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  • 1
    Electronic Resource
    Electronic Resource
    High-dose proinflammatory cytokines induce apoptosis of hair bulb keratinocytes in vivo (2000)
    Oxford, UK : Blackwell Science Ltd
    British journal of dermatology 143 (2000), S. 0 
    Details
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Background Hair loss following skin inflammation may in part be mediated by keratinocyte (KC) apoptosis. While the effects of different cytokines or other apoptosis stimulating agents such as interferon (IFN)-γ or tumour necrosis factor (TNF)-α on KC apoptosis in vitro have been addressed in several studies, little is known about the effects of proinflammatory cytokines on KC apoptosis in vivo. Objectives To study the effects of intradermally injected TNF-α, interleukin (IL)-1β and IFN-γ on KC apoptosis in the back skin of C57BL/6 mice. Methods Apoptosis in epidermal and hair bulb KCs was analysed by immunohistology using TUNEL staining. Results Injection of TNF-α induced a significantly higher number of apoptotic cells within the epidermis than vehicle; all three proinflammatory cytokines together further increased their number. Intrafollicular hair bulb KCs were much more susceptible to apoptosis induction by TNF-α or IL-1β; their injection significantly upregulated apoptosis after 6 h, which was further increased after 24 h. The combination of all cytokines together accelerated intrafollicular apoptosis after 6 h by doubling the number of apoptotic cells per hair bulb, compared with the effects of TNF-α or IL-1β alone. Conclusions These data suggest that programmed cell death of proliferating KCs in vivo can be induced by proinflammatory cytokines.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-2133.2000.03784.x
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  • 2
    Electronic Resource
    Electronic Resource
    Retracted: Enhanced Inhibition of Tumour Growth and Metastasis, and Induction of Antitumour Immunity by IL-2-IgG2b Fusion Protein (2002)
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 55 (2002), S. 0 
    Details
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Budagian V, Nanni P, Lollini PL, Musiani P, Di Carlo E, Bulanova E, Paus R, Bulfone-Paus S. Enhanced Inhibition of Tumour Growth and Metastasis, and Induction of Antitumour Immunity by IL-2-IgG2b Fusion Protein. Scand J Immunol 2002;55:484–492Cytokine-immunoglobulin (Ig)-fusion proteins have attracted increasing interest as antitumour agents. Here, we have investigated the antimetastatic and antitumour responses elicited in vivo by mammary adenocarcinoma cells (TS/A) engineered to secrete interleukin (IL)-2-IgG fusion proteins. TS/A cells were transfected with DNA coding for IL-2-IgG2b, IgG2b or IL-2, and injected subcutaneously into syngeneic mice. Animals injected with TS/A-IL-2 or TS/A-IL-2-IgG2b both efficiently rejected tumours, whereas treatment with parental cells or TS/A-IgG2b was lethal. Interestingly, only mice vaccinated with IL-2-IgG2b fusion protein-secreting cells showed a long-lasting protective immunity against a later challenge with parental tumour cells. Moreover, the metastatic potential of TS/A-IL-2-IgG2b-transfected cells was dramatically decreased compared with TS/A-IL-2-cells, with a virtual absence of lung metastases after intravenous injection. Adenocarcinomas secreting IL-2-IgG2b exhibited a more prominent, early and persistent infiltration of CD4+, CD8+ and natural killer (NK) cells than TS/A-IL-2 cells. Therefore, upon transfection into adenocarcinoma cells, the IgG2b part of IL-2 fusion protein exerts intriguing added antitumour properties over IL-2 alone, thus contributing to a long-lasting tumour immunity, probably by the recruitment of specific immune effector cells. These findings suggest a promising new oncotherapeutic strategy for poorly immunogenic tumours: vaccination with tumour cells engineered to secrete IL-2-IgG2b fusion protein.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1365-3083.2002.01081.x
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    Paper (German National Licenses)
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