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000157717 0247_ $$2doi$$a10.1084/jem.20202411
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000157717 0247_ $$2ISSN$$a0022-1007
000157717 0247_ $$2ISSN$$a1540-9358
000157717 0247_ $$2ISSN$$a1540-9538
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000157717 037__ $$aDZNE-2021-01174
000157717 041__ $$aEnglish
000157717 082__ $$a610
000157717 1001_ $$0P:(DE-HGF)0$$aHeindl, Steffanie$$b0
000157717 245__ $$aChronic T cell proliferation in brains after stroke could interfere with the efficacy of immunotherapies.
000157717 260__ $$aNew York, NY$$bRockefeller Univ. Press$$c2021
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000157717 520__ $$aNeuroinflammation is an emerging focus of translational stroke research. Preclinical studies have demonstrated a critical role for brain-invading lymphocytes in post-stroke pathophysiology. Reducing cerebral lymphocyte invasion by anti-CD49d antibodies consistently improves outcome in the acute phase after experimental stroke models. However, clinical trials testing this approach failed to show efficacy in stroke patients for the chronic outcome 3 mo after stroke. Here, we identify a potential mechanistic reason for this phenomenon by detecting chronic T cell accumulation-evading the systemic therapy-in the post-ischemic brain. We observed a persistent accumulation of T cells in mice and human autopsy samples for more than 1 mo after stroke. Cerebral T cell accumulation in the post-ischemic brain was driven by increased local T cell proliferation rather than by T cell invasion. This observation urges re-evaluation of current immunotherapeutic approaches, which target circulating lymphocytes for promoting recovery after stroke.
000157717 536__ $$0G:(DE-HGF)POF4-352$$a352 - Disease Mechanisms (POF4-352)$$cPOF4-352$$fPOF IV$$x0
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000157717 650_2 $$2MeSH$$aAnimals
000157717 650_2 $$2MeSH$$aAutopsy
000157717 650_2 $$2MeSH$$aBrain: immunology
000157717 650_2 $$2MeSH$$aBrain: pathology
000157717 650_2 $$2MeSH$$aBrain Ischemia: drug therapy
000157717 650_2 $$2MeSH$$aBrain Ischemia: immunology
000157717 650_2 $$2MeSH$$aBrain Ischemia: pathology
000157717 650_2 $$2MeSH$$aCell Proliferation
000157717 650_2 $$2MeSH$$aFemale
000157717 650_2 $$2MeSH$$aHumans
000157717 650_2 $$2MeSH$$aImmunotherapy
000157717 650_2 $$2MeSH$$aIntegrin alpha4: immunology
000157717 650_2 $$2MeSH$$aLymphocyte Count
000157717 650_2 $$2MeSH$$aMale
000157717 650_2 $$2MeSH$$aMice, Inbred C57BL
000157717 650_2 $$2MeSH$$aNatalizumab: pharmacology
000157717 650_2 $$2MeSH$$aNatalizumab: therapeutic use
000157717 650_2 $$2MeSH$$aNeuronal Plasticity: drug effects
000157717 650_2 $$2MeSH$$aRecovery of Function: drug effects
000157717 650_2 $$2MeSH$$aStroke: immunology
000157717 650_2 $$2MeSH$$aStroke: physiopathology
000157717 650_2 $$2MeSH$$aStroke: therapy
000157717 650_2 $$2MeSH$$aT-Lymphocytes: immunology
000157717 7001_ $$0P:(DE-HGF)0$$aRicci, Alessio$$b1
000157717 7001_ $$0P:(DE-HGF)0$$aCarofiglio, Olga$$b2
000157717 7001_ $$0P:(DE-2719)2811347$$aZhou, Qihui$$b3$$udzne
000157717 7001_ $$0P:(DE-2719)2811333$$aArzberger, Thomas$$b4$$udzne
000157717 7001_ $$0P:(DE-HGF)0$$aLenart, Nikolett$$b5
000157717 7001_ $$0P:(DE-HGF)0$$aFranzmeier, Nicolai$$b6
000157717 7001_ $$0P:(DE-HGF)0$$aHortobagyi, Tibor$$b7
000157717 7001_ $$0P:(DE-HGF)0$$aNelson, Peter T$$b8
000157717 7001_ $$0P:(DE-HGF)0$$aStowe, Ann M$$b9
000157717 7001_ $$0P:(DE-HGF)0$$aDenes, Adam$$b10
000157717 7001_ $$0P:(DE-2719)2231621$$aEdbauer, Dieter$$b11$$udzne
000157717 7001_ $$0P:(DE-HGF)0$$aLiesz, Arthur$$b12
000157717 773__ $$0PERI:(DE-600)1477240-1$$a10.1084/jem.20202411$$gVol. 218, no. 8, p. e20202411$$n8$$pe20202411$$tJournal of experimental medicine$$v218$$x1540-9538$$y2021
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000157717 9201_ $$0I:(DE-2719)1110004$$kAG Edbauer$$lCell Biology of Neurodegeneration$$x0
000157717 9201_ $$0I:(DE-2719)5000080$$kAG Zhou$$lAdaptive Immunity in Neurodegeneration$$x1
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