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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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The ionic and biochemical basis for T-cell activation and proliferation. Potential causes of impaired T-cell function.

TL;DR: The major component of the T-cell response appears to be transmembrane Ca2+ uptake, presumably through C2+ channels as discussed by the authors, and ligand-gated channels are regulated differently from the Ca2− channels of excitable cells.
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Activation of p42erk2MAPK and p90rskby IL-2 Occurs Independently of Protein Kinase C

TL;DR: It is demonstrated that IL-2 stimulation results in the activation of MAPK and p90rsk and that this activation occurs in a PKC-independent manner.
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Expression and activation of the steroidogenic enzyme CYP11A1 is associated with IL-13 production in T cells from peanut allergic children.

TL;DR: The data suggest that the CYP11A1-CD4+Tcell-IL-13 axis in activated CD4+ T cells from PA children is associated with development of PA reactions and may represent a novel target for therapeutic intervention in PA children.
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Diagnosis and evaluation of primary panhypogammaglobulinemia: a molecular and genetic challenge.

TL;DR: You will receive an online assessment regarding your application of this article to your practice and be eligible to receive 2 MOC Part II Self-Assessment credits from the American Board of Allergy and Immunology.
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Ecto-5′-Nucleotidase. II. Effect of 12-O-Tetradecanoylphorbol 13-Acetate on the Expression of Enzyme in Normal and Neoplastic B-Cell Lines

TL;DR: Data suggested that in the Ig-secreting B-cell lymphoma lines, there was an association between the inducibility of 5'-NT and the capacity of these cell lines to undergo plasma-cytoid-like transformation in response to TPA.