Biochimica et biophysica acta
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Biochim. Biophys. Acta · Jan 2012
ReviewThe two faces of mast cells in food allergy and allergic asthma: the possible concept of Yin Yang.
The purpose of this review is to discuss the role of mast cells in allergic inflammation. We have focused on inflammation associated with allergic asthma and food allergy. Mast cells are 'first line of defense' innate/adaptive immune cells and are widely distributed in tissues in surfaces exposed to the environment. ⋯ Recent studies revealed that mast cells, besides the classical role of pro-inflammatory effector cell, have also emerged as modulators of allergic sensitization and down-regulators of allergic inflammation. Therefore, mast cells can be regarded as 'Ying Yan' modulators in allergic responses in intestinal tract and airways. This article is part of a Special Issue entitled: Mast Cells in Inflammation.
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Biochim. Biophys. Acta · Nov 2011
ReviewEmerging pathways in asthma: innate and adaptive interactions.
Allergic asthma is a complex and chronic airway inflammatory disorder, and the prevalence of asthma has increased. Adaptive antigen-dependent immunity is a classical pathway of asthmatic pathology. Recent studies have focused on innate antigen-independent immunity in asthma. ⋯ Finding specific mechanisms of innate and/or adaptive immunity in asthma are timely goals for further research. Integration of bioinformatics and systems biology tools, particularly in relation to microbiome analysis, may be helpful in providing an understanding to allergic immune responses. This article is part of a Special Issue entitled Biochemistry of Asthma.
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Biochim. Biophys. Acta · Oct 2011
ReviewAutosomal dominant polycystic kidney disease: genetics, mutations and microRNAs.
Autosomal dominant polycystic kidney disease (ADPKD) is a common, monogenic multi-systemic disorder characterized by the development of renal cysts and various extrarenal manifestations. Worldwide, it is a common cause of end-stage renal disease. ADPKD is caused by mutation in either one of two principal genes, PKD1 and PKD2, but has large phenotypic variability among affected individuals, attributable to PKD genic and allelic variability and, possibly, modifier gene effects. ⋯ The purpose of this article is to provide a comprehensive review of the genetics of ADPKD, including mechanisms responsible for disease development, the role of gene variations and mutations in disease presentation, and the putative role of microRNAs in ADPKD etiology. The emerging and important role of genetic testing and the advent of novel molecular diagnostic applications also are reviewed. This article is part of a Special Issue entitled: Polycystic Kidney Disease.
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Biochim. Biophys. Acta · Oct 2011
ReviewFibrosis and progression of autosomal dominant polycystic kidney disease (ADPKD).
The age on onset of decline in renal function and end-stage renal disease (ESRD) in autosomal polycystic kidney disease (ADPKD) is highly variable and there are currently no prognostic tools to identify patients who will progress rapidly to ESRD. In ADPKD, expansion of cysts and loss of renal function are associated with progressive fibrosis. Similar to the correlation between tubulointerstitial fibrosis and progression of chronic kidney disease (CKD), in ADPKD, fibrosis has been identified as the most significant manifestation associated with an increased rate of progression to ESRD. ⋯ Since fibrosis is a major component of ADPKD it follows that preventing or slowing fibrosis should retard disease progression with obvious therapeutic benefits. The development of effective anti-fibrotic strategies in ADPKD is dependent on understanding the precise mechanisms underlying initiation and progression of fibrosis in ADPKD and the role of the intrinsic genetic defect in these processes. This article is part of a Special Issue entitled: Polycystic Kidney Disease.
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Biochim. Biophys. Acta · May 2011
ReviewThe pro- and anti-inflammatory properties of the cytokine interleukin-6.
Interleukin-6 is a cytokine not only involved in inflammation and infection responses but also in the regulation of metabolic, regenerative, and neural processes. In classic signaling, interleukin-6 stimulates target cells via a membrane bound interleukin-6 receptor, which upon ligand binding associates with the signaling receptor protein gp130. Gp130 dimerizes, leading to the activation of Janus kinases and subsequent phosphorylation of tyrosine residues within the cytoplasmic portion of gp130. ⋯ It turns out that regenerative or anti-inflammatory activities of interleukin-6 are mediated by classic signaling whereas pro-inflammatory responses of interleukin-6 are rather mediated by trans-signaling. This is important since therapeutic blockade of interleukin-6 by the neutralizing anti-interleukin-6 receptor monoclonal antibody tocilizumab has recently been approved for the treatment of inflammatory diseases. This article is part of a Special Issue entitled: 11th European Symposium on Calcium.