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Wenwen Jin
Researcher at National Institutes of Health
Publications - 45
Citations - 9363
Wenwen Jin is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Inflammation & Immune system. The author has an hindex of 28, co-authored 42 publications receiving 8523 citations. Previous affiliations of Wenwen Jin include Cornell University.
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Journal ArticleDOI
Conversion of Peripheral CD4+CD25− Naive T Cells to CD4+CD25+ Regulatory T Cells by TGF-β Induction of Transcription Factor Foxp3
Wanjun Chen,Wenwen Jin,Neil J. Hardegen,Ke Jian Lei,Li Li,Nancy J. Marinos,George McGrady,Sharon M. Wahl +7 more
TL;DR: Novel evidence is presented that conversion of naive peripheral CD4+CD25− T cells into anergic/suppressor cells that are CD25+, CD45RB−/low and intracellular CTLA-4+ can be achieved through costimulation with T cell receptors (TCRs) and transforming growth factor β (TGF-β).
Journal ArticleDOI
Conversion of proepithelin to epithelins: roles of SLPI and elastase in host defense and wound repair.
Jing Zhu,Carl Nathan,Wenwen Jin,Davis Sim,Gillian S. Ashcroft,Sharon M. Wahl,Lynne Lacomis,Hediye Erdjument-Bromage,Paul Tempst,Paul Tempst,Clifford D. Wright,Aihao Ding +11 more
TL;DR: It is found that SLPI/elastase act via PEPI/EPIs to operate a switch at the interface between innate immunity and wound healing, and supplying PEPi corrects the wound-healing defect in SLPI null mice.
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Secretory leukocyte protease inhibitor mediates non-redundant functions necessary for normal wound healing.
Gillian S. Ashcroft,Ke-Jian Lei,Wenwen Jin,Glenn Longenecker,Ashok B. Kulkarni,Teresa Greenwell-Wild,Hollie Hale-Donze,George McGrady,Xiao Yu Song,Sharon M. Wahl +9 more
TL;DR: It is proposed that SLPI is a pivotal endogenous factor necessary for optimal wound healing in mice null for the gene encoding SLPI, which show impaired cutaneous wound healing with increased inflammation and elastase activity.
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TGF-β Released by Apoptotic T Cells Contributes to an Immunosuppressive Milieu
TL;DR: Evidence that apoptotic T cells release TGF-β, thereby contributing to an immunosuppressive milieu is presented, broadening the potential mechanisms whereby induction of immune tolerance or deficiency occurs through T cell deletion.
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Engagement of Cytotoxic T Lymphocyte–associated Antigen 4 (CTLA-4) Induces Transforming Growth Factor β (TGF-β) Production by Murine CD4+ T Cells
TL;DR: It is reported here that cross-linking of CTLA-4 induces transforming growth factor β (TGF-β) production by murine CD4+ T cells, which may serve as a counterbalance for CD28 costimulation of IL-2 and CD4- T cell activation.