期刊
JOURNAL OF NEUROIMMUNOLOGY
卷 230, 期 1-2, 页码 33-41出版社
ELSEVIER
DOI: 10.1016/j.jneuroim.2010.08.014
关键词
CD4+CD25+regulatory T cells; Neuroprotection; HIV-1; Macrophage; Blood brain barrier; Single photon emission; computed tomography
资金
- NIH [P20 RR15635, I P01 NS043985-01, 2R37 NS36126, 5 P01 MH64570-03]
- NATIONAL CENTER FOR RESEARCH RESOURCES [P20RR015635] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF MENTAL HEALTH [P01MH064570, P01MH057556, P30MH062261] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS036126, R37NS036126, P01NS031492, P01NS043985, R01NS070190, R01NS034239] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [P01DA026146, P01DA028555] Funding Source: NIH RePORTER
CD4+CD25+ regulatory T cells (Treg) transform the HIV-1 infected macrophage from a neurotoxic to a neuroprotective phenotype. This was demonstrated previously in a murine model of HIV-1 encephalitis induced by intracranial injection of HIV-1/vesicular stomatitis virus-infected bone marrow macrophages. In this report, relationships between Treg ingress of end organ tissues, notably the brain, and neuroprotection were investigated. Treg from EGFP-transgenic donor mice were expanded, labeled with indium-111. and adoptively transferred. Treg distribution was assayed by single photon emission computed tomography and immunohistochemistry. Treg readily migrated across the blood brain barrier and were retained within virus-induced neuroinflammatory sites. In non-inflamed peripheral tissues (liver and spleen) Treg were depleted. These observations demonstrate that Treg migrate to sites of inflammation where they modulate immune responses. (C) 2010 Elsevier B.V. All rights reserved.
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