Allergy via Alexandros G.Sfakianakis on Inoreader

Source:  Allergy via Alexandros G.Sfakianakis on Inoreader    Tag:  hemizygous
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Allergy via Alexandros G.Sfakianakis on Inoreader

Increased vitamin D levels at birth and in early infancy increase offspring allergy risk-evidence for involvement of epigenetic mechanisms
Saturday, August 15, 2015 7:56 PM Kristin M. Junge, Tobias Bauer, Stefanie Geissler, Frank Hirche, Loreen Thürmann, Mario Bauer, Saskia Trump, Matthias Bieg, Dieter Weichenhan, Lei Gu, Jan-Philipp Mallm, Naveed Ishaque, Oliver Mücke, Stefan Röder, Gunda Herberth, Ulrike Diez, Michael Borte, Karsten Rippe, Christoph Plass, Carl Hermann, Gabriele I. Stangl, Roland Eils, Irina Lehmann

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Although a beneficial effect of vitamin D on health is widely accepted, its role in allergy development has been controversial. Both allergy-preventing and allergy-promoting effects have been reported. Thus, a deeper mechanistic understanding of how vitamin D is related to the regulation of immune reactivity and allergic inflammation is required. Vitamin D was shown to modify gene expression1 through binding of the vitamin D receptor to vitamin D response elements. However, only 26% of the genes identified as regulated by vitamin D have a vitamin D response element in proximity to their transcription start site (TSS),1 indicating that additional mechanisms are involved in the transcriptional control by vitamin D.


Group 2 innate lymphoid cells mediate ozone-induced airway inflammation and hyperresponsiveness in mice
Saturday, August 15, 2015 7:56 PM Qi Yang, Moyar Q. Ge, Blerina Kokalari, Imre G. Redai, Xinxin Wang, David M. Kemeny, Avinash Bhandoola, Angela Haczku

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Asthmatic patients are highly susceptible to air pollution and in particular to the effects of ozone (O3) inhalation, but the underlying mechanisms remain unclear.


GATA3 haploinsufficiency does not block allergic sensitization or atopic disease
Saturday, August 15, 2015 7:56 PM Monica G. Lawrence, Jennifer W. Leiding, Jonathan J. Lyons, Amy P. Hsu, Celeste C. Nelson, Nina Jones, Alan Fitzgerald, Wade W. Chien, Lisa Workman, Thomas A. Platts-Mills, Carmen Brewer, Rachel I. Gafni, Kelly D. Stone, Joshua D. Milner, Steven M. Holland

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GATA3 is the major transcription factor that drives TH2 differentiation and inhibits T-bet-driven TH1 differentiation from naive CD4+ T cells in response to TH2-skewing conditions.1 GATA3 is also expressed in the developing parathyroid glands, inner ear, and kidneys and is critical to vertebrate embryonic development.2Gata3 homozygous knockout mice (Gata3?/?) have a total block of T-cell differentiation and die in utero,3,4 whereas hemizygous conditional deletion of Gata3 in CD4+ T cells (Gata3fl/+) leads to impaired IL-4 and IgE production, TH1 cytokine production even in TH2-priming conditions, and failure to control parasitic infection, suggesting a Gata3 gene dosage effect on IL-4-mediated TH2 responses.


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