Scientists report a new group of monocytes they call SatM. Studies in mice show that SatM may be responsible for causing fibrosis and creates a new drug target for an ailment that has little effective therapies.
Fibrosis is a form of scarring that could if uncontrolled cause deleterious thickening of tissues. Although it is known that fibrosis is caused by an activated immune system, which specific cells are responsible continuous to elude researchers.
Scientists may have found this subgroup, as they report in Nature a class of monocyte cells with strange morphology. "The cells had a bi-lobed segmented nuclear shape and many cytoplasmic granules. We therefore called them 'Segregated nucleus atypical monocytes (SatM)'", said the author.
To identify this subgroup, the researchers looked at immune cell subpopulations that predominantly appeared in fibrosis. "These cells were regulated by C/EBPβ," observed the author.
Detailed examination of immune cells showed that the C/EBPβ mutant mice, unlike normal mice, produced no SatM, whereas no other observed immune cell population was changed. The mice were also significantly more resistant to fibrosis. On the other hand, when the mutant mice were exposed to SatM, their susceptibility to fibrosis rose.
Although researchers describe SatM as a subset of monocytes, SatM showed characteristics that suggested they were hybrids of different immune cells. According to the author, gene analysis found SatM "showed granulocyte markers, but SatM are definitely not granulocytes. These cell type is one of monocyte."
Additional study found the progenitor cells responsible for producing SatM. Adoptive transfer of these progenitors into mutant mice unable to produce SatM resulted in a SatM population, and C/EBPβ was found to be essential for maintaining the progenitors.
The ability to isolate cells specifically related to fibrosis gives hope for new therapies.
Oddly shaped immune cells cause fibrosis
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