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Wenda Gao

Researcher at Beth Israel Deaconess Medical Center

Publications -  99
Citations -  17909

Wenda Gao is an academic researcher from Beth Israel Deaconess Medical Center. The author has contributed to research in topics: Interleukin 21 & FOXP3. The author has an hindex of 41, co-authored 89 publications receiving 16636 citations. Previous affiliations of Wenda Gao include Tufts University & Third Military Medical University.

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Musculin Deficiency Aggravates Colonic Injury and Inflammation in Mice with Inflammatory Bowel Disease.

TL;DR: MSC deficiency may enhance the inflammatory reactions in the gut via excessive secretion of IL-22, leading to aggravated colonic epithelial injury under IBD.
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Development of monoclonal antibodies against Sj29 and its possible application for schistosomiasis diagnosis.

TL;DR: A double antibody sandwich ELISA established to detect Schistosoma japonicum may have a potential diagnostic capability to distinguish current from past infections and assess drug treatment responses.
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Adenovirus-Mediated PD-L1 Over-Expression Has Differential Effects on Allograft Survival in Murine Islet and Heart Transplant Models.

TL;DR: The hypothesis that membrane-bound PD-L1 should prolong allograft survival due to its increased ability to crosslink PD-1 receptor was tested and showed no graft-protecting effect, in contrast to its strong inhibition of T and B cell activation in vitro when applied in a plate-bound form.
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An IgA mimicry of IgG that binds Polymeric Immunoglobulin Receptor for mucosa transcytosis.

TL;DR: For the first time, the engineering of an IgA mimicry of IgG is reported, with its Fc portion in fusion with the 18-aa tail piece of sIgA and the J chain, possessing sIGA’s full binding activity towards polymeric immunoglobulin receptor that mediates mucosa transcytosis.
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L2pB1 Cells Contribute to Tumor Growth Inhibition.

TL;DR: In this article, the authors investigated the effect of the loss of L2pB1 cells in a B16F10 melanoma model using an inducible knock-in and knockout mouse model.