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Trafficking of FoxP3+ regulatory T cells: myths and facts

100%
Kim C. H.
Archivum Immunologiae et Therapiae Experimentalis
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2007
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vol. 55
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issue 3
151-159
EN
Fork head box P3 (FoxP3+) regulatory T cells (Tregs) are specialized T cells for the prevention of hyperimmune responses and autoimmunity. Tumors and pathogens can hijack FoxP3+ Tregs to evade host immune responses. There is an increasing body of evidence that trafficking of FoxP3+ Tregs is important for their effective suppression of target cells. Because of their distinctive functions and gene expression phenotype, the migratory behavior of FoxP3+ Tregs has been somewhat mystified. The myths are that they have unique trafficking receptors and migratory behaviors that are different from those of conventional T cells. Another related myth is that FoxP3+ regulatory T cell subsets have a fixed trafficking behavior from the time they are generated in the thymus. Recent progress in trafficking receptors and the migratory behavior of FoxP3+ Tregs are reviewed here and the validity of these myths examined.
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Lack of migration and neurological benefits after infusion of umbilical cord blood cells in ischemic brain injury

100%
Zawadzka M., Lukasiuk K., Machaj E. K., Pojda Z., Kaminska B.
Acta Neurobiologiae Experimentalis
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2009
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vol. 69
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issue 1
46-51
EN
The finding of stem/progenitor cells in postnatal bone marrow and umbilical cord blood, opens up a possibility of using stem cells to treat neurologic diseases. There is a controversy, whether intravenously administered human umbilical cord blood cells (HUCBC) migrate to the brain, differentiate and improve recovery after ischemia. In this study, 1-3 ?10^6 cells from non-cultured (non-committed) mononuclear HUCBC fraction were intravenously infused 1, 2, 3 or 7 days after a transient middle cerebral artery occlusion (MCAo) in adult rats. We found few human cells only in the ischemic area, localized mostly around blood vessels with few positive cells in the brain parenchyma. Timing of HUCBC delivery after ischemia or injection of Cyclosporin A at the time of delivery, had no effect on the number of human cells detected in the ischemic brain. Infusion of HUCBC did not reduce infarct volume and did not improve neurologic deficits after MCAo, suggesting that HUCBC failed to migrate/survive in the ischemic brain and did not provide significant neurological benefits.
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