Abstract
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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 33-41 |
| Number of pages | 9 |
| Journal | Journal of Neuroimmunology |
| Volume | 230 |
| Issue number | 1-2 |
| DOIs | |
| State | Published - Jan 2011 |
Keywords
- Blood brain barrier
- CD4+CD25+ regulatory T cells
- HIV-1
- Macrophage
- Neuroprotection
- Single photon emission computed tomography
ASJC Scopus subject areas
- Immunology and Allergy
- Immunology
- Neurology
- Clinical Neurology