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Updated: May 19, 2026
Development and Functional Characterization of Murine Tolerogenic Dendritic Cells
Published on: May 18, 2018
Murine corneal stroma cells inhibit LPS-induced dendritic cell maturation partially through TGF-β2 secretion in vitro
Jian-Min Lu1, Xiu-Jun Song, Hui-Fang Wang
1Department of Ophthalmology, Third Hospital of Hebei Medical University, Shijiazhuang, China.
Insights
Corneal stroma cells (CSCs) secrete transforming growth factor beta 2 (TGF-β(2)), which partially inhibits dendritic cell (DC) maturation. This finding explains how immature DCs are maintained in the cornea.
Area of Science:
- Ophthalmology
- Immunology
- Cell Biology
Background:
- The cornea's central region exclusively contains immature dendritic cells (DCs), unlike the periphery.
- Factors influencing DC maturation within the cornea remain incompletely understood.
Purpose of the Study:
- To investigate whether corneal stroma cells (CSCs) inhibit DC maturation by secreting cytokines.
- To determine the role of transforming growth factor beta 2 (TGF-β(2)) in this inhibition.
Main Methods:
- Analyzing TGF-β(2) mRNA and protein levels in CSCs using RT-PCR and ELISA.
- Inducing DC maturation with lipopolysaccharide (LPS) and CSC culture supernatant (with/without TGF-β(2) neutralizing antibodies).
- Assessing DC phenotypic markers (CD80, CD86, MHC II) and functional capacity (T-cell stimulation, endocytosis).
Main Results:
- CSCs express TGF-β(2) mRNA and secrete high levels of TGF-β(2) protein.
- CSC supernatant partially inhibited LPS-induced DC maturation, reducing CD80, CD86, and MHC II expression in a dose-dependent manner.
- Inhibition was associated with decreased T-cell stimulation and increased endocytosis, partially reversible by TGF-β(2) neutralization.
Conclusions:
- Corneal stroma cells partially inhibit lipopolysaccharide-induced dendritic cell maturation in vitro.
- Transforming growth factor beta 2 is a key mediator of this inhibitory effect.
Purpose:
The peripheral cornea contains mature and immature resident dendritic cells (DCs) while the central cornea is exclusively equipped with immature DCs. There must be some factors that cause immature DCs. This study investigated whether corneal stroma cells (CSCs) inhibit DC maturation by secreting cytokines.
Methods:
The messenger ribonucleic acid (mRNA) and protein level of transforming growth factor beta 2 (TGF-β(2)) was analyzed using reverse transcription polymerase chain reaction (RT-PCR) and enzyme-linked immunosorbent assay (ELISA). Immature DCs were induced to mature in the presence of lipopolysaccharide (LPS) and with concentrations of CSC culture supernatant (containing and not containing neutralizing TGF-β(2) antibodies). Then, the DC phenotypic and functional maturation were analyzed.
Results:
CSCs exhibited positive expressions of TGF-β(2) mRNA and secreted high concentrations of TGF-β(2) protein. In the presence of LPS, DCs, which were treated with a CSC culture supernatant, displayed reduced expressions of cluster of differentiation 80 (CD80), CD86, and major histocompatibility complex II (MHC II) in a dose-dependent manner. Moreover, treated DCs showed lower T-cell stimulation capacity and a higher endocytosis function. However, these phenotypic and functional modifications were partially reversed after the application of neutralizing TGF-β(2) antibodies.
Conclusions:
This study demonstrates that CSCs can partially inhibit LPS-induced DC maturation through TGF-β(2) secretion in vitro.
