PubMed · 1679876
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
M P Glauser, G Zanetti, J D Baumgartner, J Cohen. 1991-09-21. Septic shock: pathogenesis.. https://doi.org/10.1016/0140-6736(91)91452-z
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
HPV infections of the epidermis and anogenital tract occur frequently in healthy individuals, and 'high risk' HPV types are a major risk factor for cervical cancer. The first line of defense against HPV is the innate immune system, which provides non specific protection against a variety of pathogens and also enhances the adaptive immune response. However, HPV-infected cells often evade innate immune recognition and elimination. HPV gene expression and release of virus occur in superficial squamous cells where virus antigens are not readily detected, and keratinocytes are not lysed during HPV infection so there is no inflammatory response. In addition, HPV early proteins inhibit specific components of the innate immune system. E6 and E7 inhibit signaling by type I interferons and decrease expression of multiple interferon-inducible genes. E5 and E7 inhibit expression of major histocompatibility complex class I proteins on the cell surface. HPV-infected cells are resistant to lysis by natural killer (NK) cells, but are sensitive to cytokine-activated NK cells. Activated macrophages also kill HPV-infected cells and control malignant development. Thus, innate immunity is important for prevention of HPV infections, but HPV often persists due to evasion or inactivation of innate defenses.
BACKGROUND: The biological properties of interleukin (IL)-10 in tolerance induction and inhibition of alloreactivity have suggested a therapeutic use of this cytokine as an additional or alternative prophylaxis for graft-versus-host disease (GvHD). However, the effects of exogenous IL-10 on GvHD are mainly studied in animal models, and the results remain conflicting. This study aims to demonstrate, for the first time, whether the addition of exogenous IL-10 can reduce the severity of graft-versus-host reactions (GvHR) in humans. METHODS: The regulatory role of exogenous IL-10 in GvHR was investigated using an in vitro human skin explant model. The effects of IL-10 on skin GvHR were tested in parallel with allo-antigen induced T-cell proliferation, cytolytic reactivity, and cytokine production. RESULTS: In the presence of IL-10, the mixed lymphocyte reaction (MLR) primed responder cells showed significantly lower proliferative and cytolytic responses compared with the responder cells from the control MLR carried out in the absence of IL-10. The responder cells from IL-10 containing MLR induced significantly less severe skin GvHR and displayed a significantly reduced T-cell activation and cytokine production. A significant correlation was observed between the levels of TNF-alpha production and the sensitivity to IL-10 modulation of GvHR. CONCLUSIONS: The addition of exogenous IL-10 strongly inhibited the broad alloreactivity initiated by primary MLR and significantly reduced the overall severity of skin GvHR induced by MLR primed responder cells. Responder cells producing high TNF-alpha following allogeneic stimulation appeared to be less sensitive to IL-10 modulation of GvHR.
UNLABELLED: The prevalence of allergic diseases, such as allergic asthma, allergic rhinitis and atopic dermatitis, has increased during the last decade. It is generally accepted that the increased prevalence of allergic diseases is due to a disturbed T-helper lymphocyte (T(h)) T(h1)-T(h2) balance, leading to more expression of T(h2) features. Decreased postnatal microbiological stimulation (i.e. improvements in public health, reduction in family size, increased usage of antibiotics) results in an increased possibility of ongoing postnatal T(h2) reactions. Furthermore, increased postnatal allergen exposure, especially to house dust mite, is known to facilitate the existence of T(h2) features. Therefore, identification of early markers of allergy such as increased total IgE in cord blood offers the possibility to initiate adequate primary prevention in subjects at risk. Primary prevention measures constitute merely of avoidance of early allergen contacts (foods and inhalants) and avoidance of pollution exposure (i.e. passive smoking). At the moment, insufficient data are available concerning the preventive effect of medication on the development of allergic diseases. However, studies on the early use of cetirizine suggest that the occurrence of asthma can be prevented or delayed in young children suffering from atopic eczema. CONCLUSION: because identification of the atopic newborn is now possible, adequate early prevention can be instigated.