ArticleBMC immunology2019
Distinct variations of antibody secreting cells and memory B cells during the course of Kawasaki disease.
Article in BMC immunology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Immunophenotype of Kawasaki Disease: Insights into Pathogenesis and Treatment Response.Life (Basel, Switzerland) · 2025Review
- lute: estimating the cell composition of heterogeneous tissue with varying cell sizes using gene expression.BMC genomics · 2025Article
- Single cell sequencing technology reveals the correlation between B lymphocytes and vascular inflammatory symptoms of Kawasaki disease.Translational pediatrics · 2025Article
- Receptor Binding Domain-Specific B Cell Memory Responses Among Individuals Vaccinated Against SARS-CoV-2.Vaccines · 2024Article
- Article
- Antibodies, repertoires and microdevices in antibody discovery and characterization.Lab on a chip · 2024Review
- The immune landscape of SARS-CoV-2-associated Multisystem Inflammatory Syndrome in Children (MIS-C) from acute disease to recovery.iScience · 2021Article
- Kawasaki syndrome: role of superantigens revisited.The FEBS journal · 2021Review
- A Diagnostic Model for Kawasaki Disease Based on Immune Cell Characterization From Blood Samples.Frontiers in pediatrics · 2021Article
- Severe COVID-19, multisystem inflammatory syndrome in children, and Kawasaki disease: immunological mechanisms, clinical manifestations and management.Rheumatology international · 2021Review
- Single-Cell Technologies for the Study of Antibody-Secreting Cells.Frontiers in immunology · 2021Review
- Antibodies and Immunity During Kawasaki Disease.Frontiers in cardiovascular medicine · 2020Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundBoth antibody secreting cells (ASCs) and memory B cells are essential for the maintenance of humoral immunity. To date, limit studies have focused on the two populations in Kawasaki disease (KD). To address the status of humoral immunity during KD, our current concentration is on the variations of ASCs and memory B cells, as well as their subsets in both acute and remission stages of KD.
methodsASCs were defined as the population with high expressions of CD27 and CD38 among CD3-CD20- lymphocytes. Based on the expression of surface marker CD138 and intracellular marker IgG, ASCs were further divided into two subsets. Memory B cells were characterized by the expressions of IgD, CD27 and IgM, upon which memory B cells were further categorized into CD27 + IgD- (switched memory, Sm), CD27-IgD- (Double negative, DN) and CD27 + IgD + IgM+ (marginal zone, MZ) B cells. Collectively, six populations were analyzed using flow cytometry. The blood samples were collected from KD patients in different stages and healthy controls.
resultsIn the acute stage, the percentages of ASCs, CD138+ ASCs, and IgG+ ASCs were significantly increased. In contrast, the percentages of memory B cells including Sm and MZ B cells were significantly decreased. Correlation analysis found ASCs positively correlated with the level of serum IgM, whereas MZ B cells not only positively correlated with the level of serum IgG, IgA, and IgM, but also positively correlated with the level of serum complement C3 and C4 and negatively correlated with the value of C-reactive protein (CRP). In the remission stage, the percentages of IgG+ ASCs and MZ B cells were significantly reduced, whereas other subsets presented heterogeneous variations.
conclusionsOur study provided direct evidence that ASCs contributed to the pathogenesis of KD, and it was the first time to describe the variation of memory B cells in this disease. Among the subsets, only IgG+ ASCs presented a significant increase in the acute stage and decreased after IVIG administration, indicating the involvement of IgG+ ASCs in the inflammation of KD and also suggesting that IVIG played an inhibitory role in the expression of cytoplasmic IgG.
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