The antioxidant response element in the prdx6 promoter region, a cis-acting regulator element, is activated by oxidative stress. Transcription of the PRDX6 gene is regulated by nuclear factor erythroid 2-related factors 1, 2, and 3 as transcription factors via binding to the ARE. Among the Nrfs, Nrf2 positively regulates transcription of the PRDX6 gene. As PRDXs are antioxidants, they support survival and tumor maintenance by protecting cells from oxidative stress-induced apoptosis. In a recent study, over expression of PRDX 6 attenuates cisplatin-induced Niraparib 1038915-60-4 apoptosis in human ovarian cancer cells. In contrast, reduction of PRDX6 expression increased peroxide-induced cell death in liver cancer cells. The invasion and metastasis promoting actions of PRDX6 has been found in lung cancer cells through activation of Akt via activation of phosphoinositiede 3-kinase and p38 kinase. The activity of PRDX6 contributes to the metastatic ability of lung cancer cells by stimulating invasion components including PI3K, Akt, and uPA. The small CSC population is suggested to possess self-renewal potential and the ability to differentiate and thereby generating the heterogenous cell population of the originating tumor. These findings have been also demonstrated for pancreatic cancer. In addition CSC are proposed to mediate uncontrolled growth, therapy resistance, invasion and metastasis. Recent reports indicate that the emergence of CSCs occurs in part as a result of epithelial-mesenchymal-transition. EMT is an evolutionarily conserved development process during that cells lose epithelial characteristics and gain mesenchymal properties. These observations include that IFN-c, IL-17, and neutrophils are found in lungs of asthma patients and treatments targeting TH2 cells failed to be effective. It is interestingly noted here that not only TH2- associated diseases have increased over the past decades in parallel with elevated hygiene conditions, but also TH1-associated inflammatory and autoimmune diseases. There are patients with a coincidence of allergic and autoimmune disease. Moreover, allergic diseases show a substantial autoimmune profile and TH1 response plays an important role in chronicity and tissue injury in atopic diseases. Our results, Rapamycin 53123-88-9 combined with the observations described above, does not support the fact that skewing of T helper cell differentiation is an immunological mechanism for the hygiene hypothesis at least in school age children. In newborn children, the situation might be different. It has been shown that reduced IFN-c secretion after ex-vivo restimulation of cord blood cells with phorbol 12-myristate 13- acetate was associated with reduced allergen-specific IgE. The different results between newborn and school age children might be based on different development status of the immune system or on the different methods to assess the IFN-c expression. It is important to note here that our data shows direct analyses of the cells without any cultures, representing a direct in vivo situation compared to cultures of cells for several days. Although the present study did not allow us to investigate immunological mechanisms in deep or even to discover new mechanisms.