Subject(s)
Anaphylaxis , Mice , Animals , Anaphylaxis/etiology , Neutrophils , Receptors, IgG , Immunoglobulin G , Disease Models, AnimalSubject(s)
Basophils , Receptors, IgE , Cell Degranulation , Humans , Immunoglobulin E , Leukocyte Count , Mast CellsABSTRACT
Taniguchi et al (Research Articles, 17 July 2020, p. 269) claim that the cytokine interleukin-33 induces accumulation of tumor-associated macrophages expressing the immunoglobulin E receptor FcεRI. Although these findings hold great therapeutic promise, we provide evidence that the anti-FcεRI antibody used in this study is not specific for FcεRI on macrophages, which raises concerns about the validity of some of the conclusions.
Subject(s)
Interleukin-33 , Neoplasms , Humans , Interleukin-33/genetics , Neoplasms/genetics , Neoplastic Stem Cells , Receptors, IgE , Transforming Growth Factor betaABSTRACT
IL-6 excess is central to the pathogenesis of multiple inflammatory conditions and is targeted in clinical practice by immunotherapy that blocks the IL-6 receptor encoded by IL6R We describe two patients with homozygous mutations in IL6R who presented with recurrent infections, abnormal acute-phase responses, elevated IgE, eczema, and eosinophilia. This study identifies a novel primary immunodeficiency, clarifying the contribution of IL-6 to the phenotype of patients with mutations in IL6ST, STAT3, and ZNF341, genes encoding different components of the IL-6 signaling pathway, and alerts us to the potential toxicity of drugs targeting the IL-6R.
