Circulating immune complex in the mucocutaneous lymphnode syndrome

Furuse, Akio; Matsuda, Ichiro

doi:10.1007/bf00445669

Cited by 16 publications

(8 citation statements)

References 9 publications

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“…Studies have shown that decreased levels of C1q might be related to increased levels of C1qAb (12). Plasma levels of C1q-CIC in the present study differed from those in other reports, which might be related to the time of measurement and methods employed (13)(14)(15). The present study did not show significant differences in plasma concentrations of C1q-CIC between the KD group and healthy control or febrile control groups.…”

Section: Discussioncontrasting

confidence: 89%

Early decreased plasma levels of factor B and C5a are important biomarkers in children with Kawasaki disease

Zou

Song

et al. 2015

Pediatr Res

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Background:The mechanisms underpinning Kawasaki disease (KD) are incompletely understood. There is an unmet need for specific biomarkers for the early diagnosis of KD. Methods: Eighty-five KD patients suffering from acute-phase and subacute-phase KD, 40 healthy children, and 40 febrile children comprised the study cohort. An enzyme-linked immunosorbent assay was used to measure plasma levels of C1q, C1q-circulating immune complex (C1q-CIC), mannan-binding lectin-associated serine protease (MASP)-1, factor B, C4d, C3d, C5a, C5b-9 and CD59. results: Plasma concentrations of factor B and C5a in the acute phase were lower than those in healthy and febrile control groups (all P < 0.05). Compared with acute-phase KD patients, plasma concentrations of C1q, factor B, and C3d in KD patients were increased significantly (P < 0.05), but those of C4d, MASP-1 and CD59 decreased significantly (P < 0.05), in patients with sub-acute KD. conclusion: These data suggest that more than one pathway in the complement system is activated in KD. Importantly, decreased plasma concentrations of factor B and C5a in the acute phase (6-10 d) could be employed as biomarkers for the early diagnosis of KD. k awasaki disease (KD) is an acute, self-limiting, nonspecific systemic vascular inflammatory syndrome. KD is considered to be caused by infectious agents in genetically susceptible children. The diagnosis of KD is dependent upon clinical manifestations; definitive diagnostic markers are lacking. The pathogenesis of KD is characterized by immune injury to endothelial cells (1) that results in systemic vasculitis or aneurysms in coronary arteries (2).Vascular endothelial cells are a source of complement and complement regulatory factors. Activated complement can form complement fragments (e.g., C3, C4d, Bb) and the membrane attack complex (MAC) on the cell surface (3). The MAC can mediate the inflammatory response by killing anucleate cells and bacteria, as well as causing cells to secrete a large number of cytokines and growth factors (4). Animal studies have shown that coronary atherosclerotic lesions appear not only during complement activation, but also during complement deposition, which results in tissue injury (5). It also has been demonstrated that complement components are accumulated in cryoglobulinemic vasculitis (6). Other studies have reported dysfunction of vascular endothelial cells (7) and the classical pathway of complement activation in all three layers of aneurysms (8).With the evidence stated above, we speculated that activation of the complement system might be involved in the pathogenesis of KD, and that activated complement factors could be employed as early diagnostic markers for KD. To test this hypothesis, we investigated plasma levels of various complement components in children with acute KD and subacute KD. RESULTS Changes in Plasma Concentrations of Complement FactorsC1q and C1q-circulating immune complex (C1q-CIC). C1q is a factor of the classical pathway of complement activation. The plasma level of C1q was sig...

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Section: Discussioncontrasting

confidence: 89%

Early decreased plasma levels of factor B and C5a are important biomarkers in children with Kawasaki disease

Zou

Song

et al. 2015

Pediatr Res

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“…Circulating immune complexes have been detected in Kawasaki disease using the Raji cell method, Clq method, and precipitation with polyethylene glycol method (8,11,12). Not only IgG-CIC but also IgA-CIC by precipitation test with polyethylene glycol have been reported (22).…”

Section: Discussionmentioning

confidence: 99%

High Levels of IgA‐Containing Circulating Immune Complex and Secretory IgA in Kawasaki Disease

Ohshio¹,

Furukawa²,

Khine³

et al. 1987

Microbiology and Immunology

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Sera of patients with Kawasaki disease were studied for the levels of IgA-containing (C3-fixing) circulating immune complexes (IgA-CIC), IgG-contain ing (IgG-)CIC, total IgA, secretory IgA, and complement component (C3) by means of enzyme-linked immunosorbent assays or single radial immunodiffusion methods. There was significantly high level of IgA-CIC, but not IgG-CIC. The levels of total IgA, secretory IgA, and C3 were significantly elevated. Significantly high levels of secretory IgA were found in 22 (51 %) of 43 patients.

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“…Its aetiology remains unknown in These suggestive findings include increases in serum immunoglobulin E levels [10], the presence of circulating immune complexes [4,5,12,19], the emergence of heterophilic antibodies [21], abnormalities in the regulatory T-cell subsets (increases in helper T-cells and decrease in suppressor T-cells) [11], and hyperactivity of suppressor T-cells [15]. Recently, serum factors that impair in vitro PBL response to mitogens were reported in patients with some infectious diseases (eg.…”

Section: Discussionmentioning

confidence: 97%

Inhibition of lymphocyte DNA synthesis by plasma from patients with Kawasaki disease

et al. 1986

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Plasma obtained from patients with Kawasaki disease during the acute phase markedly inhibited DNA synthesis in autologous peripheral blood lymphocytes (PBLs) stimulated by phytohaemagglutinin-P (PHA-P) or concanavalin A (Con A). The inhibition became less marked with the progression of the disease and there was no effect on DNA synthesis in PBLs stimulated by pokeweed mitogen (PWM). The plasma also inhibited DNA synthesis in PBLs obtained from healthy adults. The postulated suppressors markedly inhibited DNA synthesis in PBLs from healthy adults stimulated by PHA-P, Con A, purified protein derivative (PPD) or mixed lymphocyte culture reaction (MLR) but they had little effect on the DNA synthesis stimulated by PWM or protein A. With respect to the mechanism, the suppression was found to be potentiated by an increase in the concentration of the patients' plasma, and not to be associated with cytotoxicity nor with a deficiency of factor(s) indispensable for PBL proliferation. It was also evident that the suppression was not related to the concentration of the stimulant, to the lengths of the culturing period nor to the presence of prostaglandins.

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Circulating immune complex in the mucocutaneous lymphnode syndrome

Cited by 16 publications

References 9 publications

Early decreased plasma levels of factor B and C5a are important biomarkers in children with Kawasaki disease

Early decreased plasma levels of factor B and C5a are important biomarkers in children with Kawasaki disease

High Levels of IgA‐Containing Circulating Immune Complex and Secretory IgA in Kawasaki Disease

Inhibition of lymphocyte DNA synthesis by plasma from patients with Kawasaki disease

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