<p>Multisystem Inflammatory Syndrome in Children (MIS-C) is a rare but serious condition that develops weeks after SARS-CoV-2 exposure and involves systemic inflammation affecting multiple organs. Its exact pathophysiology remains unclear, with proposed mechanisms including cytokine storms, antibody-dependent enhancement, and genetic predispositions. This study aimed to evaluate the effects of immunomodulatory therapy-intravenous immunoglobulins (IVIG) and glucocorticosteroids (GCS) on peripheral immune cell composition in 24 children with MIS-C. Innate and adaptive immune cells populations were analyzed by flow cytometry before and after treatment (IVIG 2&#xa0;g/kg; GCS 1–2&#xa0;mg/kg/day). Prior to therapy, patients showed elevated counts and altered phenotypes of neutrophils, monocytes, and T cells. Following treatment, a reduction in CD64 expression on neutrophils and monocytes was observed, along with decreased numbers of inflammatory cells, indicating an immunomodulatory effect of IVIG and GCS. An increase in CD56 expression on monocytes suggested additional phenotypic changes within this compartment. These findings highlight CD64 as a marker of inflammatory activation in MIS-C and demonstrate that therapy reduces its expression, potentially reflecting diminished inflammation. Further research is needed to assess long-term immune effects of treatment in children with MIS-C.</p>

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Therapy-induced modulation of cellular response in Multisystem Inflammatory Syndrome in Children (MIS-C) - insights into selected immune cells’ markers expression

  • Karolina Bukowska-Strakova,
  • Izabela Siemińska,
  • Karolina Leś,
  • Małgorzata Stec,
  • Katarzyna Ptak,
  • Izabela Szymońska,
  • Anna Olchawa-Czech,
  • Nina Mól,
  • Przemysław Błyszczuk,
  • Jarek Baran,
  • Przemko Kwinta,
  • Maciej Siedlar

摘要

Multisystem Inflammatory Syndrome in Children (MIS-C) is a rare but serious condition that develops weeks after SARS-CoV-2 exposure and involves systemic inflammation affecting multiple organs. Its exact pathophysiology remains unclear, with proposed mechanisms including cytokine storms, antibody-dependent enhancement, and genetic predispositions. This study aimed to evaluate the effects of immunomodulatory therapy-intravenous immunoglobulins (IVIG) and glucocorticosteroids (GCS) on peripheral immune cell composition in 24 children with MIS-C. Innate and adaptive immune cells populations were analyzed by flow cytometry before and after treatment (IVIG 2 g/kg; GCS 1–2 mg/kg/day). Prior to therapy, patients showed elevated counts and altered phenotypes of neutrophils, monocytes, and T cells. Following treatment, a reduction in CD64 expression on neutrophils and monocytes was observed, along with decreased numbers of inflammatory cells, indicating an immunomodulatory effect of IVIG and GCS. An increase in CD56 expression on monocytes suggested additional phenotypic changes within this compartment. These findings highlight CD64 as a marker of inflammatory activation in MIS-C and demonstrate that therapy reduces its expression, potentially reflecting diminished inflammation. Further research is needed to assess long-term immune effects of treatment in children with MIS-C.