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Creator:: Shepherd, David M.
Abstract:: The immune system has been identified as a very sensitive target for the toxic effects of 2,3,7,S-tetrachlorodibenzo-p-dioxin (TCDD). Exposure to TCDD has been shown to disrupt the generation of both cell-mediated and humoral T cell-dependent immunity in laboratory animals; however, the mechanism remains unknown. In this dissertation, the hypothesis is...
Resource Type:: Dissertation
Full Text:: activation AN ABSTRACT OF THE DISSERTATION OF David M. Shepherd for the degree of Doctor of Philosophy

Creator:: Prell, Rodney A.
Resource Type:: Dissertation
Full Text:: . David Barnes, Dr. Christopher Bayne, Dr. Jerry Heidel, and Dr. Henry Schaup, thank you for your

Creator:: Choi, Jin-Young, 1964
Abstract:: Exposure to TCDD suppresses the generation of immune responses through unknown mechanisms. Interestingly, TCDD enhances inflammatory responses to various stimuli. The goal of the studies presented in this thesis was to examine the role of hyperinflammation in TCDD-induced immunotoxicity. Previously we observed an increase in Mac-1⁺ cells in the spleen...
Resource Type:: Dissertation
Full Text:: thank to my committee members: Dr. Christopher Bayne, Dr. Jerry Heidel, Dr David Williams, Dr. Olaf

Creator:: Funatake, Castle J.
Abstract:: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) and related compounds are well-recognized for their immunosuppressive activity, which is mediated through an intracellular receptor and transcription factor, aryl hydrocarbon receptor (AhR). Laboratory animals exposed to TCDD are less resistant to infection and have severely impaired humoral and cell-mediated immune responses. This dissertation addressed the hypothesis that...
Resource Type:: Dissertation
Full Text:: David M. Shepherd Technical support; critical review of manuscript Elena S. Spanjaard Technical support

ScholarsArchive@OSU