scholarly journals Tissue-Derived Hedgehog Proteins Modulate Th Differentiation and Disease

2013 ◽  
Vol 190 (6) ◽  
pp. 2641-2649 ◽  
Author(s):  
Anna L. Furmanski ◽  
Jose Ignacio Saldana ◽  
Masahiro Ono ◽  
Hemant Sahni ◽  
Nikolaos Paschalidis ◽  
...  
2006 ◽  
Vol 34 (04) ◽  
pp. 667-684 ◽  
Author(s):  
Chia-Yang Li ◽  
Jau-Ling Suen ◽  
Bor-Luen Chiang ◽  
Pei-Dawn Lee Chao ◽  
Shih-Hua Fang

Our previous studies had reported that morin decreased the interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-α) production in lipopolysaccharide (LPS)-activated macrophages, suggesting that morin may promote helper T type 2 (Th2) response in vivo. Dendritic cells (DCs) are the most potent antigen presenting cells and known to play a major role in the differentiation of helper T type 1 (Th1) and Th2 responses. This study aimed to reveal whether morin is able to control the Th differentiation through modulating the maturation and functions of DCs. Bone marrow-derived dendritic cells (BM-DCs) were incubated with various concentrations of morin and their characteristics were studied. The results indicated that morin significantly affects the phenotype and cytokine expression of BM-DCs. Morin reduced the production of IL-12 and TNF-α in BM-DCs, in response to LPS stimulation. In addition, the proliferative response of stimulated alloreactive T cells was significantly decreased by morin in BM-DCs. Furthermore, allogeneic T cells secreted higher IL-4 and lower IFN-γ in response to morin in BM-DCs. In conclusion, these results suggested that morin favors Th2 cell differentiation through modulating the maturation and function of BM-DCs.


Development ◽  
2009 ◽  
Vol 136 (15) ◽  
pp. 2613-2621 ◽  
Author(s):  
M. Peeters ◽  
K. Ottersbach ◽  
K. Bollerot ◽  
C. Orelio ◽  
M. de Bruijn ◽  
...  

2010 ◽  
Vol 285 (32) ◽  
pp. 24584-24590 ◽  
Author(s):  
Jennifer M. Kavran ◽  
Matthew D. Ward ◽  
Oyindamola O. Oladosu ◽  
Sabin Mulepati ◽  
Daniel J. Leahy

JOR Spine ◽  
2019 ◽  
Vol 2 (4) ◽  
Author(s):  
Frances C. Bach ◽  
Kim M. Rooij ◽  
Frank M. Riemers ◽  
Joseph W. Snuggs ◽  
Willem A. M. Jong ◽  
...  

2016 ◽  
Vol 34 (15_suppl) ◽  
pp. e16020-e16020
Author(s):  
Taoufik Nedjadi ◽  
Abdelbaset Buhmeida ◽  
Mourad Assidi ◽  
Adel Al-Ammari ◽  
Ahmed Al-Sayyad ◽  
...  

2008 ◽  
Vol 11 (2) ◽  
pp. 128-132 ◽  
Author(s):  
Dinesh Rakheja ◽  
Richard L. Boriack

Systemic fetal dysmorphogenesis in disorders of postsqualene cholesterol biosynthesis is thought to be caused by disruption of Hedgehog signaling. Because precholesterol sterols such as 7-dehydrocholesterol and lathosterol can replace cholesterol in the activation of Hedgehog proteins, it is currently believed that cholesterol deficiency-related Hedgehog signaling block occurs further downstream, probably at the level of Smoothened. Experimentally, such a block in Hedgehog signaling occurs at sterol levels of <40 μg/mg protein. Recently, we studied autopsy material from 2 infants with fatal cholesterol biosynthetic disorders (Smith-Lemli-Opitz syndrome and X-linked dominant chondrodysplasia punctata) in which the hepatic cholesterol levels were far greater. In this study, we demonstrate abnormal accumulation of sterol precursors of cholesterol in membrane lipid rafts (detergent resistance membranes) prepared from liver tissues of these 2 infants: 8-dehydrocholesterol and 7-dehydrocholesterol in lipid rafts of the infant with Smith-Lemli-Opitz syndrome and cholest-8(9)-ene-3β-ol in lipid rafts of the infant with X-linked dominant chondrodysplasia punctata. We suggest that such alterations in the lipid raft sterol environment may affect the biology of cells and the development of fetuses with cholesterol biosynthetic disorders.


2003 ◽  
Vol 51 (11) ◽  
pp. 1557-1566 ◽  
Author(s):  
Rosa Sacedón ◽  
Alberto Varas ◽  
Carmen Hernández-López ◽  
Cruz Gutiérrez-deFrías ◽  
Tessa Crompton ◽  
...  

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