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001-es BibID:	BIBFORM001996
Első szerző:	Eidsmo, Liv
Cím:	FasL and TRAIL induce epidermal apoptosis and skin ulceration upon exposure to Leishmania major / Liv Eidsmo, Caroline Fluur, Bence Rethi, Sofia Eriksson Ygberg, Nicolas Ruffin, Angelo De Milito, Hannah Akuffo, Francesca Chiodi
Dátum:	2007
Megjegyzések:	Receptor-mediated apoptosis is proposed as an important regulator of keratinocyte homeostasis in human epidermis. We have previously reported that Fas/FasL interactions in epidermis are altered during cutaneous leishmaniasis (CL) and that keratinocyte death through apoptosis may play a pathogenic role for skin ulceration. To further investigate the alterations of apoptosis during CL, a keratinocyte cell line (HaCaT) and primary human epidermal keratinocytes were incubated with supernatants from Leishmania major-infected peripheral blood mononuclear cells. An apoptosis-specific microarray was used to assess mRNA expression in HaCaT cells exposed to supernatants derived from L. major-infected cultures. Fas and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) mRNA and protein expression were significantly up-regulated, and apoptosis was detected in both HaCaT and human epidermal keratinocyte cells. The keratinocyte apoptosis was partly inhibited through blocking of Fas or FasL and even more efficiently through TRAIL neutralization. Up-regulation of Fas on keratinocytes in epidermis and the presence of FasL-expressing macrophages and T cells in dermis were previously reported by us. In this study, keratinocytes expressing TRAIL, as well as the proapoptotic receptor TRAIL-R2, were detected in skin biopsies from CL cases. We propose that activation of Fas and TRAIL apoptosis pathways, in the presence of inflammatory mediators at the site of infection, leads to tissue destruction and ulceration during CL.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban apoptosis skin leishmania
Megjelenés:	The American Journal of Pathology. - 170 : 1 (2007), p. 227-239. -
További szerzők:	Fluur, Caroline Réthi Bence (1973-) (biológus, immunológus) Ygberg, Sofia Eriksson Ruffin, Nicolas De Milito, Angelo Akuffo, Hannah Chiodi, Francesca
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001-es BibID:	BIBFORM005613
Első szerző:	Réthi Bence (biológus, immunológus)
Cím:	Priming of T cells to Fas-mediated proliferative signals by interleukin-7 / Bence Rethi, Nancy Vivar, Stefano Sammicheli, Caroline Fluur, Nicolas Ruffin, Ann Atlas, Eva Rajnavolgyi, Francesca Chiodi
Dátum:	2008
Megjegyzések:	T-cell depletion associated with HIV infection or cytoreductive therapies triggers potential T-cell regenerative mechanisms such as peripheral T-lymphocyte expansion to weak antigenic stimuli and the increased availability of interleukin-7 (IL-7), a cytokine with potent antiapoptotic and proliferative activities. Deleterious mechanisms also associated with lymphopenia, such as increased Fas expression and apoptosis of T cell, however, may result in opposing effects. In this study, we show that Fas molecules, primarily associated with T-cell depletion in lymphopenic settings, may also contribute to compensatory T-cell expansion through transmitting costimulatory signals to suboptimally activated T cells. Proliferation of T lymphocytes in response to concomitant Fas and T-cell receptor (TCR) triggering was shown to be increased in HIV-infected individuals compared with noninfected controls. As IL-7 levels are often elevated in lymphopenic individuals in association with increased Fas expression, we analyzed whether IL-7 Would influence Fas-mediated proliferative signals in T cells. We show that IL-7 is able to increase the efficacy of Fas to induce proliferation of suboptimally activated T cells. Thus, high IL-7 levels associated with lymphopenic conditions may simultaneously induce sensitivity to Fas-mediated apoptosis in nonactivated T cells and increase Fas-induced costimulatory signals in T cells recognizing low-affinity antigens.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Virus TYPE-1 Infection HIV-1 Infection Homeostatic Proliferation Receptro Expression Sooty Mangabeys Down-regulation Up-regulation Activation Apoptosis
Megjelenés:	Blood. - 112 : 4 (2008), p. 1195-1204. -
További szerzők:	Vivar, Nancy Sammicheli, Stefano Fluur, Caroline Ruffin, Nicolas Atlas, Ann Rajnavölgyi Éva (1950-) (immunológus) Chiodi, Francesca
Internet cím:	elektronikus változat DOI elektronikus változat
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