Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress

Research output: Contribution to journalJournal articlepeer-review

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Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress. / Fanelli, Giorgia; Gonzalez-Cordero, Anai; Gardner, Peter J; Peng, Qi; Fernando, Milan; Kloc, Magdalena; Farrar, Conrad A; Naeem, Arifa; Garred, Peter; Ali, Robin R; Sacks, Steven H.

In: Scientific Reports, Vol. 7, 14625, 2017.

Research output: Contribution to journalJournal articlepeer-review

Harvard

Fanelli, G, Gonzalez-Cordero, A, Gardner, PJ, Peng, Q, Fernando, M, Kloc, M, Farrar, CA, Naeem, A, Garred, P, Ali, RR & Sacks, SH 2017, 'Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress', Scientific Reports, vol. 7, 14625. https://doi.org/10.1038/s41598-017-15212-z

APA

Fanelli, G., Gonzalez-Cordero, A., Gardner, P. J., Peng, Q., Fernando, M., Kloc, M., Farrar, C. A., Naeem, A., Garred, P., Ali, R. R., & Sacks, S. H. (2017). Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress. Scientific Reports, 7, [14625]. https://doi.org/10.1038/s41598-017-15212-z

Vancouver

Fanelli G, Gonzalez-Cordero A, Gardner PJ, Peng Q, Fernando M, Kloc M et al. Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress. Scientific Reports. 2017;7. 14625. https://doi.org/10.1038/s41598-017-15212-z

Author

Fanelli, Giorgia ; Gonzalez-Cordero, Anai ; Gardner, Peter J ; Peng, Qi ; Fernando, Milan ; Kloc, Magdalena ; Farrar, Conrad A ; Naeem, Arifa ; Garred, Peter ; Ali, Robin R ; Sacks, Steven H. / Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress. In: Scientific Reports. 2017 ; Vol. 7.

Bibtex

@article{b65b10a60b32459087670f573f62eb93,
title = "Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress",
abstract = "Age-related macular degeneration (AMD) is a major cause of blindness and is associated with complement dysregulation. The disease is a potential target for stem cell therapy but success is likely to be limited by the inflammatory response. We investigated the innate immune properties of human induced-pluripotent stem cell (iPSC)-derived RPE cells, particularly with regard to the complement pathway. We focused on collectin-11 (CL-11), a pattern recognition molecule that can trigger complement activation in renal epithelial tissue. We found evidence of constitutive and hypoxia-induced expression of CL-11 in iPS-RPE cells, and in the extracellular fluid. Complement activation on the cell surface occurred in conjunction with CL-11 binding. CL-11 has been shown to activate inflammatory responses through recognition of L-fucose, which we confirmed by showing that fucosidase-treated cells, largely, failed to activate complement. The presence of CL-11 in healthy murine and human retinal tissues confirmed the biological relevance of CL-11. Our data describe a new trigger mechanism of complement activation that could be important in disease pathogenesis and therapeutic interventions.",
author = "Giorgia Fanelli and Anai Gonzalez-Cordero and Gardner, {Peter J} and Qi Peng and Milan Fernando and Magdalena Kloc and Farrar, {Conrad A} and Arifa Naeem and Peter Garred and Ali, {Robin R} and Sacks, {Steven H}",
year = "2017",
doi = "10.1038/s41598-017-15212-z",
language = "English",
volume = "7",
journal = "Scientific Reports",
issn = "2045-2322",
publisher = "nature publishing group",

}

RIS

TY - JOUR

T1 - Human stem cell-derived retinal epithelial cells activate complement via collectin 11 in response to stress

AU - Fanelli, Giorgia

AU - Gonzalez-Cordero, Anai

AU - Gardner, Peter J

AU - Peng, Qi

AU - Fernando, Milan

AU - Kloc, Magdalena

AU - Farrar, Conrad A

AU - Naeem, Arifa

AU - Garred, Peter

AU - Ali, Robin R

AU - Sacks, Steven H

PY - 2017

Y1 - 2017

N2 - Age-related macular degeneration (AMD) is a major cause of blindness and is associated with complement dysregulation. The disease is a potential target for stem cell therapy but success is likely to be limited by the inflammatory response. We investigated the innate immune properties of human induced-pluripotent stem cell (iPSC)-derived RPE cells, particularly with regard to the complement pathway. We focused on collectin-11 (CL-11), a pattern recognition molecule that can trigger complement activation in renal epithelial tissue. We found evidence of constitutive and hypoxia-induced expression of CL-11 in iPS-RPE cells, and in the extracellular fluid. Complement activation on the cell surface occurred in conjunction with CL-11 binding. CL-11 has been shown to activate inflammatory responses through recognition of L-fucose, which we confirmed by showing that fucosidase-treated cells, largely, failed to activate complement. The presence of CL-11 in healthy murine and human retinal tissues confirmed the biological relevance of CL-11. Our data describe a new trigger mechanism of complement activation that could be important in disease pathogenesis and therapeutic interventions.

AB - Age-related macular degeneration (AMD) is a major cause of blindness and is associated with complement dysregulation. The disease is a potential target for stem cell therapy but success is likely to be limited by the inflammatory response. We investigated the innate immune properties of human induced-pluripotent stem cell (iPSC)-derived RPE cells, particularly with regard to the complement pathway. We focused on collectin-11 (CL-11), a pattern recognition molecule that can trigger complement activation in renal epithelial tissue. We found evidence of constitutive and hypoxia-induced expression of CL-11 in iPS-RPE cells, and in the extracellular fluid. Complement activation on the cell surface occurred in conjunction with CL-11 binding. CL-11 has been shown to activate inflammatory responses through recognition of L-fucose, which we confirmed by showing that fucosidase-treated cells, largely, failed to activate complement. The presence of CL-11 in healthy murine and human retinal tissues confirmed the biological relevance of CL-11. Our data describe a new trigger mechanism of complement activation that could be important in disease pathogenesis and therapeutic interventions.

U2 - 10.1038/s41598-017-15212-z

DO - 10.1038/s41598-017-15212-z

M3 - Journal article

C2 - 29116192

VL - 7

JO - Scientific Reports

JF - Scientific Reports

SN - 2045-2322

M1 - 14625

ER -

ID: 196041862