tamhsc.edu
                [2 ]Department of Neurosurgery, Neuroscience Research Institute, Baylor Scott & White Health, Temple, TX 76504, USA
                Author notes
                [* ]Correspondence: lshapiro@ 123456medicine.tamhsc.edu ; Tel.: +1-254-724-6267
                Article
                brainsci-07-00011
                10.3390/brainsci7010011
                5297300
                28124982
                © 2017 by the authors; licensee MDPI, Basel, Switzerland.

                This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

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