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Fredrik Ivars

Researcher at Lund University

Publications -  52
Citations -  3393

Fredrik Ivars is an academic researcher from Lund University. The author has contributed to research in topics: T cell & Natural killer T cell. The author has an hindex of 25, co-authored 52 publications receiving 3092 citations. Previous affiliations of Fredrik Ivars include Pasteur Institute.

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CD4+CD25+ regulatory T cells down-regulate co-stimulatory molecules on antigen-presenting cells.

TL;DR: It is found that CD4+CD25+ T cells down‐regulated the expression of the co‐stimulatory molecules CD80 and CD86 on dendritic cells, suggesting that distinct mechanisms regulate theexpression of these molecules.
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Dystroglycan is selectively cleaved at the parenchymal basement membrane at sites of leukocyte extravasation in experimental autoimmune encephalomyelitis

TL;DR: It is shown here that macrophage-derived gelatinase (matrix metalloproteinase [MMP]-2 and MMP-9) activity is crucial for leukocytes penetration of the parenchymal BM, the first description of selective in situ proteolytic damage of a BBB-specific molecule at sites of leukocyte infiltration.
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Cytotoxic T lymphocyte antigen-4-dependent down-modulation of costimulatory molecules on dendritic cells in CD4+ CD25+ regulatory T-cell-mediated suppression.

TL;DR: It is proposed that Treg cells down‐modulate B7‐molecules on DCs in a CTLA‐4‐dependent way, thereby enhancing suppression of T‐cell activity.
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Identification of Human S100A9 as a Novel Target for Treatment of Autoimmune Disease via Binding to Quinoline-3-Carboxamides

TL;DR: The specific binding of quinoline-3-carboxamides to S100A9 explains the immunomodulatory activity of this class of compounds and defines S 100A9 as a novel target for treatment of human autoimmune diseases.
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Endothelial basement membrane laminin alpha5 selectively inhibits T lymphocyte extravasation into the brain.

TL;DR: It is shown that targeting lymphocyte interactions with endothelial basement membrane laminins provides a means of inhibiting disease without compromising innate immune responses, and that T lymphocytes use mechanisms distinct from other immune cells to penetrate the endothelium basement membrane barrier.