The DOI matches its Crossref record; 49 of the 49 references it cites were found in a registry or an index.
Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome
Open accessAbstract
Antiphospholipid syndrome (APS) is defined by recurrent pregnancy loss and thrombosis in the presence of antiphospholipid (aPL) Ab's.Currently, therapy for pregnant women with APS is focused on preventing thrombosis, but anticoagulation is only partially successful in averting miscarriage.We hypothesized that complement activation is a central mechanism of pregnancy loss in APS and tested this in a model in which pregnant mice receive human IgG containing aPL Ab's.Here we identify complement component C5 (and particularly its cleavage product C5a) and neutrophils as key mediators of fetal injury, and we show that Ab's or peptides that block C5a-C5a receptor interactions prevent pregnancy complications.The fact that F(ab)′2 fragments of aPL Ab's do not mediate fetal injury and that C4-deficient mice are protected from fetal injury suggests that activation of the complement cascade is initiated via the classical pathway.Studies in factor B-deficient mice, however, indicate that alternative pathway activation is required and amplifies complement activation.In contrast, activating FcγRs do not play an important role in mediating aPL Ab-induced fetal injury.Our findings identify the key innate immune effectors engaged by pathogenic autoantibodies that mediate poor pregnancy outcomes in APS and provide novel and important targets for prevention of pregnancy loss in APS.
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Cites
Natural killer cells and pregnancy
Moffett-King, A. (2002) · Nature Reviews Immunology · doi:10.1038/nri886 · Cited by 1,235
Rai, R., Cohen, H., Dave, M., & Regan, L. (1997) · BMJ · doi:10.1136/bmj.314.7076.253 · Cited by 1,113
FcR γ chain deletion results in pleiotrophic effector cell defects
Takai, T., Li, M., Sylvestre, D., Clynes, R., & Ravetch, J. V. (1994) · Cell · doi:10.1016/0092-8674(94)90115-5 · Cited by 951
Kutteh, W. H. (1996) · American Journal of Obstetrics and Gynecology · doi:10.1016/s0002-9378(96)70610-5 · Cited by 803
Mast Cells: A Cellular Link Between Autoantibodies and Inflammatory Arthritis
Lee, D. M., Friend, D. S., Gurish, M. F., Benoist, C., Mathis, D., & Brenner, M. B. (2002) · Science · doi:10.1126/science.1073176 · Cited by 750
Complement-dependent Clearance of Apoptotic Cells by Human Macrophages
Mevorach, D., Mascarenhas, J. O., Gershov, D., & Elkon, K. B. (1998) · The Journal of Experimental Medicine · doi:10.1084/jem.188.12.2313 · Cited by 700
Arthritis Critically Dependent on Innate Immune System Players
Ji, H., Ohmura, K., Mahmood, U., Lee, D. M., Hofhuis, F. M. A., Boackle, S. A., Takahashi, K., Holers, V. M., Walport, M., Gerard, C., et al. (2002) · Immunity · doi:10.1016/s1074-7613(02)00275-3 · Cited by 693
Self-citationComplement C3 Activation Is Required for Antiphospholipid Antibody-induced Fetal Loss
Holers, V. M., Girardi, G., Mo, L., Guthridge, J. M., Molina, H., Pierangeli, S. S., Espinola, R., Xiaowei, L. E., Mao, D., Vialpando, C. G., et al. (2002) · The Journal of Experimental Medicine · doi:10.1084/jem.200116116 · Cited by 626
Self-citationWipke, B. T., & Allen, P. M. (2001) · The Journal of Immunology · doi:10.4049/jimmunol.167.3.1601 · Cited by 585
Pregnancy Loss in the Antiphospholipid-Antibody Syndrome — A Possible Thrombogenic Mechanism
Rand, J. H., Wu, X.-X., Andree, H. A. M., Lockwood, C. J., Guller, S., Scher, J., & Harpel, P. C. (1997) · New England Journal of Medicine · doi:10.1056/nejm199707173370303 · Cited by 526
Research works printed but not linked: 7
- Stephenson, 1994, Fertil. Steril., 66, 24
- Shin, 1996, Biomembranes., 4, 123
- Li, 2000, Eur. J. Immunol., 30, 2015, 10.1002/1521-4141(200007)30:7<2015::AID-IMMU2015>3.0.CO;2-5 · doi:10.1002/1521-4141(200007)30:7<2015::aid-immu2015>3.0.co;2-5
- Ikematsu, 1998, J. Immunol., 161, 2895, 10.4049/jimmunol.161.6.2895 · doi:10.4049/jimmunol.161.6.2895
- Tesser, 2001, Arthritis Rheum., 44, S274
- Wojta, 2002, Blood., 100, 517, 10.1182/blood.V100.2.517 · DOI
- Kondo, 2001, Clin. Exp. Immunol., 124, 323, 10.1046/j.1365-2249.2001.01513.x · doi:10.1046/j.1365-2249.2001.01513.x
Cited by
The preterm parturition syndrome
Romero, R., Espinoza, J., Kusanovic, J., Gotsch, F., Hassan, S., Erez, O., Chaiworapongsa, T., & Mazor, M. (2006) · BJOG: An International Journal of Obstetrics & Gynaecology · doi:10.1111/j.1471-0528.2006.01120.x · Cited by 1,419
Interplay between inflammation and thrombosis in cardiovascular pathology
Stark, K., & Massberg, S. (2021) · Nature Reviews Cardiology · doi:10.1038/s41569-021-00552-1 · Cited by 1,033
D'Cruz, D. P., Khamashta, M. A., & Hughes, G. R. (2007) · The Lancet · doi:10.1016/s0140-6736(07)60279-7 · Cited by 992
Rother, R. P., Rollins, S. A., Mojcik, C. F., Brodsky, R. A., & Bell, L. (2007) · Nature Biotechnology · doi:10.1038/nbt1344 · Cited by 778
The Pathogenesis of the Antiphospholipid Syndrome
Giannakopoulos, B., & Krilis, S. A. (2013) · New England Journal of Medicine · doi:10.1056/nejmra1112830 · Cited by 688
Metadata
- Authors
- Girardi, G., Berman, J., Redecha, P., Spruce, L., Thurman, J. M., Kraus, D., Hollmann, T. J., Casali, P., Caroll, M. C., Wetsel, R. A., Lambris, J. D., Holers, V. M., & Salmon, J. E.
- Venue
- Journal of Clinical Investigation
- Published
- 2003-12-01
- Volume
- 112
- Issue
- 11
- Pages
- 1644-1654
- ISSN
- 0021-9738 (ISSN-L)
- OpenAlex
- W4239387674
- Cited by
- 594
- References
- 49
- FWCI
- 15.72
- Type
- journal article
- Language
- en
- Open access
- bronze
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- Girardi, G., Berman, J., Redecha, P., Spruce, L., Thurman, J. M., Kraus, D., Hollmann, T. J., Casali, P., Caroll, M. C., Wetsel, R. A., Lambris, J. D., Holers, V. M., & Salmon, J. E. (2003). Complement C5a receptors and neutrophils mediate fetal injury in the antiphospholipid syndrome. Journal of Clinical Investigation. https://doi.org/10.1172/jci200318817
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