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Daniel Hawiger

Researcher at Saint Louis University

Publications -  36
Citations -  7903

Daniel Hawiger is an academic researcher from Saint Louis University. The author has contributed to research in topics: Immune system & Dendritic cell. The author has an hindex of 18, co-authored 28 publications receiving 7423 citations. Previous affiliations of Daniel Hawiger include Yale University & Rockefeller University.

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Tolerogenic dendritic cells.

TL;DR: It is suggested that several clinical situations, including autoimmunity and certain infectious diseases, can be influenced by the antigen-specific tolerogenic role of DCs.
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Dendritic Cells Induce Peripheral T Cell Unresponsiveness under Steady State Conditions in Vivo

TL;DR: An antigen delivery system targeting these specialized antigen presenting cells in vivo using a monoclonal antibody to a DC-restricted endocytic receptor is devised, which concludes that in the absence of additional stimuli DCs induce transient antigen-specific T cell activation followed by T cell deletion and unresponsiveness.
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Inducing and expanding regulatory T cell populations by foreign antigen.

TL;DR: The conversion of truly naive CD4+ T cells into suppressor cells expressing Foxp3 is reported by targeting of peptide-agonist ligands to dendritic cells and by analysis of Foxp 3 expression at the level of single cells, showing that conversion was achieved by minute antigen doses with suboptimal dendrite cell activation.
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Dendritic cell function in vivo during the steady state: a role in peripheral tolerance.

TL;DR: It is proposed that dendritic cells play a major role in defining immunologic self, not only centrally in the thymus but also in the periphery, and overcomes at least some of the risk of developing autoimmunity and chronic inflammation.
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Immunological Unresponsiveness Characterized by Increased Expression of CD5 on Peripheral T Cells Induced by Dendritic Cells In Vivo

TL;DR: It is found that targeting encephalitogenic oligodendrocyte glycoprotein (MOG) peptide to DCs resulted in a novel form of peripheral T cell tolerance that was sufficiently profound to prevent autoimmune experimental acute encephalomyelitis (EAE).