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Jacob D. Eccles

Researcher at University of Virginia

Publications -  13
Citations -  3519

Jacob D. Eccles is an academic researcher from University of Virginia. The author has contributed to research in topics: Lymphatic Endothelium & Immunoglobulin E. The author has an hindex of 11, co-authored 13 publications receiving 2623 citations. Previous affiliations of Jacob D. Eccles include Oregon Health & Science University.

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Structural and functional features of central nervous system lymphatic vessels

TL;DR: In searching for T-cell gateways into and out of the meninges, functional lymphatic vessels lining the dural sinuses are discovered, which may call for a reassessment of basic assumptions in neuroimmunology and sheds new light on the aetiology of neuroinflammatory and neurodegenerative diseases associated with immune system dysfunction.
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Modulation of the sigma-1 receptor–IRE1 pathway is beneficial in preclinical models of inflammation and sepsis

TL;DR: The contribution of S1R to the restraint of the inflammatory response is revealed and this work identifies sigma-1 receptor (S1R) as an essential inhibitor of cytokine production in a preclinical model of septic shock.
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Roles of lymphatic endothelial cells expressing peripheral tissue antigens in CD4 T-cell tolerance induction

TL;DR: Lymphatic endothelial cells (LECs) serve as an antigen reservoir for CD4 T-cell tolerance, and MHC-II molecules on LECs are used to induce CD8 T- cell tolerance via LAG-3.
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TH1 signatures are present in the lower airways of children with severe asthma, regardless of allergic status

TL;DR: The lower airways of children with severe asthma display a dominant TH1 signature and atypical cytokine profiles that link to allergic status and deviate from established paradigms and warrant further assessment of the pathogenicity of TH1 cells in patients withsevere asthma.
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Regulation of T-cell Tolerance by Lymphatic Endothelial Cells.

TL;DR: The ability of lymphatic endothelial cells to alter immune responses under steady-state or inflammatory conditions is explored, and the therapeutic potential of bypassing lymphatichelial cell-induced tolerance to enhance cancer immunotherapy is discussed.