Kawasaki disease: Aetiopathogenesis and therapeutic utility of intravenous immunoglobulin

Galeotti, Caroline; Bayry, Jagadeesh; Koné‐Paut, Isabelle; Kaveri, Srini V.

doi:10.1016/j.autrev.2009.12.004

Cited by 92 publications

(75 citation statements)

References 96 publications

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“…The vasculitis involves the small-and medium-sized arteries, and symptoms include high fever, rash, cervical lymphadenopathy, conjunctivitis, and mucocutaneous changes. The most concerning life-long morbidity involves formation of ectasia or aneurysm of the coronary arteries [6]. The majority of children with KD are under 5 years old, with peak incidence between 18 and 24 months.…”

Section: Kawasaki Diseasementioning

confidence: 99%

“…KD is believed to represent an aberrant inflammatory response to an infectious trigger in a genetically predisposed individual [6]. Activation of monocytes, macrophages, and inflammatory cytokines such as tumor necrosis alpha (TNF-α), interleukin (IL)-1, and IL-6 contributes largely to the inflammatory state characteristic of KD [6].…”

Section: Immunologic Theories Behind Kdmentioning

confidence: 99%

“…Activation of monocytes, macrophages, and inflammatory cytokines such as tumor necrosis alpha (TNF-α), interleukin (IL)-1, and IL-6 contributes largely to the inflammatory state characteristic of KD [6]. The influx of neutrophils characterizes the early stage, and resultant reactive oxygen species and other mediators also contribute to endothelial inflammation and resultant dysfunction [6,7]. Specific Toll-like receptor agonists (such a TLR-2) contribute to the upregulation of costimulatory and inflammatory cytokines inducing coronary pathology in KD [7].…”

Section: Immunologic Theories Behind Kdmentioning

confidence: 99%

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Impact of Immunoglobulin Therapy in Pediatric Disease: a Review of Immune Mechanisms

Wong

White

2015

Clinic Rev Allerg Immunol

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Intravenous immunoglobulin (IVIG) provides replacement therapy in immunodeficiency and immunomodulatory therapy in inflammatory and autoimmune diseases. This paper describes the immune mechanisms underlying six major non-primary immunodeficiency pediatric diseases and the diverse immunomodulatory functions of IVIG therapy. In Kawasaki disease, IVIG plays a major, proven, and effective role in decreasing aneurysm formation, which represents an aberrant inflammatory response to an infectious trigger in a genetically predisposed individual. In immune thrombocytopenia, IVIG targets the underlying increased platelet destruction and decreased platelet production. Although theoretically promising, IVIG shows no clear clinical benefit in the prophylaxis and treatment of neonatal sepsis. Limitations in research design combined with the unique neonatal immunologic environment offer explanations for this finding. Inflammation from aberrant immune activation underlies the myelinotoxic effects of Guillain-Barré syndrome. HIV-1 exerts a broad range of immunologic effects and was found to decrease serious bacterial infections in the pre-highly active anti-retroviral therapy (HAART) era, although its practical relevance in the post-HAART era has waned. Clinical and experimental data support the role of immune mechanisms in the pathogenesis of childhood epilepsy. IVIG exerts anti-epileptic effects through targeting upregulated cytokine pathways and antibodies thought to contribute to epilepsy. Applications in six additional pediatric diseases including pediatric asthma, atopic dermatitis, cystic fibrosis, pediatric autoimmune neuropsychiatric disorders associated with streptococcal infection (PANDAS), autism, and transplantation will also be briefly reviewed. From autoimmunity to immunodeficiency, a dynamic immunologic basis underlies major pediatric diseases and highlights the broad potential of IVIG therapy.

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Section: Kawasaki Diseasementioning

confidence: 99%

Section: Immunologic Theories Behind Kdmentioning

confidence: 99%

Section: Immunologic Theories Behind Kdmentioning

confidence: 99%

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Impact of Immunoglobulin Therapy in Pediatric Disease: a Review of Immune Mechanisms

Wong

White

2015

Clinic Rev Allerg Immunol

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“…However, when it is used at higher than replacement doses (e.g., 1.5-2 g/kg) it has immunomodulatory and anti-inflammatory effects. These are believed to contribute to its efficacy in treatment of such conditions as immune thrombocytopenia, Kawasaki disease, autoimmune inflammatory neuropathies, selected autoimmune dermatological and rheumatological conditions treated for licensed indications and also in off-label therapy [1][2][3].…”

Section: Introductionmentioning

confidence: 98%

Potentiation of cytokine-induced proliferation of human Natural Killer cells by intravenous immunoglobulin G

Issekutz

Käsermann

Rowter

2015

Clinical Immunology

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“…It was demonstrated that inflammatory cytokines are essential factors for the pathogenesis of inflammation in Kawasaki disease and that coronary artery lesions were caused by abnormal activation of endothelial cells, progressive injury of the arterial media and activation/ disruption of the coagulation and fibrinolysis systems [27,28].…”

Section: Plasma Exchangementioning

confidence: 99%

Pathogenesis of Systemic Inflammatory Diseases in Childhood: ?Lessons From Clinical Trials of Anti-Cytokine Monoclonal Antibodies for Kawasaki Disease, Systemic Onset Juvenile Idiopathic Arthritis, and Cryopyrin-Associated Periodic Fever Syndrome?

Yokota¹,

Kikuchi²,

Nozawa³

et al. 2013

Pediat Therapeut

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Inflammation has often been considered a non-specific response, and to play only a bridging role in the activation of adaptive immunity. However, it is now accepted that inflammation is the product of an independent innate immune system closely linked to the adaptive immune system. The key mediators of inflammation are inflammatory cytokines, as determined by multiple lines of evidence both in vitro and in vivo. Due to the crucial role of inflammatory cytokines in the pathogenesis of autoimmune disorders, anti-cytokine treatment has been developed as a therapy for rheumatoid arthritis, juvenile idiopathic arthritis (JIA), and inflammatory bowel disease. We recently completed several clinical trials of anti-cytokine treatment for children with systemic inflammatory diseases: anti-IL-6 receptor monoclonal antibody (tocilizumab) for children with 2 subtypes of JIA (poly-JIA and systemic JIA), anti-TNF-alpha monoclonal antibody (infliximab) for children with Kawasaki disease, and anti-IL-1-beta monoclonal antibody (canakinumab) for children with cryopyrin-associated periodic syndrome. This review summarizes the basis of inflammation in terms of innate immunity and adaptive immunity in these systemic inflammatory diseases, clinical efficacy and tolerability of these biologic agents, and attempts to determine the roles of individual inflammatory cytokines in disease pathogenesis.

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Kawasaki disease: Aetiopathogenesis and therapeutic utility of intravenous immunoglobulin

Cited by 92 publications

References 96 publications

Impact of Immunoglobulin Therapy in Pediatric Disease: a Review of Immune Mechanisms

Impact of Immunoglobulin Therapy in Pediatric Disease: a Review of Immune Mechanisms

Potentiation of cytokine-induced proliferation of human Natural Killer cells by intravenous immunoglobulin G

Pathogenesis of Systemic Inflammatory Diseases in Childhood: ?Lessons From Clinical Trials of Anti-Cytokine Monoclonal Antibodies for Kawasaki Disease, Systemic Onset Juvenile Idiopathic Arthritis, and Cryopyrin-Associated Periodic Fever Syndrome?

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