Publication
2023
- Cetin, E. et al. 2023. Calprotectin blockade inhibits long-term vascular pathology following peritoneal dialysis-associated bacterial infection. Frontiers in Cellular and Infection Microbiology 13, article number: 1285193. (10.3389/fcimb.2023.1285193)
- Mazzarino, M. et al. 2023. Therapeutic targeting of chronic kidney disease-associated DAMPs differentially contributing to vascular pathology. Frontiers in Immunology 14, article number: 1240679. (10.3389/fimmu.2023.1240679)
2018
- Raby, A. and Labeta, M. 2018. Preventing peritoneal dialysis-associated fibrosis by therapeutic blunting of peritoneal toll-like receptor activity. Frontiers in Physiology 9, article number: 1692. (10.3389/fphys.2018.01692)
- Raby, A., González-Mateo, G. T., Williams, A., Topley, N., Fraser, D., López-Cabrera, M. and Labeta, M. O. 2018. Targeting toll-like receptors with soluble toll-like receptor 2 prevents peritoneal dialysis solution-induced fibrosis. Kidney International 94(2), pp. 346-362. (10.1016/j.kint.2018.03.014)
2017
- Raby, A. et al. 2017. Toll-like receptors 2 and 4 are potential therapeutic targets in peritoneal dialysis-associated fibrosis. Journal of the American Society of Nephrology 28(2), pp. 461-478. (10.1681/ASN.2015080923)
2016
- Raby, A. and Labeta, M. 2016. Therapeutic boosting of the immune response: turning to CD14 for help. Current Pharmaceutical Biotechnology 17(5), pp. 414-418. (10.2174/1389201017666160114095708)
2013
- Raby, A. et al. 2013. Targeting the TLR co-receptor CD14 with TLR2-derived peptides modulates immune responses to pathogens. Science Translational Medicine 5(185), article number: 185ra64. (10.1126/scitranslmed.3005544)
2012
- Durno, K., Holst, B., Wilkes, A., Shah, S., Labeta, M. O., Hall, J. E. and Szakmany, T. 2012. STLR-2 levels can discriminate between infective and non-infective origins of multi-organ dysfunction on ICU admission: a pilot study. Critical Care Medicine 40(12), pp. U138-U139. (10.1097/01.ccm.0000424713.57752.27)
- Holst, B., Raby, A., Hall, J. E. and Labeta, M. O. 2012. Complement takes its Toll: an inflammatory crosstalk between Toll-like receptors and the receptors for the complement anaphylatoxin C5a. Anaesthesia 67(1), pp. 60-64. (10.1111/j.1365-2044.2011.07011.x)
2011
- Colmont, C. S. et al. 2011. Human peritoneal mesothelial cells respond to bacterial ligands through a specific subset of Toll-like receptors. Nephrology Dialysis Transplantation 26(12), pp. 4079-4090. (10.1093/ndt/gfr217)
- Raby, A. et al. 2011. TLR activation enhances C5a-induced pro-inflammatory responses by negatively modulating the second C5a receptor, C5L2. European Journal of Immunology 41(9), pp. 2741-2752. (10.1002/eji.201041350)
2009
- Raby, A. et al. 2009. Soluble TLR2 reduces inflammation without compromising bacterial clearance by disrupting TLR2 triggering. The Journal of Immunology 183(1), pp. 506-517. (10.4049/jimmunol.0802909)
2006
- Labeta, M. O., LeBouder, E., Rey-Nores, J. E. and Affolter, M. 2006. Modulation of neonatal microbial recognition: TLR-mediated innate immune responses are specifically and differentially modulated by human milk. Journal of Immunology 176, pp. 3742-52.
2003
- LeBouder, E. et al. 2003. Soluble forms of Toll-like receptor (TLR)2 capable of modulating TLR2 signaling are present in human plasma and breast milk. The Journal of Immunology 171(12), article number: 6680. (10.4049/jimmunol.171.12.6680)
- Labeta, M. O., Vargas, F., Fernandez-Alvarez, J. and Somoza, N. 2003. Evidence of expression of endotoxin receptors CD14, toll-like receptors TLR4 and TLR2 and associated molecule MD-2 and of sensitivity to endotoxin (LPS) in islet beta cells. Clinical & Experimental Immunology 133(2), pp. 208-18. (10.1046/j.1365-2249.2003.02211.x)
2001
- Labeta, M. O., Nores, J. E. R., Vigar, M. . A. and Harris, C. L. 2001. The lipopolysaccharide co-receptor CD14 is present and functional in seminal plasma and expressed on spermatozoa. Immunology 104(3), pp. 317-23. (10.1046/j.1365-2567.2001.01312.x)
2000
- Labeta, M. et al. 2000. Innate recognition of bacteria in human milk is mediated by a milk-derived highly expressed pattern recognition receptor, soluble CD14. Journal of Experimental Medicine 191, pp. 1807-1812. (10.1084/jem.191.10.1807)
Erthyglau
- Cetin, E. et al. 2023. Calprotectin blockade inhibits long-term vascular pathology following peritoneal dialysis-associated bacterial infection. Frontiers in Cellular and Infection Microbiology 13, article number: 1285193. (10.3389/fcimb.2023.1285193)
- Mazzarino, M. et al. 2023. Therapeutic targeting of chronic kidney disease-associated DAMPs differentially contributing to vascular pathology. Frontiers in Immunology 14, article number: 1240679. (10.3389/fimmu.2023.1240679)
- Raby, A. and Labeta, M. 2018. Preventing peritoneal dialysis-associated fibrosis by therapeutic blunting of peritoneal toll-like receptor activity. Frontiers in Physiology 9, article number: 1692. (10.3389/fphys.2018.01692)
- Raby, A., González-Mateo, G. T., Williams, A., Topley, N., Fraser, D., López-Cabrera, M. and Labeta, M. O. 2018. Targeting toll-like receptors with soluble toll-like receptor 2 prevents peritoneal dialysis solution-induced fibrosis. Kidney International 94(2), pp. 346-362. (10.1016/j.kint.2018.03.014)
- Raby, A. et al. 2017. Toll-like receptors 2 and 4 are potential therapeutic targets in peritoneal dialysis-associated fibrosis. Journal of the American Society of Nephrology 28(2), pp. 461-478. (10.1681/ASN.2015080923)
- Raby, A. and Labeta, M. 2016. Therapeutic boosting of the immune response: turning to CD14 for help. Current Pharmaceutical Biotechnology 17(5), pp. 414-418. (10.2174/1389201017666160114095708)
- Raby, A. et al. 2013. Targeting the TLR co-receptor CD14 with TLR2-derived peptides modulates immune responses to pathogens. Science Translational Medicine 5(185), article number: 185ra64. (10.1126/scitranslmed.3005544)
- Durno, K., Holst, B., Wilkes, A., Shah, S., Labeta, M. O., Hall, J. E. and Szakmany, T. 2012. STLR-2 levels can discriminate between infective and non-infective origins of multi-organ dysfunction on ICU admission: a pilot study. Critical Care Medicine 40(12), pp. U138-U139. (10.1097/01.ccm.0000424713.57752.27)
- Holst, B., Raby, A., Hall, J. E. and Labeta, M. O. 2012. Complement takes its Toll: an inflammatory crosstalk between Toll-like receptors and the receptors for the complement anaphylatoxin C5a. Anaesthesia 67(1), pp. 60-64. (10.1111/j.1365-2044.2011.07011.x)
- Colmont, C. S. et al. 2011. Human peritoneal mesothelial cells respond to bacterial ligands through a specific subset of Toll-like receptors. Nephrology Dialysis Transplantation 26(12), pp. 4079-4090. (10.1093/ndt/gfr217)
- Raby, A. et al. 2011. TLR activation enhances C5a-induced pro-inflammatory responses by negatively modulating the second C5a receptor, C5L2. European Journal of Immunology 41(9), pp. 2741-2752. (10.1002/eji.201041350)
- Raby, A. et al. 2009. Soluble TLR2 reduces inflammation without compromising bacterial clearance by disrupting TLR2 triggering. The Journal of Immunology 183(1), pp. 506-517. (10.4049/jimmunol.0802909)
- Labeta, M. O., LeBouder, E., Rey-Nores, J. E. and Affolter, M. 2006. Modulation of neonatal microbial recognition: TLR-mediated innate immune responses are specifically and differentially modulated by human milk. Journal of Immunology 176, pp. 3742-52.
- LeBouder, E. et al. 2003. Soluble forms of Toll-like receptor (TLR)2 capable of modulating TLR2 signaling are present in human plasma and breast milk. The Journal of Immunology 171(12), article number: 6680. (10.4049/jimmunol.171.12.6680)
- Labeta, M. O., Vargas, F., Fernandez-Alvarez, J. and Somoza, N. 2003. Evidence of expression of endotoxin receptors CD14, toll-like receptors TLR4 and TLR2 and associated molecule MD-2 and of sensitivity to endotoxin (LPS) in islet beta cells. Clinical & Experimental Immunology 133(2), pp. 208-18. (10.1046/j.1365-2249.2003.02211.x)
- Labeta, M. O., Nores, J. E. R., Vigar, M. . A. and Harris, C. L. 2001. The lipopolysaccharide co-receptor CD14 is present and functional in seminal plasma and expressed on spermatozoa. Immunology 104(3), pp. 317-23. (10.1046/j.1365-2567.2001.01312.x)
- Labeta, M. et al. 2000. Innate recognition of bacteria in human milk is mediated by a milk-derived highly expressed pattern recognition receptor, soluble CD14. Journal of Experimental Medicine 191, pp. 1807-1812. (10.1084/jem.191.10.1807)
Research
My research interest and activities have focused on the molecular mechanisms underlying microbial recognition by the innate immune system, in particular by Toll-like receptors (TLR). This family of innate immune receptors plays a pivotal role in infection clearance by mediating a prompt and efficient proinflammatory response to an array of microorganisms and their components, and by controlling the nature and magnitude of the adaptive immune response. My group’s early research focused on the immunobiology of the TLR co-receptor, CD14, which amplifies TLR-mediated responses. Recently, our research focus has been extended to include the regulation of the TLR-mediated inflammatory response to infection, the regulation by TLRs of other innate immune receptors, in particular those for the complement anaphylatoxin C5a, the design and characterisation of a TLR-based novel strategy to boost the immune response, and the role of TLRs in kidney-related pathologies.
Published key findings include: 1) the detection and characterisation of the TLR co-receptor soluble CD14 (sCD14) in human breast milk; 2) demonstration of the differential effect of sCD14 on human B cells; 3) the identification and characterisation of a naturally-occurring soluble form of TLR2 (sTLR2) capable of regulating pro-inflammatory responses; 4) demonstration of the presence of protein components of milk capable of enhancing and inhibiting TLR signalling; 5) the in vitro and in vivo characterisation of the anti-inflammatory capacity of sTLR2; 6) the identification and characterisation of a pro-inflammatory crosstalk between TLRs and complement receptors; 8) the description of a novel TLR2 peptide-based strategy to boost the immune response; 9) the description of the role and therapeutic target potential of TLR2 and TLR4 in peritoneal dialysis-associated fibrosis.