The DOI matches its Crossref record; 38 of the 38 references it cites were found in a registry or an index.
Emerging Roles for the Immune System in Traumatic Brain Injury
Open accessAbstract
Traumatic brain injury (TBI) affects an ever-growing population of all ages with long-term consequences on health and cognition. Many of the issues that TBI patients face are thought to be mediated by the immune system. Primary brain damage that occurs at the time of injury can be exacerbated and prolonged for months or even years by chronic inflammatory processes, which can ultimately lead to secondary cell death, neurodegeneration, and long-lasting neurological impairment. Researchers have turned to rodent models of TBI in order to understand how inflammatory cells and immunological signaling regulate the post-injury response and recovery mechanisms. In addition, the development of numerous methods to manipulate genes involved in inflammation has recently expanded the possibilities of investigating the immune response in TBI models. As results from these studies accumulate, scientists have started to link cells and signaling pathways to pro- and anti-inflammatory processes that may contribute beneficial or detrimental effects to the injured brain. Moreover, emerging data suggest that targeting aspects of the immune response may offer promising strategies to treat TBI. This review will cover insights gained from studies that approach TBI research from an immunological perspective and will summarize our current understanding of the involvement of specific immune cell types and cytokines in TBI pathogenesis.
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Citations
Cites
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
From inflammation to sickness and depression: when the immune system subjugates the brain
Dantzer, R., O'Connor, J. C., Freund, G. G., Johnson, R. W., & Kelley, K. W. (2008) · Nature Reviews Neuroscience · doi:10.1038/nrn2297 · Cited by 7,395
Neutrophil recruitment and function in health and inflammation
Kolaczkowska, E., & Kubes, P. (2013) · Nature Reviews Immunology · doi:10.1038/nri3399 · Cited by 5,472
Caspase-11 cleaves gasdermin D for non-canonical inflammasome signalling
Kayagaki, N., Stowe, I. B., Lee, B. L., O’Rourke, K., Anderson, K., Warming, S., Cuellar, T., Haley, B., Roose-Girma, M., Phung, Q. T., et al. (2015) · Nature · doi:10.1038/nature15541 · Cited by 3,686
Activation and regulation of the inflammasomes
Latz, E., Xiao, T. S., & Stutz, A. (2013) · Nature Reviews Immunology · doi:10.1038/nri3452 · Cited by 2,884
Mild traumatic brain injury in U.S. soldiers returning from Iraq
Hoge, C. W., McGurk, D., Thomas, J. L., Cox, A. L., Engel, C. C., & Castro, C. A. (2008) · New England Journal of Medicine · doi:10.1056/nejmoa072972 · Cited by 2,775
Chronic traumatic encephalopathy in athletes: Progressive tauopathy after repetitive head injury
McKee, A. C., Cantu, R. C., Nowinski, C. J., Hedley-Whyte, E. T., Gavett, B. E., Budson, A. E., Santini, V. E., Lee, H.-S., Kubilus, C. A., & Stern, R. A. (2009) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e3181a9d503 · Cited by 2,295
Apolipoprotein E controls cerebrovascular integrity via cyclophilin A
Bell, R. D., Winkler, E. A., Singh, I., Sagare, A. P., Deane, R., Wu, Z., Holtzman, D. M., Betsholtz, C., Armulik, A., Sallstrom, J., et al. (2012) · Nature · doi:10.1038/nature11087 · Cited by 1,293 · cited 1×
“Moreover, transgenic overexpression of APOEε4 in mice was also found to cause worsened brain pathology, BBB breakdown, and neurological impairments following brain injury (159, 160).”
BackgroundTakahashi, K., Rochford, C. D. P., & Neumann, H. (2005) · The Journal of Experimental Medicine · doi:10.1084/jem.20041611 · Cited by 1,124
Inflammation after trauma: Microglial activation and traumatic brain injury
Ramlackhansingh, A. F., Brooks, D. J., Greenwood, R. J., Bose, S. K., Turkheimer, F. E., Kinnunen, K. M., Gentleman, S., Heckemann, R. A., Gunanayagam, K., Gelosa, G., et al. (2011) · Annals of Neurology · doi:10.1002/ana.22455 · Cited by 999
Yeh, F. L., Wang, Y., Tom, I., Gonzalez, L. C., & Sheng, M. (2016) · Neuron · doi:10.1016/j.neuron.2016.06.015 · Cited by 943
Inflammation and neuroprotection in traumatic brain injury.
Corps, K. N., Roth, T. L., & McGavern, D. B. (2015) · JAMA Neurology · doi:10.1001/jamaneurol.2014.3558 · Cited by 853
Jay, T. R., Miller, C. M., Cheng, P. J., Graham, L. C., Bemiller, S., Broihier, M. L., Xu, G., Margevicius, D., Karlo, J. C., Sousa, G. L., et al. (2015) · Journal of Experimental Medicine · doi:10.1084/jem.20142322 · Cited by 682
Walsh, J. G., Muruve, D. A., & Power, C. (2014) · Nature Reviews Neuroscience · doi:10.1038/nrn3638 · Cited by 637 · cited 1×
“Since the finding that inflammasome proteins are upregulated after TBI in human patients (98), significant attention has been paid to identify the inflammasome-associated signaling events that are engaged in response to brain trauma (14, 99, 100).”
BackgroundAging-induced type I interferon response at the choroid plexus negatively affects brain function
Baruch, K., Deczkowska, A., David, E., Castellano, J. M., Miller, O., Kertser, A., Berkutzki, T., Barnett-Itzhaki, Z., Bezalel, D., Wyss-Coray, T., et al. (2014) · Science · doi:10.1126/science.1252945 · Cited by 615
Mortimer, J. A., Van Duijn, C. M., Chandra, V, Fratiglioni, L., Graves, A. B., Heyman, A., Jorm, A. F., Kokmen, E., Kondo, K., Rocca, W. A., et al. (1991) · International Journal of Epidemiology · doi:10.1093/ije/20.supplement_2.s28 · Cited by 594
DICER1 loss and Alu RNA induce age-related macular degeneration via the NLRP3 inflammasome and MyD88
Tarallo, V., Hirano, Y., Gelfand, B. D., Dridi, S., Kerur, N., Kim, Y., Cho, W. G., Kaneko, H., Fowler, B. J., Bogdanovich, S., et al. (2012) · Cell · doi:10.1016/j.cell.2012.03.036 · Cited by 592
Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?
Johnson, V. E., Stewart, W., & Smith, D. H. (2010) · Nature Reviews Neuroscience · doi:10.1038/nrn2808 · Cited by 587
Roberts, G. W., Gentleman, S. M., Lynch, A., Murray, L., Landon, M., & Graham, D. I. (1994) · Journal of Neurology, Neurosurgery & Psychiatry · doi:10.1136/jnnp.57.4.419 · Cited by 569
The role of interleukin-1 in neuroinflammation and Alzheimer disease: an evolving perspective
Shaftel, S. S., Griffin, W. S. T., & O'Banion, M. K. (2008) · Journal of Neuroinflammation · doi:10.1186/1742-2094-5-7 · Cited by 565
Soares, H., Hicks, R., Smith, D., & McIntosh, T. (1995) · The Journal of Neuroscience · doi:10.1523/jneurosci.15-12-08223.1995 · Cited by 379
NLRP3 inflammasome is expressed and functional in mouse brain microglia but not in astrocytes
Gustin, A., Kirchmeyer, M., Koncina, E., Felten, P., Losciuto, S., Heurtaux, T., Tardivel, A., Heuschling, P., & Dostert, C. (2015) · PLoS ONE · doi:10.1371/journal.pone.0130624 · Cited by 369
Dealing with danger in the CNS: the response of the immune system to injury
Gadani, S. P., Walsh, J. T., Lukens, J. R., & Kipnis, J. (2015) · Neuron · doi:10.1016/j.neuron.2015.05.019 · Cited by 342
Self-citationA Molecular Platform in Neurons Regulates Inflammation after Spinal Cord Injury
de Rivero Vaccari, J. P., Lotocki, G., Marcillo, A. E., Dietrich, W. D., & Keane, R. W. (2008) · The Journal of Neuroscience · doi:10.1523/jneurosci.0157-08.2008 · Cited by 332
de Rivero Vaccari, J. P., Lotocki, G., Alonso, O. F., Bramlett, H. M., Dietrich, W. D., & Keane, R. W. (2009) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2009.46 · Cited by 312
Amyloid-β Dynamics Correlate with Neurological Status in the Injured Human Brain
Brody, D. L., Magnoni, S., Schwetye, K. E., Spinner, M. L., Esparza, T. J., Stocchetti, N., Zipfel, G. J., & Holtzman, D. M. (2008) · Science · doi:10.1126/science.1161591 · Cited by 295
Head Injury and Amyotrophic Lateral Sclerosis
Chen, H., Richard, M., Sandler, D. P., Umbach, D. M., & Kamel, F. (2007) · American Journal of Epidemiology · doi:10.1093/aje/kwm153 · Cited by 279
Morganti, J. M., Jopson, T. D., Liu, S., Riparip, L.-K., Guandique, C. K., Gupta, N., Ferguson, A. R., & Rosi, S. (2015) · The Journal of Neuroscience · doi:10.1523/jneurosci.2405-14.2015 · Cited by 253 · cited 14×
“A later CCI study also pointed to beneficial effects of IL-6 by showing that its deficiency leads to significantly poorer performance on behavioral tests as well as higher IL-1β protein levels in the cortex, suggesting that IL-6 may be an important regulator of IL-1β in TBI (117).”
BackgroundInfluentialAmyloid precursor protein secretases as therapeutic targets for traumatic brain injury
Loane, D. J., Pocivavsek, A., Moussa, C. E.-H., Thompson, R., Matsuoka, Y., Faden, A. I., Rebeck, G. W., & Burns, M. P. (2009) · Nature Medicine · doi:10.1038/nm.1940 · Cited by 246
Immune Surveillance of the CNS following Infection and Injury
Russo, M. V., & McGavern, D. B. (2015) · Trends in Immunology · doi:10.1016/j.it.2015.08.002 · Cited by 191
Hsieh, C. L., Niemi, E. C., Wang, S. H., Lee, C. C., Bingham, D., Zhang, J., Cozen, M. L., Charo, I., Huang, E. J., Liu, J., et al. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.3252 · Cited by 174
Understanding the Role of T Cells in CNS Homeostasis
Ellwardt, E., Walsh, J. T., Kipnis, J., & Zipp, F. (2016) · Trends in Immunology · doi:10.1016/j.it.2015.12.008 · Cited by 156
Muccigrosso, M. M., Ford, J., Benner, B., Moussa, D., Burnsides, C., Fenn, A. M., Popovich, P. G., Lifshitz, J., Walker, F. R., Eiferman, D. S., et al. (2016) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2016.01.009 · Cited by 146 · cited 1×
“org December 2016 | Volume 7 | Article 556 deficits that could be linked to TBI-mediated microglia priming (54).”
BackgroundThe immunology of traumatic brain injury: a prime target for Alzheimer’s disease prevention
Giunta, B., Obregon, D., Velisetty, R., Sanberg, P. R., Borlongan, C. V., & Tan, J. (2012) · Journal of Neuroinflammation · doi:10.1186/1742-2094-9-185 · Cited by 112
Washington, P. M., Morffy, N., Parsadanian, M., Zapple, D. N., & Burns, M. P. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.3017 · Cited by 103 · cited 1×
“These studies have shown that brain trauma can spur the aberrant release and deposition of both amyloid beta (Aβ) and tau (144).”
BackgroundCcr2 deletion dissociates cavity size and tau pathology after mild traumatic brain injury
Gyoneva, S., Kim, D., Katsumoto, A., Kokiko-Cochran, O. N., Lamb, B. T., & Ransohoff, R. M. (2015) · Journal of Neuroinflammation · doi:10.1186/s12974-015-0443-0 · Cited by 95 · cited 6×
“A recent article by Saber et al. used an FPI injury model to explore the effect of TREM2 on TBIinduced neuroinflammation, tissue loss, and neurological function (83).”
BackgroundInfluentialZanier, E. R., Marchesi, F., Ortolano, F., Perego, C., Arabian, M., Zoerle, T., Sammali, E., Pischiutta, F., & De Simoni, M.-G. (2016) · Journal of Neurotrauma · doi:10.1089/neu.2015.4041 · Cited by 94 · cited 2×
“term functional impairments and elevated myeloid cell activation (50)”
BackgroundMethodBennett, R. E., & Brody, D. L. (2014) · Journal of Neurotrauma · doi:10.1089/neu.2013.3320 · Cited by 64
Cited by
Huang, S., Ge, X., Yu, J., Han, Z., Yin, Z., Li, Y., Chen, F., Wang, H., Zhang, J., & Lei, P. (2018) · The FASEB Journal · doi:10.1096/fj.201700673r · Cited by 388
Meningeal lymphatic dysfunction exacerbates traumatic brain injury pathogenesis.
Bolte, A. C., Dutta, A. B., Hurt, M. E., Smirnov, I., Kovacs, M. A., McKee, C. A., Ennerfelt, H. E., Shapiro, D., Nguyen, B. H., Frost, E. L., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-18113-4 · Cited by 357
Xia, X., Wang, Y., Huang, Y., Zhang, H., Lu, H., & Zheng, J. C. (2019) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2019.101694 · Cited by 202
Parihar, V. K., Maroso, M., Syage, A., Allen, B. D., Angulo, M. C., Soltesz, I., & Limoli, C. L. (2018) · Experimental Neurology · doi:10.1016/j.expneurol.2018.03.009 · Cited by 127
Co-transplantation of autologous Treg cells in a cell therapy for Parkinson’s disease
Park, T.-Y., Jeon, J., Lee, N., Kim, J., Song, B., Kim, J.-H., Lee, S.-K., Liu, D., Cha, Y., Kim, M., et al. (2023) · Nature · doi:10.1038/s41586-023-06300-4 · Cited by 128
Metadata
- Authors
- McKee, C. A., & Lukens, J. R.
- Venue
- Frontiers in Immunology
- Publisher
- Frontiers Media SA
- Published
- 2016-12-05
- Volume
- 7
- Pages
- 556-556
- ISSN
- 1664-3224 (ISSN-L)
- OpenAlex
- W2560167144
- Cited by
- 263
- References
- 38
- FWCI
- 15.66
- Type
- journal article
- Language
- en
- Open access
- gold
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