Jack T. Lin
Stanford University
24 Papers
198 Citations
Jack T. Lin is an academic researcher from Stanford University. The author has contributed to research in topics: T cell & Cytotoxic T cell. The author has an hindex of 13, co-authored 21 publications. Previous affiliations of Jack T. Lin include Dartmouth College.
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Papers
Exploiting a natural conformational switch to engineer an interleukin-2 'superkine'
Aron M. Levin,Darren L. Bates,Aaron M. Ring,Carsten Krieg,Jack T. Lin,Leon Su,Ignacio Moraga,Miro E. Raeber,Gregory R. Bowman,Paul Novick,Vijay S. Pande,C. Garrison Fathman,Onur Boyman,K. Christopher Garcia +13 more
TL;DR: In vitro evolution has mimicked the functional role of CD25 in enhancing IL-2 potency and regulating target cell specificity, which has implications for immunotherapy.
TGF-β1 Uses Distinct Mechanisms to Inhibit IFN-γ Expression in CD4+ T Cells at Priming and at Recall: Differential Involvement of Stat4 and T-bet
TL;DR: TGF-β1 inhibited the development of IFN-γ-expressing cells in a dose-dependent fashion and in the absence of APC, indicating that TGF- β1 can inhibit Th1 development by acting directly on the CD4+ T cell.
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Therapeutic effect of CD137 immunomodulation in lymphoma and its enhancement by Treg depletion
Roch Houot,Matthew J. Goldstein,Holbrook E Kohrt,June Helen Myklebust,Ash A. Alizadeh,Jack T. Lin,Jonathan M. Irish,James A. Torchia,Arne Kolstad,Lieping Chen,Ronald Levy +10 more
TL;DR: It is demonstrated that anti-CD137 therapy has potent antilymphoma activity in vivo and could be further enhanced by depletion of regulatory T cell (T(regs), which support the evaluation of anti- CD137 therapy in clinical trials for patients with lymphoma.
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Genetic regulation of autoimmune disease: BALB/c background TGF-beta 1-deficient mice develop necroinflammatory IFN-gamma-dependent hepatitis.
TL;DR: This represents the first murine model of hepatitis that develops spontaneously, is restricted by genetic background, and is dependent upon the Th1 cytokine IFN-γ, and that thus recapitulates these important aspects of AIH.
CD28 co-stimulation regulates the effect of transforming growth factor-β1 on the proliferation of naive CD4+ T cells
TL;DR: Evidence that CD28 co-stimulation modifies the effects of TGF-beta1 on T cell proliferation is presented and it is suggested that engagement of CD28 may activate additional downstream pathways that modulate the responses of naïve T cells to TGF -beta1.
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