The DOI matches its Crossref record; 42 of the 42 references it cites were found in a registry or an index.
Role of the MyD88 transduction signaling pathway in endothelial activation by antiphospholipid antibodies
Abstract
Antiphospholipid syndrome (APS) is an autoimmune disease characterized by the persistent presence of antiphospholipid antibodies (aPLs) and recurrent thrombosis or fetal loss. The thrombophilic state has been partially related to the induction of a proinflammatory and procoagulant endothelial cell (EC) phenotype induced by anti–β2-glycoprotein I (β2-GPI) antibodies that bind β2-GPI expressed on the EC surface. Anti–β2-GPI antibody binding has been shown to induce nuclear factor-κB (NF-κB) translocation leading to a proinflammatory EC phenotype similar to that elicited by interaction with microbial products (lipopolysaccharide [LPS]) and proinflammatory cytokines (interleukin 1β [IL-1β], tumor necrosis factor α [TNF-α]). However, the upstream signaling events are not characterized yet. To investigate the endothelial signaling cascade activated by anti–β2-GPI antibodies, we transiently cotransfected immortalized human microvascular endothelial cells (HMEC-1) with dominant-negative constructs of different components of the pathway (ΔTRAF2, ΔTRAF6, ΔMyD88) together with reporter genes (NF-κB luciferase and pCMV-β-galactosidase). Results showed that both human anti–β2-GPI IgM monoclonal antibodies as well as polyclonal affinity-purified anti–β2-GPI IgG display a signaling cascade comparable to that activated by LPS or IL-1. ΔTRAF6 and ΔMyD88 significantly abrogate antibody-induced as well as IL-1– or LPS-induced NF-κB activation, whereas ΔTRAF2 (involved in NF-κB activation by TNF) does not affect it. Moreover, anti– β2-GPI antibodies and LPS followed the same time kinetic of IL-1 receptor–activated kinase (IRAK) phosphorylation, suggesting an involvement of the toll-like receptor (TLR) family. Our findings demonstrate that anti–β2-GPI antibodies react with their antigen likely associated to a member of the TLR/IL-1 receptor family on the EC surface and directly induce activation.
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Cites
Toll-like receptors and innate immunity
Medzhitov, R. (2001) · Nature Reviews Immunology · doi:10.1038/35100529 · Cited by 4,308
Hoshino, K., Takeuchi, O., Kawai, T., Sanjo, H., Ogawa, T., Takeda, Y., Takeda, K., & Akira, S. (1999) · The Journal of Immunology · doi:10.4049/jimmunol.162.7.3749 · Cited by 3,374
Cervera, R., Piette, J., Font, J., Khamashta, M. A., Shoenfeld, Y., Camps, M. T., Jacobsen, S., Lakos, G., Tincani, A., Kontopoulou‐Griva, I., et al. (2002) · Arthritis & Rheumatism · doi:10.1002/art.10187 · Cited by 2,156
Unresponsiveness of MyD88-Deficient Mice to Endotoxin
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MyD88 Is an Adaptor Protein in the hToll/IL-1 Receptor Family Signaling Pathways
Medzhitov, R., Preston-Hurlburt, P., Kopp, E., Stadlen, A., Chen, C., Ghosh, S., & Janeway, C. A. (1998) · Molecular Cell · doi:10.1016/s1097-2765(00)80136-7 · Cited by 1,575
TRAF6 deficiency results in osteopetrosis and defective interleukin-1, CD40, and LPS signaling
Lomaga, M. A., Yeh, W.-C., Sarosi, I., Duncan, G. S., Furlonger, C., Ho, A., Morony, S., Capparelli, C., Van, G., Kaufman, S., et al. (1999) · Genes & Development · doi:10.1101/gad.13.8.1015 · Cited by 1,267
HMEC-1: Establishment of an Immortalized Human Microvascular Endothelial Cell Line
Ades, E. W., Candal, F. J., Swerlick, R. A., George, V. G., Summers, S., Bosse, D. C., & Lawley, T. J. (1992) · Journal of Investigative Dermatology · doi:10.1111/1523-1747.ep12613748 · Cited by 1,265
Muzio, M., Bosisio, D., Polentarutti, N., D’amico, G., Stoppacciaro, A., Mancinelli, R., van’t Veer, C., Penton-Rol, G., Ruco, L. P., Allavena, P., et al. (2000) · The Journal of Immunology · doi:10.4049/jimmunol.164.11.5998 · Cited by 1,060
Self-citationIRAK: A Kinase Associated with the Interleukin-1 Receptor
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Cited by
The Pathogenesis of the Antiphospholipid Syndrome
Giannakopoulos, B., & Krilis, S. A. (2013) · New England Journal of Medicine · doi:10.1056/nejmra1112830 · Cited by 688
Björkbacka, H., Kunjathoor, V. V., Moore, K. J., Koehn, S., Ordija, C. M., Lee, M. A., Means, T., Halmen, K., Luster, A. D., Golenbock, D. T., et al. (2004) · Nature Medicine · doi:10.1038/nm1008 · Cited by 634
Pathogenesis of antiphospholipid syndrome: understanding the antibodies
Meroni, P. L., Borghi, M. O., Raschi, E., & Tedesco, F. (2011) · Nature Reviews Rheumatology · doi:10.1038/nrrheum.2011.52 · Cited by 620
Self-citationViall, C. A., Chen, Q., Liu, B., Hickey, A., Snowise, S., Salmon, J. E., Stone, P. R., & Chamley, L. W. (2013) · Journal of Autoimmunity · doi:10.1016/j.jaut.2013.08.005 · Cited by 69
Metadata
- Authors
- Raschi, E., Testoni, C., Bosisio, D., Borghi, M. O., Koike, T., Mantovani, A., & Meroni, P. L.
- Venue
- Blood
- Publisher
- American Society of Hematology
- Published
- 2003-05-01
- Volume
- 101
- Issue
- 9
- Pages
- 3495-3500
- ISSN
- 0006-4971 (ISSN-L)
- 1528-0020
- OpenAlex
- W1982207491
- Cited by
- 306
- References
- 42
- FWCI
- 13.04
- Type
- journal article
- Language
- en
- Open access
- closed
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