CD64, CD11a and CD18 leukocytes expression in children with SARS-CoV-2 multisystem inflammatory syndrome versus children with Kawasaki disease: Similar but not the same

García-Salido, Alberto; Carcelén, Sandra Cuenca; Castillo-Robleda, Ana

doi:10.1016/j.medcle.2020.09.002

Cited by 1 publication

(2 citation statements)

References 5 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Elevated levels of CCL2 (monocyte chemoattractant protein-1), IL-1α, and IL-1 receptor antagonist (12), a decrease in the proportion of classic, CD14 high monocytes, and an increase in the proportion of nonclassical CD14 low , CD16 high monocytes with CD64 high expression are indicative of an activated, cytokine-producing phenotype. High percentages of neutrophils also express high levels of CD64 and neutrophils and monocytes express high levels of S100A-family alarmins, suggestive of an active inflammatory process (15,23,24). In addition, cell surface expression of intercellular adhesion molecule 1 on both neutrophils and monocytes are indicative of leukocyte activation (13).…”

Section: Innate Immunitymentioning

confidence: 99%

“…Mild to moderate lymphopenia is a hallmark of disease in MIS-C with decreased absolute numbers of B cells, α/β T cells (CD4 + and CD8 + ), and γ/δ T cells. Cellular migration, consumption, and recruitment may contribute to this leukopenia, mediated by interleukin (IL)-17, chemokine (C-C motif) ligand (CCL) 20 and CCL28 (T helper cell mucosal recruitment) (10, 13), CCL19, chemokine (C-X-C motif) ligand 10 (CXCL10), and CUB domain containing protein 1 (T cell and Natural Killer cell recruitment to affected tissues) (22, 23), and upregulation of the surface α L β 2 integrin, CD11a/CD18 (leukocyte activation, differentiation, and endothelial adhesion) (24, 25).…”

Section: Immunologic Mechanisms Of the Systemic Inflammatory Process ...mentioning

confidence: 99%

See 1 more Smart Citation

Multisystem Inflammatory Syndrome in Children: Host Immunologic Responses

Mazer

Bulut

Brodsky

et al. 2022

Pediatric Critical Care Medicine

View full text Add to dashboard Cite

Several weeks into the COVID-19 pandemic, a new syndrome causing sudden critical illness in children was identified (1)(2)(3)(4). Multisystem inflammatory syndrome in children (MIS-C), also called Pediatric Inflammatory Multisystem Syndrome Temporally associated with Severe acute respiratory syndrome coronavirus 2 (5), is a clinical syndrome of systemic inflammation, strongly associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) virus, that has some similarities to, but is clinically and biologically distinct from, Kawasaki disease shock, macrophage activation syndrome, and toxic shock syndrome (TSS) (6-8). MIS-C typically afflicts infected (and often asymptomatic) children 4-6 weeks after exposure to SARS-CoV-2 and can cause multiple organ involvement affecting the heart, lungs, kidneys, brain, skin, and gastrointestinal system (1). These patients often present with cardiogenic or distributive shock and/or with severe abdominal pathology requiring admission to the PICU (9). Feldstein et al (1) studied a cohort of 539 MIS-C patients throughout the United States and demonstrated a nearly 75% ICU admission rate, 45% vasopressor requirement with less than 2% mortality, with the majority of patients achieving a complete recovery. Although MIS-C is a rare new clinical entity, formative studies are shaping the basic immunopathologic mechanisms behind the syndrome (2). The focus of this review is to synthesize the currently published immunologic profiles of patients with MIS-C into a robust mechanistic schema, which will identify future areas of study to complete the identification of the immunologic pathophysiology of MIS-C and to create a template that can be applied to several other autoinflammatory and post-infectious processes. A PATHOLOGIC IMMUNE RESPONSE, DIRECT SARS-COV-2 EFFECT, OR POST-INFECTIOUS SYNDROME?The prevailing (nonmutually exclusive) hypotheses for the pathogenic etiology of MIS-C include: 1) a post-infectious autoimmune-mediated inflammatory process, 2) a cytokine storm instigated by a superantigen response, and 3) a dysregulated immune response to chronic exposure to SARS-CoV-2 viral antigens. There are data to support all three theories in the literature and the underlying etiology is likely complex and multifactorial.

show abstract