In this study, we describe a simple system in which human keratinocytes can be redirected to an alternative differentiation pathway. We transiently transfected freshly isolated human skin keratinocytes with the single transcription factor OCT4. Within 2 days these cells displayed expression of endogenous embryonic genes and showed reduced genomic methylation.
View Article and Find Full Text PDFEpidermal stem cells are a population of somatic stem cells responsible for maintaining and repairing the epidermis of the skin. A malfunctioning epidermal stem cell compartment results in loss of the epidermis and death of the whole organism. Since the epidermis continually renews itself by sloughing a layer of cells every day, it is in a constant state of cellular turnover and requires continual cell replacement for life.
View Article and Find Full Text PDFUnderdeveloped nations are relatively protected from the worldwide asthma epidemic; the hygiene hypothesis suggests this is due to suppression of Th2-mediated inflammation by increased exposure to pathogens and their products. Although microbial exposures can promote Th2-suppressing Th1 responses, even Th2-skewing infections, such as helminths, appear to suppress atopy, suggesting an alternate explanation for these observations. To investigate whether induction of regulatory responses by helminths may counter allergic inflammation, we examined the effects of helminth infection in a murine model of atopic asthma.
View Article and Find Full Text PDFComplement is one of primary defense mechanisms against intravascular microorganisms and could play a role in the immune response to malignancy and hence its clinical behavior. We evaluated if the sole coding polymorphism of C1qA associates with outcome in patients with breast carcinoma. Genotyping for C1qA[276A/G] was performed in 63 breast cancer subjects with localized tumor and compared with that in 38 breast cancer subjects with metastasis.
View Article and Find Full Text PDFJ Allergy Clin Immunol
December 2005
Asthma and atopy are characterized by T(H)2-type patterns of inflammation. The hygiene hypothesis suggests that early-life environmental exposure to microbes, other pathogens, and their products promotes innate immune responses that suppress atopy; the current epidemic of allergic disease may result from a dearth of such stimuli. Antiatopic responses engendered by these exposures include both T(H)1-type and regulatory-type patterns, the latter including mechanisms of antigen-presenting cells as well as those of lymphoid origin, and are characterized by prominent IL-10 and/or TGF-beta effects.
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