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Arthur A. Vandenbark

Researcher at Oregon Health & Science University

Publications -  134
Citations -  7372

Arthur A. Vandenbark 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 41, co-authored 134 publications receiving 6920 citations. Previous affiliations of Arthur A. Vandenbark include Veterans Health Administration & United States Department of Veterans Affairs.

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CD4 T-cell epitopes of human α B-crystallin

TL;DR: Findings suggest that autoreactive α B‐crystallin‐specific Th1 cells may have the potential to contribute to MS pathogenesis.
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Rationally designed mutations convert complexes of human recombinant T cell receptor ligands into monomers that retain biological activity.

TL;DR: These studies demonstrated that RTLs encoding the Ag-binding/TCR recognition domain of MHC class II molecules are innately very robust structures, capable of retaining potent biological activity separate from the Ig-fold domains of the progenitor class II structure, with prevention of aggregation accomplished by modification of an exposed surface that was buried in the progensitor structure.
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Interleukin 7 is a potent co-stimulator of myelin specific t cells that enhances the adoptive transfer of experimental autoimmune encephalomyelitis

TL;DR: The results suggest that IL-7 may be a critical co-stimulatory factor that enhances the extrathymic expansion of inflammatory T cells and may play an important role in the pathogenesis of a number of inflammatory autoimmune disorders.
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Activation Pathways Implicate Anti-HLA-DP and Anti-LFA-1 Antibodies as Lead Candidates for Intervention in Chronic Berylliosis

TL;DR: Results indicate a prominent role for HLA-DP and LFA-1 in BAL CD4+ T cell activation and further suggest that specific Abs to these molecules could serve as a possible therapy for chronic beryllium disease.
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T lymphocytes promote the development of bone marrow-derived APC in the central nervous system.

TL;DR: It is demonstrated that T cells modulate the development of BM-derived CNS APC in an Ag-independent fashion and may be relevant to pathogenesis in experimental autoimmune encephalomyelitis, multiple sclerosis, and/or other CNS diseases involving myelomonocytic lineage cells.