Peripheral Immune Response to CNS Injury
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EDITORIAL
Peripheral Immune Response to CNS Injury Keith R. Pennypacker
Received: 24 July 2012 / Accepted: 26 July 2012 / Published online: 11 August 2012 # Springer Science+Business Media, LLC 2012
Despite considerable research effort in the area of acute neural injury, no therapeutic breakthroughs have been discovered in recent years. Alternative approaches for pharmacological intervention are needed to target the processes associated with these neuropathologies. The peripheral immune system plays a role in the delayed neurodegeneration occurring in stroke and traumatic brain injury as well as in chronic neural diseases. Broadly inhibiting the immune response to neural injury has not been successful. A further understanding of the immune–brain interaction during injury could provide more specific targets for treatment. This issue is devoted to examination of the immune response to neural injury and provides insight into potential molecular targets for drug treatment. Dr. Becker reviews her laboratory’s work examining the cellular immune responses directed toward brain antigens in both animal models of stroke and patients after ischemic stroke. These responses have been identified as TH1(+) linked to exacerbated stroke outcome and antigen-specific TREG which results in a more positive outcome. The development of a TH1(+) response is correlated with an inflammatory background, such as a systemic inflammatory stimulus in experimental stroke or a systemic infection in stroke patients. The conclusion is that systemic inflammation alters the microenvironment in the brain and lymph nodes leading to the development of an autoimmune response to brain antigens after cerebral ischemic injury. Dr. Garbuzova examines the involvement of innate and adaptive immune systems in amyotrophic lateral sclerosis (ALS). Modulation of the immune system has been reported to provide beneficial outcome in ALS animal models, but these results have not translated to human patients. Regulatory B lymphocytes in experimental stroke are a potential protective cell type as cited by Drs. Offner and Hurn. K. R. Pennypacker (*) Department of Molecular Pharmacology and Physiology, School of Biomedical Sciences, Morsani College of Medicine, University of South Florida, Tampa, FL, USA e-mail: [email protected]
Lack of B cells leads to increased infarct volume while restoration of B cells reverses this effect. Regulatory B cells that produce IL-10 are protective. Agents that enhance their presence would be applicable as a novel therapy for stroke. The manuscript of Hetz et al. describes that when cellular therapies are used to treat traumatic brain injury (TBI), there is a reduction in cellular degeneration due to decreased inflammation. These cell therapies interact with reactive macrophages in the spleen. This interaction at the spleen culminates in the systemic immune response switching to an anti-inflammatory mode. The report from Dr. Yenari’s laboratory furthers the role of inflammation in contributing to the exacerbation of stroke. This r
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