Publications by authors named "Lola Domenici"

3 Publications

  • Page 1 of 1

Dendritic cells with lymphocyte-stimulating activity differentiate from human CD133 positive precursors.

Blood 2011 Apr 8;117(15):3983-95. Epub 2011 Feb 8.

Department of Anatomy, Histology and Forensic Medicine, University of Florence, Florence, Italy.

CD133 is a hallmark of primitive myeloid progenitors. We have addressed whether human cord blood cells selected for CD133 can generate dendritic cells, and Langerhans cells in particular, in conditions that promote that generation from CD34(+) progenitors. Transforming growth factor-β1 (TGF-β1) and anti-TGF-β1 antibody, respectively, were added in some experiments. With TGF-β, monocytoid cells were recognized after 7 days. Immunophenotypically immature dendritic cells were present at day 14. After 4 more days, the cells expressed CD54, CD80, CD83, and CD86 and were potent stimulators in mixed lymphocyte reaction; part of the cells expressed CD1a and langerin, but not Birbeck granules. Without TGF-β, only a small fraction of cells acquired a dendritic shape and expressed the maturation-related antigens, and lymphocytes were poorly stimulated. With anti-TGF-β, the cell growth was greatly hampered, CD54 and langerin were never expressed, and lymphocytes were stimulated weakly. In conclusion, CD133(+) progenitors can give rise in vitro, through definite steps, to mature, immunostimulatory dendritic cells with molecular features of Langerhans cells, although without Birbeck granules. Addition of TGF-β1 helps to stimulate cell growth and promotes the acquisition of mature immunophenotypical and functional features. Neither langerin nor Birbeck granules proved indispensable for lymphocyte stimulation.
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April 2011

Rosiglitazone reduces the inflammatory response in a model of vascular injury in rats.

Shock 2009 Dec;32(6):638-44

Department of Experimental Medicine, Excellence Centre for Cardiovascular Diseases, Second University of Naples, Naples, Italy.

Thiazolidinediones are ligands that bind to and activate the nuclear peroxisome proliferator-activated receptor gamma. They are widely used as insulin sensitizers for the treatment of type 2 diabetes. Several studies have implicated the peroxisome proliferator-activated receptor gamma agonists rosiglitazone and pioglitazone in inflammatory events. To assess the anti-inflammatory properties of rosiglitazone, we investigated its effects on the molecular and cellular inflammatory response induced by a carotid injury in the rat. Male Wistar rats were randomized into a rosiglitazone-treated group (10 mg kg(-1) day(-1)) and a control group (0.9% w/v NaCl). The drug or vehicle was administered by gavage for 7 days before carotid injury and for up to 21 days after injury. The inflammatory markers p38 mitogen-activated protein kinase, cyclooxygenase 2, nuclear factor-kappaB, and heat shock protein 47 and the influx and activity of cells in response to injury were measured. Rosiglitazone treatment significantly reduced the expression of the inflammatory markers compared with control group. p38 mitogen-activated protein kinase and nuclear factor-kappaB started to decrease a few hours after injury, whereas cyclooxygenase 2 and heat shock protein 47 expression decreased 7 and 14 days, respectively, after injury. Rosiglitazone also reduced neointima formation and inflammatory cell infiltration. In conclusion, rosiglitazone negatively regulated the inflammatory events involved in tissue repair at molecular and cellular levels. These results suggest that rosiglitazone plays a protective role in inflammatory vascular diseases.
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December 2009

A role for transforming growth factor-beta1 in maintaining the differentiated state of Langerhans cells in human epidermis.

Ital J Anat Embryol 2006 Jul-Sep;111(3):133-49

Department of Anatomy, Histology and Forensic Medicine of the University of Florence, Florence, Italy.

Since during the generation of dendritic cells transforming growth factor (TGF)-beta1 is required to generate specifically Langerhans cells, we have addressed whether TGF-beta1 also affects the number and immunophenotype of Langerhans cells within the epidermis. Isolated human epidermal sheets were cultured as follows: serum free; with serum; serum free with TGF-beta1; with serum plus anti-TGF-betal; with serum plus an irrelevant antibody of the same isotype as anti-TGF-beta1. The expression of Langerhans cell antigens was analyzed by immunofluorescence and the preservation of epidermal structure and the expression of E-cadherin by electron microscopy. The number, surface area and perimeter length of Langerhans cells were measured and the results subjected to analysis of variance. Independent of serum, the architecture of the isolated epidermis was well preserved and E-cadherin was expressed for at least 48 h. In cultures without serum, Langerhans cells appeared well preserved when stained for MHC-II antigens. On the contrary, their number, surface area and perimeter length were significantly decreased upon labeling for CD1a and langerin, indicating altered expression and distribution of these differentiation specific antigens. These alterations were not accompanied by the expression of antigens of mature dendritic cells and were almost entirely prevented by serum. TGF-beta1, 1.0 ng/mL, had similar effects as serum on CD1a and langerin expression and distribution within cells, whereas anti-TGF-beta1 antibodies neutralized the effect of serum. The results indicate that Langerhans cells depend on soluble factors for the maintenance of the differentiated state within epidermis and that TGF-beta1 is a major one of such factors.
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April 2007