Dermal Fibroblasts Induce Maturation of Dendritic Cells

Saalbach, Anja; Klein, Charlotte; Sleeman, Jonathan; Sack, Ulrich; Kauer, Friederike; Gebhardt, Carl; Averbeck, Marco; Anderegg, Ulf; Simon, Jan C.

doi:10.4049/jimmunol.178.8.4966

Cited by 58 publications

(55 citation statements)

References 37 publications

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“…It has been reported that expression of maturation markers is not altered on murine bone marrow-derived DCs from CD18 Ϫ/Ϫ mice (52). However, in another study, it was shown that ␤2 integrins expressed on human DCs interacted with Thy1 and ICAM-1 expressed on fibroblasts to induce phenotypic maturation of DCs (53). It was recently reported that signaling via ␤2 integrins on human DCs is required for expression of maturation marker CD86 in response to biomaterials (54).…”

Section: Discussionmentioning

confidence: 99%

Activated Apoptotic Cells Induce Dendritic Cell Maturation via Engagement of Toll-like Receptor 4 (TLR4), Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin (DC-SIGN), and β2 Integrins

Pathak

Sköld

Mohanram

et al. 2012

Journal of Biological Chemistry

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Background: Activated apoptotic lymphocytes provide activation/maturation signals to human monocyte-derived dendritic cells (DCs). Results: Cell-cell contact-dependent signaling involved ␤2 integrins, DC-SIGN, and TLR4, which resulted in activation of multiple signaling pathways. Conclusion: These studies provide mechanistic insight into DC responses during encounter with cells undergoing immunogenic cell death. Significance: Learning how DCs respond to certain cell death has implications for vaccine design.

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Section: Discussionmentioning

confidence: 99%

Activated Apoptotic Cells Induce Dendritic Cell Maturation via Engagement of Toll-like Receptor 4 (TLR4), Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin (DC-SIGN), and β2 Integrins

Pathak

Sköld

Mohanram

et al. 2012

Journal of Biological Chemistry

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“…Efficiency of separation was examined by anti-CD16 staining and flow cytometric analysis. Human monocytes were separated from blood of healthy volunteers by magnetic cell separation using anti-CD14-beads (Miltenyi Biotec) as described previously [39]. …”

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confidence: 99%

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

et al. 2011

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Human Thy-1 (CD90) has been shown to mediate adhesion of inflammatory cells to activated microvascular endothelial cells via interaction with Mac-1 (CD11b/CD18) in vitro. Since there are no data showing the physiological relevance of Thy-1 for the recruitment of inflammatory cells in vivo, different inflammation models were investigated in Thy-1-deficient mice and littermate controls. In thioglycollate-induced peritonitis, the number of neutrophils and monocytes was significantly diminished in Thy-1-deficient mice. During acute lung inflammation, the extravasation of eosinophils and monocytes into the lung was significantly reduced in Thy-1-deficient mice. Moreover, during chronic lung inflammation, the influx of eosinophils and monocytes was also strongly decreased. These effects were independent of Thy-1 expression on T cells, as shown by the transplantation of WT BM into the Thy-1-deficient mice. In spite of the strong Thy-1 expression on T cells in the chimeric mice, the extravasation of the inflammatory cells in these mice was significantly diminished, compared to control mice. Finally, the altered number and composition of infiltrating leukocytes in Thy-1-deficient mice modified the chemokine/cytokine and protease expression at the site of inflammation. In conclusion, Thy-1 is involved in the control of inflammatory cell recruitment and, thus, also in conditioning the inflammatory microenvironment.Key words: Extravasation . Inflammation . Thy-1 Supporting Information available online IntroductionThe recruitment of inflammatory cells to sites of inflammation plays an important role in the pathogenesis of several inflammatory diseases. Leukocyte adhesion to endothelial cells (ECs) follows a multistep process, including the capture of free leukocytes out of the blood stream, rolling, firm adhesion, and transendothelial diapedesis. The importance of several adhesion molecules in this series of events has been described previously [1]. In ICAM-1-deficient mice, neutrophil recruitment was significantly reduced, but it was not completely blocked in a chemical peritonitis model or in a lipopolysaccharide 645(LPS)-induced airway inflammation model, indicating the involvement of additional adhesion molecules [2,3]. Furthermore, leukocyte recruitment in experimental colitis was not affected by blocking ICAM-1 or MadCAM, whereas the blocking of VCAM-1 resulted in a significant attenuation of colitis [4]. Thus, under specific inflammatory conditions, certain adhesion molecules mediate adhesion and transmigration of leukocytes into the perivascular tissue.Recently, human Thy-1 expressed on ECs was identified as an adhesion molecule mediating the binding of neutrophils and monocytes to activated microvascular ECs [5]. Thy-1 is a highly glycosylated GPI-anchored surface protein and a member of the immunoglobulin superfamily [6,7,8]. In humans, Thy-1 is expressed on ECs at sites of inflammation or in tumours whereas ECs do not express Thy-1 in healthy tissue [5,9]. Thy-1 is also expressed on fibroblasts, neurons, and a su...

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“…However, we could not resolve the effects on the gene expression of TGFB1 (Figure 5d [27][28][29][30][31] and DCs [32][33][34][35][36] via signals mediated by the soluble factors, and/or direct cell-cell contact resulting in cell ligations such as CD40-CD40L and ICAM-1-LFA-1. Previously, we reported that fibroblasts produce several cytokines such as RANTES, MCP-1, IL-6, IL-8, and the growth-related gene product following HLA-II stimulation.…”

Section: The Effects Of the Culture Supernatants Of Th Cells Activatementioning

confidence: 99%

Fibroblasts stimulated via HLA-II molecules produce prostaglandin E2 and regulate cytokine production from helper T cells

Kato-Kogoe

Ohyama

Nishimura

et al. 2010

Laboratory Investigation

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Fibroblasts act as important immune regulatory cells via their ability to cross-talk with T cells accumulating in lesions.Our previous study showed that fibroblasts produce several cytokines and chemokines by crosslinking HLA class II (HLA-II) molecules with monoclonal antibodies or by making T-cell receptor-peptide-HLA complexes. It is thus conceivable that the interaction of T cells and fibroblasts via HLA-II affects fibroblast responses to stimuli. This study used human gingival fibroblasts (HGF) to investigate possible effects of these fibroblast-derived soluble factors on the differentiation of naïve T cells and on the subsequent fibroblast responses. After mixed lymphocyte reaction culture between naïve T cells and allogeneic dendritic cells in the presence of culture supernatant from HGF stimulated via HLA-DQ molecules (DQ-sup), but not via DR, T cells exhibited a Th2-shifted phenotype, thereby producing quantitatively more IL-13 and IL-5 compared with interferon-g. Astonishingly, analyses to identify possible factors affecting the Th2 polarization secreted from HLA-IIstimulated HGF, prostaglandin E 2 , was detected only in DQ-sup. The Th2 polarization of naïve T cells was blocked in the presence of supernatants from indomethacin-treated HGF with HLA-DQ stimulation. In addition, we found that the culture supernatants of Th cells activated following mixed lymphocyte reaction culture in the presence of DQ-sup had the potential to induce gene expression of type I and III collagens in HGF. These results suggested that fibroblasts stimulated via HLA-DQ molecules promote Th2 polarization in Th-cell responses and showed the counter activation of collagen synthesis, implicating orchestrated responses among these cells in the fibrosis of chronic inflammatory lesions.

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Dermal Fibroblasts Induce Maturation of Dendritic Cells

Cited by 58 publications

References 37 publications

Activated Apoptotic Cells Induce Dendritic Cell Maturation via Engagement of Toll-like Receptor 4 (TLR4), Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin (DC-SIGN), and β2 Integrins

Activated Apoptotic Cells Induce Dendritic Cell Maturation via Engagement of Toll-like Receptor 4 (TLR4), Dendritic Cell-specific Intercellular Adhesion Molecule 3 (ICAM-3)-grabbing Nonintegrin (DC-SIGN), and β2 Integrins

Thy‐1 (CD90) regulates the extravasation of leukocytes during inflammation

Fibroblasts stimulated via HLA-II molecules produce prostaglandin E2 and regulate cytokine production from helper T cells

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