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Does in vitro replicative senescence of human CD8+ cells reflect the phenotypic changes observed during in vivo ageing?

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Brzezinska A.
|
2005
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vol. 52
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issue 4
931-935
EN
Immunosenescence is viewed as a remodeling process with the exhaustion of naïve T cells and filling up of the immunological space with memory cells. In this study some phenotypic changes of CD8+ human cells during in vivo ageing were compared with those observed in long term cultures of lymphocytes derived from cord blood or from peripheral blood from donors of different age. Both in vivo and in vitro a significant decrease of the fraction of CD8+CD28+ cells was observed. Comparing the proportions of other T cell subpopulations (the CD4/CD8+ ratio, CD56, CD57, CD27) made it possible to conclude that replicative senescence in vitro partially reflects in vivo ageing.
2
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Role of T-lymphocytes in Radiation-Impaired Wound Healing

100%
Schäffer M., Stülten C., Viebahn R.
Polish Journal of Surgery
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2007
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vol. 79
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issue 4
312-318
EN
Radiation impairs healing, although the underlying mechanisms are not clearly defined. T-lymphocytes have been shown to be critical for wound healing. We hypothesized that radiation-impaired healing may affect different subtypes of T cells.The aim of the study. We studied the effect of local electron irradiation on standard parameters of dermal wound healing in rats and correlated the outcome of healing with the expression of different lymphocyte subtypes in the wound.Material and methods. Groups of 10 rats were irradiated using single dose 12 or 24 Gray electron radiation at the dorsal skin. Control rats were sham-irradiated. On day 5, a skin incision in the irradiated area was performed and polyvinyl alcohol sponges were inserted subcutaneously. Rats were sacrificed 10 days later to determine the wound breaking strength and reparative collagen deposition. Blood lymphocytes were analyzed by FACS. Immunohistochemistry was performed on wound sections.Results. Irradiation significantly reduced wound collagen deposition and wound breaking strength (p <0.05), leading to a 78% reduction in collagen deposition and 47% reduction in breaking strength in 24 Gy animals. Blood lymphocytes were not affected by electron-irradiation, suggesting that the wound was not affected by radiation-induced systemic effects. Impaired healing was reflected, however, in increased expression of wound CD8 cells and decreased expression of CD25 (IL-2 receptor) (p <0.01). No effect was seen on wound CD4 cells. In addition, the ratio of CD4/CD8 was significantly decreased (p <0.05).Conclusions. Radiation-impaired healing is reflected in impaired expression of wound lymphocyte subtypes. Altered lymphocyte subtypes may affect the outcome of healing in irradiated wounds.
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Proliferation and apoptosis of human T cells during replicative senescence - a critical approach.

100%
Jaruga E., Skierski J., Radziszewska E., Sikora E.
|
2000
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vol. 47
|
issue 2
293-300
EN
Normal human T lymphocytes growing in culture undergo replicative senescence. Previously, we have shown that in our conditions polyclonal T cells cease proliferation after about three weeks (Radziszewska et al., 1999, Cell Biol. Int. 23, 97-103). Now we present results of a more detailed analysis of in vitro growth as well as phenotypic changes of T cells. Cell cycle analysis showed that about 20% of cells were in the S phase untill the 17th day of culture (young cells). The highest number of mitotic cells (phase G2/M; 10%) was observed during the first week of culture. All not dividing senescent cells were stopped in the G1 phase (after the 30th day of culture). The sub-G1 fraction which represents apoptotic cells did not exceed 8% during the whole period until the 30th day of culture. During in vitro T-cell growth, a rather rapid selection to CD3+CD8+ cells occurs. In the presenescent (between the 17th and 30th day) and senescent populations the majority of cells (above 90%) were CD8 positive. We also have checked the expression of α-chain interleukin-2 (IL-2) receptor (CD25). In young and presenescent cells about one third of cells was CD25 positive, but only 15% in the pool of senescent cells. Immunoblotting analysis of p16 protein recognized previously as a marker of senescent T cells, showed its highest and transient expression in presenescent cells. A critical review of the polyclonal T cell replicative senescence model is presented.
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