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Rebecca E. Hussey

Researcher at Harvard University

Publications -  64
Citations -  9404

Rebecca E. Hussey is an academic researcher from Harvard University. The author has contributed to research in topics: Antigen & Cytotoxic T cell. The author has an hindex of 42, co-authored 64 publications receiving 9238 citations. Previous affiliations of Rebecca E. Hussey include Bristol-Myers Squibb.

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An alternative pathway of T-cell activation: A functional role for the 50 kd T11 sheep erythrocyte receptor protein

TL;DR: Given that T11 is the earliest T-lineage surface glycoprotein to appear in thymic ontogeny and is thus expressed before T3-Ti, the former may be involved in clonal expansion and/or differentiation during early development.
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Clonotypic structures involved in antigen-specific human T cell function. Relationship to the T3 molecular complex.

TL;DR: The development of monoclonal antibodies to such polymorphic T cell surface structures should provide important probes to further define the surface receptor for antigen.
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Antigen recognition by human T lymphocytes is linked to surface expression of the T3 molecular complex.

TL;DR: Evidence is provided for a direct linkage between antigen recognition by T lymphocytes and surface expression of the T3 molecular complex, which inhibits cytotoxic T lymphocyte effector function by T4 and T8 clones as well as antigen-specific T cell recognition.
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Triggering of the T3-Ti antigen-receptor complex results in clonal T-cell proliferation through an interleukin 2-dependent autocrine pathway

TL;DR: The findings demonstrate that antigen-induced proliferation is mediated through an autocrine pathway involving endogenous IL-2 production, release, and subsequent binding to IL-3-Ti receptor cross-linking.
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A soluble CD4 protein selectively inhibits HIV replication and syncytium formation.

TL;DR: Concentrations of soluble CD4 in the nanomolar range, like certain anti-CD4 monoclonal antibodies, inhibit syncytium formation and HIV infection by binding gp120-expressing cells, and class II specific T-cell interactions are uninhibited by solubleCD4 protein, whereas they are virtually abrogated by equivalent amounts of anti-T4 antibody.