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Halina Offner

Researcher at Oregon Health & Science University

Publications -  315
Citations -  15366

Halina Offner is an academic researcher from Oregon Health & Science University. The author has contributed to research in topics: Experimental autoimmune encephalomyelitis & T cell. The author has an hindex of 61, co-authored 311 publications receiving 14301 citations. Previous affiliations of Halina Offner include Veterans Health Administration & United States Department of Veterans Affairs.

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Immunization with a synthetic T-cell receptor V-region peptide protects against experimental autoimmune encephalomyelitis.

TL;DR: This is the first report demonstrating the use of a synthetic T CR V-region peptide to induce specific regulatory immunity and has important implications for the regulation of human disease characterized by common TCR V-gene usage.
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Experimental Stroke Induces Massive, Rapid Activation of the Peripheral Immune System:

TL;DR: Data show for the first time that focal cerebral ischemia results in dynamic and widespread activation of inflammatory cytokines, chemokines, and CCR in the peripheral immune system.
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Splenic Atrophy in Experimental Stroke Is Accompanied by Increased Regulatory T Cells and Circulating Macrophages

TL;DR: New evidence is provided to support the contention that damage to the brain caused by cerebral ischemia provides a powerful negative signal to the peripheral immune system that ultimately induces a drastic state of immunosuppression caused by cell death as well as an increased presence of CD4+FoxP3+ regulatory T cells.
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Decreased FOXP3 levels in multiple sclerosis patients.

TL;DR: This study is the first to establish that MS patients have abnormalities in FOXP3 message and protein expression levels in peripheral CD4+CD25+ T cells (Tregs) that are quantitatively related to a reduction in functional suppression induced during suboptimal T‐cell receptor (TCR) ligation.
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T- and B-cell-deficient mice with experimental stroke have reduced lesion size and inflammation.

TL;DR: The data quantify the damaging effect of T and B lymphocytes on early, evolving ischemic brain injury, and further implicate interleukin-1β in brain and interferon-γ and MIP-2 in spleen as inflammatory factors produced by cells other than T andB cells.