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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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Plasticity of Invariant NKT Cell Regulation of Allergic Airway Disease Is Dependent on IFN-γ Production

TL;DR: IFN-γ is identified as playing a critical role in dictating the consequences of iNKT cell activation in the initiation phase of the development of AHR and airway inflammation.
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Transcription of IL-2 and IL-4 genes is not inhibited by cyclosporin A in competent T cells.

TL;DR: It is shown that transcription of the IL-2 and IL-4 genes occurs normally throughout this "progression" phase, even in the presence of CsA, and indicates that the augmentation in the progression phase is both NF-AT-independent and C'sA-resistant.
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Allergic Airway Hyperresponsiveness-Enhancing γδ T Cells Develop in Normal Untreated Mice and Fail to Produce IL-4/13, Unlike Th2 and NKT Cells

TL;DR: It is concluded that both the development and the cytokine potential of the AHR-enhancing γδ T cells differs critically from that of Th2 cells and NKT cells, despite similar influences of these cell populations on AHR.
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MEF2C regulates c-Jun but not TNF-α gene expression in stimulated mast cells

TL;DR: The results demonstrate the novel and important, MEKK2‐dependent role of MEF2C in induction of c‐Jun expression in mast cells activated through FcϵRI, a pathway distinct from that involving MEKK 2‐MEK5‐ERK5 in the regulation of mast cell cytokine production.
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The Role of RSV Infection in Asthma Initiation and Progression: Findings in a Mouse Model

TL;DR: Experimental models of RSV infection in mice are discussed and a new investigative approach in which mice are initially infected as neonates and then reinfected later in life is highlighted, shedding light on the mechanisms underlying the association between early severe RSV infections and development of asthma later in childhood.