M
Ming O. Li
Researcher at Memorial Sloan Kettering Cancer Center
Publications - 131
Citations - 18959
Ming O. Li is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: T cell & Immune system. The author has an hindex of 57, co-authored 110 publications receiving 15725 citations. Previous affiliations of Ming O. Li include University of Washington & Columbia University.
Papers
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Journal ArticleDOI
Transforming growth factor-beta regulation of immune responses.
TL;DR: This review highlights the findings that have advanced the understanding of TGF-beta in the immune system and in disease.
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The cellular and molecular origin of tumor-associated macrophages.
Ruth A. Franklin,Will Liao,Abira Sarkar,Myoungjoo V. Kim,Myoungjoo V. Kim,Michael R. Bivona,Kang Liu,Eric G. Pamer,Ming O. Li +8 more
TL;DR: In mice, mammary tumor growth induces the accumulation of tumor-associated macrophage that are phenotypically and functionally distinct from mammary tissue macrophages, which reveal the ontogeny of TAMs and a discrete tumor-elicited inflammatory response, which may provide new opportunities for cancer immunotherapy.
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TGF-β: A Master of All T Cell Trades
Ming O. Li,Richard A. Flavell +1 more
TL;DR: This work has defined the cytokine transforming growth factor-beta as a critical regulator of thymic T cell development as a crucial player in peripheral T cell homeostasis, tolerance to self antigens, and T cell differentiation during the immune response.
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Transforming Growth Factor-β Controls Development, Homeostasis, and Tolerance of T Cells by Regulatory T Cell-Dependent and -Independent Mechanisms
TL;DR: In this paper, the role of transforming growth factor-beta (TGF-beta) in inhibiting T cell functions has been studied with dominant negative TGF-β receptor transgenic models.
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T Cell-Produced Transforming Growth Factor-β1 Controls T Cell Tolerance and Regulates Th1- and Th17-Cell Differentiation
TL;DR: It is shown that mice with a T cell-specific deletion of the Tgfb1 gene developed lethal immunopathology in multiple organs, and this development was associated with enhanced T cell proliferation, activation, and CD4+ T cell differentiation into T helper 1 (Th1) and Th2 cells.