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Omics · study · 2026

Myeloid-avid mTOR-inhibiting nanobiologic attenuates allograft fibrosis after lung transplantation

Listed in NCBI GEO

Chronic lung allograft dysfunction (CLAD) is characterized by fibrotic graft remodeling and limits long-term survival after pulmonary transplantation.

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Despite clinical evidence that myeloid cells drive conditions that increase the risk of CLAD development, contemporary immunosuppression primarily target lymphocytes. We evaluated an mTOR inhibiting nanobiologic (mTORi-NB) targeting myeloid cells and their progenitors in a semi-allogeneic mouse model of CLAD.

We found that the mTORi-NB preferentially targeted myeloid and endothelial cells in the allografts. Brief peri-operative therapy with the mTORi-NB reduced early macrophage graft infiltration and inhibited acute inflammation. In mTORi-NB-treated lung recipients, transcriptomic analysis revealed downregulation of fibrotic genes in macrophages and type I (AT1) and type II (AT2) alveolar epithelial cells, known drivers of pulmonary fibrogenesis.

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We also observed upregulation of anti-fibrotic genes in macrophages after treatment with mTORi-NB, as well as reduction of allograft fibrosis, associated with preservation of AT2 cells. Our findings suggest that myeloid-avid immunosuppression may be a promising approach for inhibiting CLAD.

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Life Sciences
Provenance · 1 source records, 7 field assertions
SourceKeyLast seenRaw
NCBI GEOGSE31460213 d agoJSON v1
FieldAssertionExtractorEvidence
access_levelsource · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[field].local:field:life-sciencesmapping · NCBI GEOconnector:ncbi_geo@1.0.0
concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencingsource · NCBI GEOconnector:ncbi_geo@1.0.0/gdstype
concepts[organism].NCBITaxon:10090source · NCBI GEOconnector:ncbi_geo@1.0.0/taxon
descriptionsource · NCBI GEOconnector:ncbi_geo@1.0.0/summary
publication_datesource · NCBI GEOconnector:ncbi_geo@1.0.0
titlesource · NCBI GEOconnector:ncbi_geo@1.0.0/title