Antilymphocyte autoantibodies generate T cell–C4d signatures in systemic lupus erythematosus

Liu, Chau‐Ching; Manzi, Susan; Ahearn, Joseph M.

doi:10.1016/j.trsl.2014.07.007

Cited by 4 publications

(6 citation statements)

References 41 publications

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“…In fact, TC4d-positive patients do not present with lymphopoenia. 36 However, CB-CAPs deposition may lead to deformation of the cell membrane and/or cell activation. 37 38 …”

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

“…In contrast to the absence of antiplatelet antibodies in PC4d-positive patients, anti T-cell antibodies were found on T cells of approximately 30% of TC4d-positive subjects with SLE. 36 The antigens of these antibodies have not been clearly identified. 36 Taken together, these data lead to the hypothesis that the dynamic binding of various autoantibodies to cells causes complement activation and deposition of CB-CAPs on those cells.…”

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

“… 36 The antigens of these antibodies have not been clearly identified. 36 Taken together, these data lead to the hypothesis that the dynamic binding of various autoantibodies to cells causes complement activation and deposition of CB-CAPs on those cells. This is consistent with the observation that not all cell types are simultaneously C4d or C3d positive in a given patient, and that CB-CAPs bind to different cell types in a patient-specific fashion.…”

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

“…This is consistent with the observation that not all cell types are simultaneously C4d or C3d positive in a given patient, and that CB-CAPs bind to different cell types in a patient-specific fashion. 36 …”

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

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Cell-bound complement activation products in SLE

Ramsey‐Goldman

Dervieux³

et al. 2017

Lupus Sci Med

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Diagnosis of SLE is based on clinical manifestations and laboratory findings. Timely diagnosis and treatment are important to control disease activity and prevent organ damage. However, diagnosis is challenging because of the heterogeneity in clinical signs and symptoms, and also because the disease presents with alternating periods of flare and quiescence. As SLE is an autoimmune disease characterised by the formation of autoantibodies, diagnostic immunology laboratory tests for detecting and quantifying autoantibodies are commonly used for the diagnosis and classification of SLE. These include ANA, anti-double-stranded DNA antibodies and anti-Smith antibodies, together with other antibodies such as antiphospholipid or anti-Cq1. Complement proteins C3 and C4 are commonly measured in patients with SLE, but their serum levels do not necessarily reflect complement activation. Cell-bound complement activation products (CB-CAPs) are fragments formed upon complement activation that bind covalently to haematopoietic cells. This review focuses on the complement system and, in particular, on CB-CAPs as biomarkers for the diagnosis and monitoring of SLE, vis-à-vis complement proteins and other biomarkers of complement activation.

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“…In fact, TC4d-positive patients do not present with lymphopoenia. 36 However, CB-CAPs deposition may lead to deformation of the cell membrane and/or cell activation. 37 38 …”

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

Section: Challenges In the Diagnosis And Monitoring Of Slementioning

confidence: 99%

See 2 more Smart Citations

Cell-bound complement activation products in SLE

Ramsey‐Goldman

Dervieux³

et al. 2017

Lupus Sci Med

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“…Until recently, the mechanism(s) responsible for generating the CB-CAP signature have not been systematically investigated. Our recent study has shown that anti-lymphocyte autoantibodies play a pivotal role in generating patient-specific T-cell-bound C4d (T-C4d) signatures [46], providing solid evidence for an autoantibody-mediated mechanism underlying CB-CAP generation for the first time. Of the various CB-CAP phenotypes identified to date, platelet-bound C4d (P-C4d) is characteristically distinct in that it is identified only in a relatively small fraction of SLE patients (approximately 20% in sensitivity), yet in an extremely exclusive manner (99% in specificity) [34].…”

Section: Discussionmentioning

confidence: 99%

Potential Roles of Antiphospholipid Antibodies in Generating Platelet-C4d in Systemic Lupus Erythematosus

et al. 2017

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Premature, accelerated onset of atherothrombotic disease is prevalent in patients with systemic lupus erythematosus (SLE). Most, if not all, atherothrombotic diseases are likely to involve platelets and complement. Previously, we discovered that platelets bearing complement activation product C4d (P-C4d) are present in SLE patients, and are significantly associated with antiphospholipid (aPL) antibody positivity and stroke in SLE patients. The goal of the present study was to further elucidate the role of aPL and other platelet-reactive autoantibodies in the generation of P-C4d. To determine the association between P-C4d and aPL antibodies, the serum levels of aPL antibodies and P-C4d of 180 SLE patients were measured by enzyme-linked immunoassays and flow cytometry, respectively. To investigate the role of aPL antibodies, and possibly other autoantibodies as well, in mediating the generation of P-C4d, in vitro 2-step P-C4d induction experiments were performed. The results showed that the presence and levels of aPL antibodies in the serum were specifically elevated in SLE patients with positive P-C4d. The plasma and immunoglobulins purified from SLE patients who were positive for P-C4d and aPL were capable of inducing C4d deposition on normal platelets in vitro. The capacity of SLE plasma in inducing P-C4d appeared to correlate proportionately to the serum aPL levels. Collectively, the results demonstrate that both aPL and other platelet-reactive autoantibodies may participate in mediating the generation of P-C4d in SLE patients.

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