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G

Gisen Kim

Researcher at La Jolla Institute for Allergy and Immunology

Publications -  23
Citations -  5097

Gisen Kim is an academic researcher from La Jolla Institute for Allergy and Immunology. The author has contributed to research in topics: T cell & Colitis. The author has an hindex of 15, co-authored 23 publications receiving 4698 citations.

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Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid.

TL;DR: The vitamin A metabolite retinoic acid is identified as a key regulator of TGF-β–dependent immune responses, capable of inhibiting the IL-6–driven induction of proinflammatory TH17 cells and promoting anti-inflammatory Treg cell differentiation, indicating that a common metabolite can regulate the balance between pro- and anti- inflammatory immunity.
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Recognition of bacterial glycosphingolipids by natural killer T cells

TL;DR: It is shown that most mouse and human NKT cells recognize glycosphingolipids from Sphingomonas, Gram-negative bacteria that do not contain lipopolysaccharide, and that these cells might be useful in providing protection from bacteria that cannot be detected by pattern recognition receptors such as Toll-like receptor 4.
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Interleukin 10 acts on regulatory T cells to maintain expression of the transcription factor Foxp3 and suppressive function in mice with colitis

TL;DR: It is shown that interleukin 10 produced by CD11b+ myeloid cells in recombination-activating gene 1–deficient recipient mice was needed to prevent the colitis induced by transferred CD4+CD45RBhi T cells.
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Transcriptional reprogramming of mature CD4+ helper T cells generates distinct MHC class II-restricted cytotoxic T lymphocytes

TL;DR: It is found that the helper T cell fate was not fixed and that mature, antigen-stimulated CD4+ T cells terminated expression of the gene encoding ThPOK and reactivated genes of the CD8 lineage, resulting in the post-thymic termination of the helpers T cell program and the functional differentiation of distinct MHC class II–restrictedCD4+ cytotoxic T lymphocytes.
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Retinoic Acid Can Directly Promote TGF-β-Mediated Foxp3+ Treg Cell Conversion of Naive T Cells

TL;DR: The authors propose that RA does not act directly on naive T cells during activation in culture but rather indirectly via negative regulation of an accompanying population of effector or memory CD4+ CD44hi cells, and show that RA is able to counterbalance the inhibitory effects of costimulation on TGF-β-mediated Foxp3 induction.