Comment on "Tumor-initiating cells establish an IL-33-TGF-β niche signaling loop to promote cancer progression".

Taniguchi (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.

Loss of the interleukin-6 receptor causes immunodeficiency, atopy, and abnormal inflammatory responses.

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 We describe two patients with homozygous mutations in 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 , and genes encoding different components of the IL-6 signaling pathway, and alerts us to the potential toxicity of drugs targeting the IL-6R.

Rural Hospital Transfer Patterns before and after Implementation of a Statewide Trauma System.

Objective: To evaluate trauma transfer practices in rural Oregon before and after implementation of a statewide trauma system.

Methods: A pre- vs post-system implementation (historical control) analysis of trauma transfer practices was performed using a sample of rural ED trauma patients from 4 Level-3 and 5 Level-4 trauma hospitals. Medical records of patients with specific index injury diagnoses in 4 anatomic regions (head, chest, liver/ spleen, and femur/open-tibia) were reviewed for a 3-year period before statewide trauma system implementation and 3 years after hospital trauma designation.