
Researchers at Universitat de València’s Departament de Microbiologia i Ecologia take a step forwards on the study of the elements taking part in the immune system’s modulation. They have proved ‘in vivo’ that the presence of certain proteins in stem cells allows them to detect microorganisms and become mature cells in order to counteract them. This finding opens up a new field for the development of immunotherapies.
Toll-like receptors – which are proteins in the mature cells of the immune system – are in charge of starting the immune response protecting us from infections. It has been observed recently that these receptors, so called TLR, may take part in the formation of blood cells (hematopoyesis) particularly when an infection is happening.
The study published on the journal Stem Cells by the Valencian researchers is very important because they have proved ‘in vivo’ – using mouses – that the presence of TLR receptors in stem cells allows these cells to detect microorganisms y become mature cells. The study’s results enlarge the functions of TLR known so far, and they link up the formation of blood cells with the infectious processes. Stem cells, through its TLR, may detect pathogens and quickly create the most efficient cell types to eliminate this pathogen, which can be either in bone marrow or in other tissues containing stem cells.
This new mechanism suggests that during infection a selection of innate immune system cells could be produced, mediated by the pathogen, and thus it could happen in a specific way. This idea is gaining strength within the scientific community.
Moreover, this finding opens a new field for the development of immunotherapeutic strategies based on the differentiation of stem cells directed by TLR, so that the ‘in vivo’ or ‘in vitro’ manipulation of this mechanism could help to increase the innate immune response when facing heavy infections. This would apply especially to those towns and villages at risk where these strategies could be established in a proactive way.
Last update: 1 de june de 2012 13:35.
News release












