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Vanessa L. Peachee

Researcher at Virginia Commonwealth University

Publications -  8
Citations -  153

Vanessa L. Peachee is an academic researcher from Virginia Commonwealth University. The author has contributed to research in topics: Immune system & Mononuclear phagocyte system. The author has an hindex of 7, co-authored 8 publications receiving 146 citations.

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Journal ArticleDOI

Phthalate treatment does not influence levels of IgE or Th2 cytokines in B6C3F1 mice.

TL;DR: Treatment with DEHP, DINP, DIHP, and BBP did not result in significant elevations in total serum IgE, IL-4, or IL-13, and it is unlikely that these substances would produce antibody-mediated respiratory allergy.
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Comparison of primary immune responses to SRBC and KLH in rodents.

TL;DR: The effects on the primary IgM immune response in the B6C3F1 mice, thePrimary immunotoxicological rodents used by National Toxicology Program, and in the Sprague–Dawley rat, the primary rodent models used by industry are addressed.
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Effects of Administration of a Monoclonal Antibody against Mouse Tumor Necrosis Factor Alpha during Pregnancy and Lactation on the Pre- and Postnatal Development of the Mouse Immune System:

TL;DR: Administration of a monoclonal antibody against mouse TNFα during pregnancy and lactation had little or no effect on selected immune parameters in mice, with only a possible minor attenuation of spleen cell response to immunization noted in the female F1 generation at 11 weeks of age.
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Immunomodulation by Dok Din Daeng (Aeginetia indica Roxb.) extracts in female B6C3F1 mice: II. Humoral immunity, innate immunity and hematology.

TL;DR: The results from this study demonstrated that exposure to WDDD and EDDD produced minimal changes in the activities of B cells and natural killer cells, macrophages and neutrophils, and hematological parameters were not affected.
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Thalidomide modulation of the immune response in female B6C3F1 mice: a host resistance study

TL;DR: Results demonstrate that Thd immunomodulation altered host resistance to B16F10 and L. monocytogenes; and selective modulation of Thd on the immune system may be responsible for the pathogen or tumor-specific effect of this compound.