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Lionel Feigenbaum

Researcher at Science Applications International Corporation

Publications -  79
Citations -  11407

Lionel Feigenbaum is an academic researcher from Science Applications International Corporation. The author has contributed to research in topics: T cell & CD8. The author has an hindex of 51, co-authored 79 publications receiving 10598 citations. Previous affiliations of Lionel Feigenbaum include Medical University of Vienna & Johns Hopkins University.

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Tumor regression and autoimmunity after reversal of a functionally tolerant state of self-reactive CD8+ T cells

TL;DR: It is found that tumor growth and lethality were unchanged in mice even after adoptive transfer of large numbers of T cells specific for an MHC class I–restricted epitope of the self/tumor antigen gp100, illustrating that adoptive transferof T cells and IL-2 can augment the function of a cancer vaccine.
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Life without white fat: a transgenic mouse

TL;DR: The A-ZIP/F-1 phenotype suggests a mouse model for the human disease lipoatrophic diabetes (Seip-Berardinelli syndrome), indicating that the lack of fat can cause diabetes.
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Tumor-specific Th17-polarized cells eradicate large established melanoma

TL;DR: Data indicate that the appropriate in vitro polarization of effector CD4+ T cells is decisive for successful tumor eradication, and this principle should be considered in designing clinical trials involving adoptive transfer-based immunotherapy of human malignancies.
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CD28 costimulation of developing thymocytes induces Foxp3 expression and regulatory T cell differentiation independently of interleukin 2.

TL;DR: Molecular mapping of CD28 costimulation showed that Treg cell generation requires a motif that binds the tyrosine kinase Lck, precisely the same motif that is required for CD28costimulation of interleukin 2 production.
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Control of Toll-like Receptor 7 Expression Is Essential to Restrict Autoimmunity and Dendritic Cell Proliferation

TL;DR: It is demonstrated that duplication of the Tlr7 gene was the sole requirement for this accelerated autoimmunity, because reduction of TLR7 gene dosage abolished the Yaa phenotype.