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Effects of Contact Allergens on Innate Immune Cells Open Access


Other title
Allergic Contact Dermatitis
Contact Hypersensitivity
Contact Allergen
Type of item
Degree grantor
University of Alberta
Author or creator
Green, Christopher D
Supervisor and department
Elliott, John (Medical Microbiology and Immunology)
Examining committee member and department
Ingham, Robert (Medical Microbiology and Immunology)
Baldwin, Troy (Medical Microbiology and Immunology)
Vliagoftis, Harissios (Medicine)
Ostergaard, Hanne (Medical Microbiology and Immunology)
Elliott, John (Medical Microbiology and Immunology)
Foley, Edan (Medical Microbiology and Immunology)
Department of Medical Microbiology and Immunology
Date accepted
Graduation date
Master of Science
Degree level
The characteristics which cause a particular chemical to be a contact irritant, a contact allergen, or have no apparent interaction with our skin are not well understood, but undoubtedly complex. We propose that contact allergens, which are those chemicals that have the capacity to induce sensitization and the subsequent development of allergic contact dermatitis, possess two fundamental, but independent, properties: (1) the ability to create a non-self T-cell epitope by reacting with self-proteins within the skin, and (2) the ability to simultaneously activate the innate immune system to provide the necessary co-stimulatory signals required for sensitization. The latter property is the focus of this thesis. We first developed and characterized a proinflammatory cytokine-based assay, using the human monocytic cell line THP-1 as a model innate immune cell. Release of TNF-α, IL-8, IL-6 and IL-1β were measured following exposure of THP-1 cells to an array of contact allergens. We found that contact allergens, but not contact irritants, elicited robust innate immune cell activation. We then utilized parental and human Toll-like receptor 4 (hTLR4) transfected HEK293 cells to screen selected contact allergens to determine if they, like Nickel, also signal through hTLR4. We independently found that two Nickel-related contact allergens, Cobalt and Palladium, also elicit immune responses through hTLR4, while the eleven other contact allergens tested do not. Lastly, we attempted to find, or create, a THP-1 based reporter assay which would be suitable for high-throughput investigations to discover novel signaling pathways used by other contact allergens. While these efforts ultimately proved unsuccessful, direct measurement of inflammatory cytokines from THP-1 cells should prove to be a useful tool for the purposes of siRNA screens or related approaches.
Permission is hereby granted to the University of Alberta Libraries to reproduce single copies of this thesis and to lend or sell such copies for private, scholarly or scientific research purposes only. Where the thesis is converted to, or otherwise made available in digital form, the University of Alberta will advise potential users of the thesis of these terms. The author reserves all other publication and other rights in association with the copyright in the thesis and, except as herein before provided, neither the thesis nor any substantial portion thereof may be printed or otherwise reproduced in any material form whatsoever without the author's prior written permission.
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