| Literature DB >> 24793464 |
Lydia Celia Madjene1, Maguelonne Pons1, Luca Danelli1, Julien Claver1, Liza Ali1, Iris K Madera-Salcedo1, Asma Kassas1, Christophe Pellefigues1, Florian Marquet1, Albert Dadah1, Tarik Attout1, Alaa El-Ghoneimi2, Gregory Gautier1, Marc Benhamou1, Nicolas Charles1, Eric Daugas3, Pierre Launay1, Ulrich Blank4.
Abstract
Mast cells are hematopoietic cells involved in inflammation and immunity and have been recognized also as important effector cells in kidney inflammation. In humans, only a few mast cells reside in kidneys constitutively but in progressive renal diseases their numbers increase substantially representing an essential part of the interstitial infiltrate of inflammatory cells. Recent data obtained in experimental animal models have emphasized a complex role of these cells and the mediators they release as they have been shown both to promote, but also to protect from disease and fibrosis development. Sometimes conflicting results have been reported in similar models suggesting a very narrow window between these activities depending on the pathophysiological context. Interestingly in mice, mast cell or mast cell mediator specific actions became also apparent in the absence of significant mast cell kidney infiltration supporting systemic or regional actions via draining lymph nodes or kidney capsules. Many of their activities rely on the capacity of mast cells to release, in a timely controlled manner, a wide range of inflammatory mediators, which can promote anti-inflammatory actions and repair activities that contribute to healing, but in some circumstances or in case of inappropriate regulation may also promote kidney disease.Entities:
Keywords: Fibrosis lupus nephritis; Mast cell chymase; Mast cells; Renal disease
Mesh:
Year: 2014 PMID: 24793464 DOI: 10.1016/j.molimm.2014.03.002
Source DB: PubMed Journal: Mol Immunol ISSN: 0161-5890 Impact factor: 4.407