scispace - formally typeset
H

Helen Sabzevari

Researcher at National Institutes of Health

Publications -  55
Citations -  3899

Helen Sabzevari is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Cytotoxic T cell & CD8. The author has an hindex of 29, co-authored 49 publications receiving 3683 citations. Previous affiliations of Helen Sabzevari include Scripps Research Institute.

Papers
More filters
Journal ArticleDOI

Inhibition of CD4+25+ T regulatory cell function implicated in enhanced immune response by low-dose cyclophosphamide

TL;DR: This is the first report demonstrating that CY, in addition to decreasing cell number, inhibits the suppressive capability of T(REGs), and the relevance of the loss of suppressor functionality and the changes in gene expression are discussed.
Journal ArticleDOI

IL-2-induced activation-induced cell death is inhibited in IL-15 transgenic mice.

TL;DR: IL-15 seems to contribute to enhanced immune memory by selectively propagating memory T cells and by blocking T cell death mediated by IL-2.
Journal Article

A triad of costimulatory molecules synergize to amplify T-cell activation.

TL;DR: Experiments using a four-gene construct showed that TRICOM recombinants can enhance antigen-specific T-cell responses in vivo, and demonstrate for the first time the ability of vectors to introduce three costimulatory molecules into cells, thereby activating both CD4+ and CD8+ T- cell populations to levels greater than those achieved with the use of only one or two costimulation molecules.
Journal ArticleDOI

Role of trans-cellular IL-15 presentation in the activation of NK cell-mediated killing, which leads to enhanced tumor immunosurveillance.

TL;DR: Evidence is provided that the IL-15 trans-presentation mechanism operates in vivo to augment the tumor immune surveillance mechanism and provides the scientific basis for a novel strategy to prevent cancer development/metastasis.
Journal ArticleDOI

An Anti–Transforming Growth Factor β Antibody Suppresses Metastasis via Cooperative Effects on Multiple Cell Compartments

TL;DR: It is shown that efficacy of the anti-TGF-beta antibody 1D11 in suppressing metastasis was dependent on a synergistic combination of effects on both the tumor parenchyma and microenvironment and the absence of a major effect of TGF- beta antagonism on any one cell compartment may be critical for a good therapeutic window and the avoidance of autoimmune complications.