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Erwin W. Gelfand

Researcher at University of Colorado Denver

Publications -  679
Citations -  37565

Erwin W. Gelfand is an academic researcher from University of Colorado Denver. The author has contributed to research in topics: Immunoglobulin E & T cell. The author has an hindex of 99, co-authored 675 publications receiving 36059 citations. Previous affiliations of Erwin W. Gelfand include University of Colorado Hospital & University of Virginia.

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Critical roles for interleukin-4 and interleukin-5 during respiratory syncytial virus infection in the development of airway hyperresponsiveness after airway sensitization.

TL;DR: It is concluded that both IL-5, particularly during acute infection, and IL-4 are critical in mediating the effects of RSV infection on allergic airway sensitization, resulting in the development of AHR and lung eosinophilia.
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IFN-γ Production during Initial Infection Determines the Outcome of Reinfection with Respiratory Syncytial Virus

TL;DR: Provision of IFN-γ during primary infection in infancy may be a potential therapeutic approach to alter the course of RSV-mediated long-term sequelae and protection against AHR and lung histopathology on reinfection.
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Reduction of antigen-induced airway hyperreactivity and eosinophilia in ICAM-1-deficient mice.

TL;DR: It is concluded that ICAM-1 is an important ligand mediating T-cell proliferation in response to antigen, eosinophil migration into the airways, and the development of airway hyperreactivity (AHR) in allergen-sensitized and -challenged mice.
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Mast cell-derived tumour necrosis factor is essential for allergic airway disease.

TL;DR: The present results demonstrate the significance of mast cells in the development of airway disease and highlight the importance of mast cell-derived tumour necrosis factor in these responses.
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Hematopoietic stem cell transplantation in 29 patients hemizygous for hypomorphic IKBKG/NEMO mutations.

Charline Miot, +50 more
- 21 Sep 2017 - 
TL;DR: Overall, HSCT can cure most clinical features of patients with a variety of IKBKG mutations, and the underlying mutation does not appear to have any influence, as patients with the same mutation had different outcomes.