Immunoglobulin M antibodies present in the acute phase of Kawasaki syndrome lyse cultured vascular endothelial cells stimulated by gamma interferon.

Leung, Donald Y.M.; Collins, Tucker; Lapierre, Lynne A.; Geha, Raif S.; Pober, Jordan S.

doi:10.1172/jci112454

Cited by 237 publications

(102 citation statements)

References 31 publications

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“…Furthermore, a significant positive correlation was observed between titres for IgM AECA and the extent of complement-dependent cytotoxicity. These findings, which are consistent with previous reports [7][8][9], demonstrate that IgM AECA can significantly contribute to vascular injury.…”

Section: Complement-dependent Endothelial Cytotoxicity In Kawasaki DIsupporting

confidence: 93%

“…Such differences could be due in part to the time of blood sampling (within 5 days of onset) and the dilution titre (at 1 : 200 for IgG) used here. Leung et al demonstrated that acute KD sera can lyse HUVEC that have been treated with cytokines, including TNF, but do not lyse untreated HUVEC [7,8]. The authors speculated that the cytotoxic antibodies target antigens on the endothelial cells that are induced by the cytokines [7,8,16].…”

Section: Discussionmentioning

confidence: 99%

“…This may be due to differences in endothelial cell antigens of HUVEC and the coronary arteries. In addition, underlying anatomical abnormalities, genetic factors, or differences in the degree of local immune activation may predispose certain patients to the development of CAL [7]. This i.v.…”

Section: Complement-dependent Endothelial Cytotoxicity In Kawasaki DImentioning

confidence: 99%

“…Although the disease is self-limited, serious complications such as coronary artery aneurism or ectasia occur in about 20% of children affected. The following observations suggest that immunoregulatory abnormalities are involved in the pathogenesis of KD: the acute phase of this disease is characterized by a deficiency of suppressor and cytotoxic T cells; increased numbers of activated helper T cells and monocytes; polyclonal B cell activation [1,2]; and increased levels of serum cytokines such as IL-1 [3], tumour necrosis factor (TNF) [4], interferon-gamma (IFN-) [5], IL-6 [6]; and the appearance of cytotoxic antibodies against vascular endothelial cells [7][8][9].…”

Section: Introductionmentioning

confidence: 99%

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Antibodies to endothelial cells in Kawasaki disease lyse endothelial cells without cytokine pretreatment

Fujieda

Oishi

Kurashige

1997

Clinical and Experimental Immunology

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SUMMARYKawasaki disease (KD) is characterized by diffuse vasculitis and marked immune activation. To confirm the presence of antiendothelial cell antibodies (AECA) and cytotoxicity of AECA, we investigated the presence of AECA using ELISA and cytotoxicity of AECA in KD. Sera from patients with acute KD were assessed for binding to human umbilical vein endothelial cells (HUVEC) using a cell-based ELISA, and for cytotoxicity against HUVEC as indicated by the conversion of a tetrazolium salt (MTT) into a coloured product. IgM AECA were detected in 8/19 KD sera, IgG AECA were detected in 5/19 KD sera. Significant differences in both AECA titres existed between patients and febrile and afebrile controls. Six out of 19 patients showed complement-dependent cytotoxicity against HUVEC. Cytotoxicity was significantly enhanced by pretreating HUVEC with tumour necrosis factor (TNF), and reduced by incubation with gammaglobulin. Serum titres of IgM AECA in the KD patients were positively correlated with cytotoxicity. Findings suggest that IgM AECA mediates complementdependent cytotoxicity against endothelial cells in patients with KD, and gammaglobulin may reduce complement-dependent cytotoxicity of AECA against endothelial cells.

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Section: Complement-dependent Endothelial Cytotoxicity In Kawasaki DIsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Complement-dependent Endothelial Cytotoxicity In Kawasaki DImentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Antibodies to endothelial cells in Kawasaki disease lyse endothelial cells without cytokine pretreatment

Fujieda

Oishi

Kurashige

1997

Clinical and Experimental Immunology

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“…Because it forms the interface between circulating blood and the vessel wall, the endothelial cell could well be the initial site of vascular damage. Anti-endothelial cell antibodies (AEA) have been reported to occur in various diseases (3)(4)(5)(6). We have developed a radioimmunoassay (RIA) to investigate the presence of AEA in rheumatoid vasculitis.…”

Section: Antiendothelial Cell Antibodies In Patients With Rheumatoidmentioning

confidence: 99%

Anti‐endothelial cell antibodies in patients with rheumatoid vasculitis

Heurkens

Daha

Breedveld

1989

Arthritis & Rheumatism

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Diagnosis and Management of Kawasaki Disease

Gersony

1991

JAMA

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Kawasaki disease is an acute vasculitis characterized by mucosal inflammation, rash, cervical adenopathy, indurative edema of the hands and feet, and late membranous desquamation of the fingertips. Early cardiac effects include myocarditis (occasionally with congestive heart failure), pericardial inflammation, and, rarely, valve involvement. Coronary artery aneurysms are a long-term concern because coronary thrombosis with myocardial infarction can be a late manifestation. The origin of Kawasaki disease is unknown, but an infectious agent is most likely. Management consists of aspirin for control of fever and inflammatory manifestations and intravenous gamma globulin for the prevention of coronary aneurysm formation. Careful late follow-up is required, especially for patients with persistent coronary abnormalities. Giant aneurysms (greater than 8 mm) are more likely to progress to coronary obstructive disease, and coronary bypass grafts have been required for some patients. Late coronary artery manifestations in patients with mild early coronary dilatation have not been described. However, since long-term epidemiologic studies have not yet been performed, it is prudent to consider childhood Kawasaki disease to be a potential risk factor for coronary disease, especially in atherosclerosis-prone Western societies.

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Immunoglobulin M antibodies present in the acute phase of Kawasaki syndrome lyse cultured vascular endothelial cells stimulated by gamma interferon.

Abstract: Kawasaki syndrome (KS) is characterized by diffuse vasculitis and marked T cell and B cell activation. In this study, sera from 16 patients with acute KS, 15 patients in the convalescent phase of KS,and 19

Cited by 237 publications

References 31 publications

Antibodies to endothelial cells in Kawasaki disease lyse endothelial cells without cytokine pretreatment

Antibodies to endothelial cells in Kawasaki disease lyse endothelial cells without cytokine pretreatment

Anti‐endothelial cell antibodies in patients with rheumatoid vasculitis

Diagnosis and Management of Kawasaki Disease

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