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Anthony M. Jevnikar

Researcher at University of Western Ontario

Publications -  166
Citations -  8432

Anthony M. Jevnikar is an academic researcher from University of Western Ontario. The author has contributed to research in topics: Transplantation & Antigen. The author has an hindex of 49, co-authored 163 publications receiving 7849 citations. Previous affiliations of Anthony M. Jevnikar include London Health Sciences Centre & University of Groningen.

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Cutting edge: the conversion of arginine to citrulline allows for a high-affinity peptide interaction with the rheumatoid arthritis-associated HLA-DRB1*0401 MHC class II molecule.

TL;DR: It is demonstrated that the conversion of arginine to citrulline at the peptide side-chain position interacting with the shared epitope significantly increases peptide-MHC affinity and leads to the activation CD4+ T cells in DR4-IE tg mice.
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Arthritis induced by posttranslationally modified (citrullinated) fibrinogen in DR4-IE transgenic mice

TL;DR: It is demonstrated that posttranslationally modified citrullinated fibrinogen leads to a selective increase in antigenic peptide affinity for major histocompatibility complex (MHC) class II molecules that carry the RA-associated shared epitope, such as HLA-DRB1*0401 (DR4).
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Inhibitory Feedback Loop Between Tolerogenic Dendritic Cells and Regulatory T Cells in Transplant Tolerance

TL;DR: Treg and Tol-DC generated in vitro were functional based on their suppressive activity in vitro, consistent with the notion that tolerance induction is associated with a self-maintaining regulatory loop in which Tol- DC induce the generation of Treg from naive T cells and Treg programs the generation from DC progenitors.
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MHC class II, antigen presentation and tumor necrosis factor in renal tubular epithelial cells.

TL;DR: These cell lines have characteristics most consistent with a proximal tubular origin and bear characteristics of accessory cells such as processing and presentation of antigen and TNF-alpha gene expression, suggesting that PT have the capacity to participate in the pathogenesis of immune renal injury.