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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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Inhibition of complement activation decreases airway inflammation and hyperresponsiveness

TL;DR: It is suggested that prevention of complement activation may have a therapeutic role in the treatment of allergic airway inflammation and asthma in sensitized individuals.
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Increased Airways Responsiveness in Mice Depends on Local Challenge with Antigen

TL;DR: In Balb/C mice, painting the skin with ovalbumin (OVA) over a period of 14 days resulted in sensitization of the animals, which was documented by the appearance of OVA-specific IgE and IgG1 antibodies and increased total serum IgE levels as discussed by the authors.
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Activation of Ca2+-dependent K+ channels in human B lymphocytes by anti-immunoglobulin.

TL;DR: This study demonstrates that in human B lymphocytes, Ca2-dependent K+ channels can be activated by crosslinking of surface IgM, and it is likely that Na+ can permeate through these ligand-gated Ca2+ "channels" in the absence of extracellular Ca2+.
Journal Article

Platelet-activating factor induces an increase in intracellular calcium and expression of regulatory genes in human B lymphoblastoid cells.

TL;DR: Early activation events triggered by PAF binding to three Ig-secreting B cell lines provide evidence for the presence of functional PAF receptors on B lymphoblastoid cells and indicate a potential role for PAF in the regulation of B cell activation.
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Rapamycin inhibits the phosphorylation of p70 S6 kinase in IL-2 and mitogen-activated human T cells.

TL;DR: Rapamycin (RAP), a potent suppressor of T-cell proliferative responses, markedly inhibited the phosphorylation of p70s6k induced by IL-2 in Kit225 cells or by the mitogens added to resting T cells, indicating for the first time that RAP may target the pathway leading to p70 s6k phosphorylated during human T- cell proliferation.