Degree Type

Dissertation

Date of Award

2018

Degree Name

Doctor of Philosophy

Department

Veterinary Pathology

Major

Immunobiology

First Advisor

Jesse M. Hostetter

Second Advisor

Ray W. Waters

Abstract

In these studies, we used non-infected cattle and cattle naturally infected with MAP that were either in the subclinical or clinical stage of infection to test the hypothesis that infection status influences WC1+ γδ T cells frequency, proliferation, and cytokine production. We found no significant differences between subclinical and clinical cattle with regard to WC1+ γδ T cells frequency in peripheral blood or in the ileum, a primary site for MAP infection. In PBMCs taken from MAP-infected cattle, WC1+ γδ T cells responded diffrentially to stimulation with PPD-J. In the clinical group, WC1+ γδ T cells failed to proliferate and the WC1.1 subset did not produce IFN-γ or IL-10 suggesting unresponsiveness. We evaluated the cytokine profile (mRNA) of the WC1+ γδ T cell subset in the ileum. Our data indicate a significant increase in the numbers of WC1+ γδ T cells expressing IL-10 in ileal tissues obtained from clinical cattle compared to subclinical and non-infected cattle. Expression of IFN-γ, TNF-α, IL-17 and TGF-β by the WC1+ γδ T cell subset in the ileum was comparable among the examined groups. We used subclinical infected cattle to evaluate the impact of WC1+ γδ T cell depletion on cytokine production by PBMCs stimulated ex vivo with PPD-J. Independent of antigen (PPD), depletion of WC1+ γδ T cells resulted in a significant decrease in IL-4 secretion and a significant increase in IL-10 secretion suggesting a modulatory role for the WC1+ subset in this system. The present dissertation supports our hypothesis that MAP infection status influences immunological responses of WC1+ γδ T cells in peripheral blood and at the sites of MAP infection. Our data suggest that the WC1+ γδ T cell subset may contribute to the immune responses that control MAP infection during the subclinical stage and those that promote disease progression during the terminal stages of MAP infection.

DOI

https://doi.org/10.31274/etd-180810-5936

Copyright Owner

Saleh Mohammed Albarrak

Language

en

File Format

application/pdf

File Size

113 pages

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