Presence of coronary aneurysms during Kawasaki Disease (KD) correlates with lower levels of autoantibodies to both full form and spliced variant of immune regulator Del-1.
Immunol Lett
; 256-257: 34-41, 2023.
Article
in English
| MEDLINE | ID: covidwho-2302009
ABSTRACT
Kawasaki disease (KD), a rare multisystem inflammatory condition that predominantly affects children under six years of age, is the leading cause of childhood-acquired heart disease in developed countries. The pathogenesis is unknown, but studies support that an infectious stimulus triggers an autoimmune reaction in a genetically susceptible child. Recent studies demonstrated an association with autoantibody response to Del-1 (also known as EDIL3) in children with KD. Del-1 is an extracellular matrix protein that is expressed both in macrophages and vascular endothelium. Del-1 has an anti-inflammatory role by preventing leucocyte migration to inflammatory sites. Del-1 has two expression variants and genetic variants of Del-1 have been associated with the risk of intracranial aneurysms. Due to the physiologic plausibility for a role during KD, we chose to assess if autoantibodies against DEL-1 are seen in a larger cohort of children with KD and to assess if responses correlated to aneurysm formation. Contrary to prior findings, in comparison to febrile controls, autoantibodies were not overall higher in children with KD. Elevation in Post-IVIG samples in comparison to pre-IVIG and convalescent samples supports the commonality of anti-Del-1 antibodies. Autoantibodies were notably lower in children with KD who had coronary Z score elevations in comparison to those who did not.
Keywords
Full text:
Available
Collection:
International databases
Database:
MEDLINE
Main subject:
Coronary Aneurysm
/
Mucocutaneous Lymph Node Syndrome
Type of study:
Cohort study
/
Observational study
/
Prognostic study
Topics:
Long Covid
/
Variants
Limits:
Child
/
Child, preschool
/
Humans
Language:
English
Journal:
Immunol Lett
Year:
2023
Document Type:
Article
Affiliation country:
J.imlet.2023.03.007
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