【Abstract】Ischemic stroke has become a major worldwide health problem due to its high recurrence and high disability and is getting increasing attention. Recent studies have shown that immune inflammation plays an important role in all aspects of stroke. This article reviews the progress in the research about the interaction between stroke and inflammatory cells and related antibodies, and the new target to prevent the progression of stroke with a view of providing more efficacious treatment for ischemic stroke.
[1] Herisson F, Frodermann V, Courties G, et al.Direct vascular channels connect skull bone marrow and the brain surface enabling myeloid cell migration[J].Nat Neurosci, 2018,21(9):1209-1217.DOI:10.1038/s41593-018-0213-2.
[2] Herz J, Sabellek P, Lane TE, et al.Role of neutrophils in exacerbation of brain injury after focal cerebral ischemia in hyperlipidemic mice[J].Stroke, 2015,46(10):2916-2925.DOI:10.1161/STROKEAHA.115.010620.
[3] American Academy of Neurology.Use of anti-ICAM-1 therapy in ischemic stroke:results of the Enlimomab Acute Stroke Trial[J].Neurology, 2001,57:1428-1434.
[4] Cuartero MI, Ballesteros I, Moraga A, et al.N2 neutrophils, novel players in brain inflammation after stroke:modulation by the PPARγ agonist rosiglitazone[J].Stroke, 2013,44(12):3498-3508.DOI:10.1161/STROKEAHA.113.002470.
[5] Cai W, Liu S, Hu M, et al.Functional dynamics of neutrophils after ischemic stroke[J].Transl Stroke Res, 2019.DOI:10.1007/s12975-019-00694-y.[Epub ahead of print].
[6] Certo M, Endo Y, Ohta K, et al.Activation of RXR/PPARγ underlies neuroprotection by bexarotene in ischemic stroke[J].Pharmacol Res, 2015,102:298-307.DOI:10.1016/j.phrs.2015.10.009.
[7] Hu X, Li P, Guo Y, et al.Microglia/macrophage polarization dynamics reveal novel mechanism of injury expansion after focal cerebral ischemia[J].Stroke, 2012,43(11):3063-3070.DOI:10.1161/STROKEAHA.112.659656.
[8] Kim BJ, Kim MJ, Park JM, et al.Reduced neurogenesis after suppressed inflammation by minocycline in transient cerebral ischemia in rat[J].J Neurol Sci, 2009,279(1-2):70-75.DOI:10.1016/j.jns.2008.12.025.
[9] Chu HX, Broughton BR, Kim HA, et al.Evidence that Ly6C(hi) monocytes are protective in acute ischemic stroke by promoting M2 macrophage polarization[J].Stroke, 2015,46(7):1929-1937.DOI:10.1161/STROKEAHA.115.009426.
[10] Miró-Mur F, Pérez-de-Puig I, Ferrer-Ferrer M, et al.Immature monocytes recruited to the ischemic mouse brain differentiate into macrophages with features of alternative activation[J].Brain Behav Immun, 2016,53:18-33.DOI:10.1016/j.bbi.2015.08.010.
[11] Jones KA, Maltby S, Plank MW, et al.Peripheral immune cells infiltrate into sites of secondary neurodegeneration after ischemic stroke[J].Brain Behav Immun, 2018,67:299-307.DOI:10.1016/j.bbi.2017.09.006.
[12] Mracsko E, Liesz A, Stojanovic A, et al.Antigen dependently activated cluster of differentiation 8-positive T cells cause perforin-mediated neurotoxicity in experimental-stroke[J].J Neurosci, 2014,34(50):16784-16795.DOI:10.1523/JNEUROSCI.1867-14.2014.
[13] Shrestha R, Millington O, Brewer J, et al.Lymphocyte-mediated neuroprotection in vitro models of excitotoxicity involves astrocytic activation and the inhibition of MAP kinase signalling pathways[J].Neuropharmacology, 2014,76(Pt A):184-193.DOI:10.1016/j.neuropharm.2013.06.025.
[14] Perez-Alvarez MJ, Mario VG, Irene BC, et al.Role of mTORC1 controlling proteostasis after brain ischemia[J].Front Neurosci, 2018,12:60.DOI:10.3389/fnins.2018.00060.
[15] Khoshnam SE, Winlow W, Farzaneh M, et al.Pathogenic mechanisms following ischemic stroke[J].Neurol Sci, 2017,38(7):1167-1186.DOI:10.1007/s10072-017-2938-1.
[16] Youl KJ, Joohyun P, Young CJ, et al.Inflammation after ischemic stroke:the role of leukocytes and glial cells[J].Exp Neurobiol, 2016,25(5):241-251.DOI:10.5607/en.2016.25.5.241.
[17] Xie L, Li W, Hersh J, et al.Experimental ischemic stroke induces long-term T cell activation in the brain[J].J Cereb Blood Flow Metab, 2019,39(11):2268-2276.DOI:10.1177/0271-678X-18792372.
[18] Liddelow SA, Guttenplan KA, Clarke LE, et al.Neurotoxic reactive astrocytes are induced by activated microglia[J].Nature, 2017,541(7638):481-487.DOI:10.1038/nature21029.
[19] Zhu P, Hata R, Ogasawara M, et al.Targeted disruption of organic cation transporter 3(Oct3) ameliorates ischemic brain damage through modulating histamine and regulatory T cells[J].J Cereb Blood Flow Metab, 2012,32(10):1897-1908.DOI:10.1038/jcbfm.2012.92.
[20] Shrestha R, Millington O, Brewer J, et al.Lymphocyte-mediated neuroprotection in vitro models of excitotoxicity involves astrocytic activation and the inhibition of MAP kinase signalling pathways[J].Neuropharmacology, 2014,76:184-193.DOI:10.1016/j.neuropharm.2013.06.025.
[21] Li M, Li Z, Yao Y, et al.Astrocyte-derived interleukin-15 exacerbates ischemic brain injury via propagation of cellular immunity[J].Proc Natl Acad Sci USA, 2017,114(3):E396-E405.DOI:10.1073/pnas.1612930114.
[22] Bornstein NM, Aronovich B, Korczyn AD, et al.Antibodies to brain antigens following stroke[J].Neurology, 2001,56(4):529-530.DOI:10.1212/wnl.56.4.529.
[23] Becker KJ, Kalil AJ, Tanzi P, et al.Autoimmune responses to brain following stroke are associated with worse outcome[J].Stroke, 2011,42:2763-2769.DOI:10.1161/STROKEAHA.111.619593.
[24] Cho HJ, Kim SS, Sung SM, et al.Impact of thyroid autoantibodies on functional outcome in patients with acute ischemic stroke[J].J Stroke Cerebrovasc Dis, 2014,23(7):1915-1920.DOI:10.1016/j.jstrokecerebrovasdis.2014.02.008.
[25] Carbone F, Satta N, Montecucco F, et al.Anti-ApoA-1 IgG serum levels predict worse post-stroke outcomes[J].Eur J Clin Invest, 2016,46(9):805-817.DOI:10.1111/eci.12664.
[26] Hosseini H, Li Y, Kanellakis P, et al.Phosphatidylserine liposomes mimic apoptotic cells to attenuate atherosclerosis by expand-ing polyreactive IgM producing B1a lymphocytes[J].Cardiovasc Res, 2015,106(3):443-452.DOI:10.1093/cvr/cvv037.
[27] Yoichi Y, Takaki H, Toshio M, et al.Elevation of autoantibody in patients with ischemic stroke[J].Neurol Med Chir (Tokyo), 2018,58(7):303-310.DOI:10.2176/nmc.ra.2018-0022.