Errata & addenda tipped in behind back end paper. / Copies of author's previously published articles in pocket on back end-paper. / Bibliography: leaves 147-194. / xi, 194, [69] leaves, [68] leaves of plates : ill. (chiefly col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Explores the hypothesis that structures similar to lymphocyte-filled villi in rats and mice are present in the small human intestine. / Thesis (Ph.D.)--University of Adelaide, Dept. of Microbiology and Immunology, 1999

In title, [beta] is represented by the Greek letter. / Copies of author's previously published articles inserted. / Errata pages pasted onto back end-paper. / Bibliography: leaves 104-137. / viii, 137, [22] leaves, [1] leaf of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Studies milk TGF-[beta] and its receptors in the post-natal gut using a rat model to investigate a link between milk TGF-[beta] and the development of the infant gut and gut mucosal immune system. Finds maternal milk may be a major source of TGF-[beta] to the immature gut and may react with receptors on the cells of the mucosal immune system along the gastro-intestinal tract, modulating infant mucosal immune responses in the transition to the post-natal enteral feeding. / Thesis (Ph.D.)--University of Adelaide, Dept. of Paediatrics, 2000

In title, [beta] is represented by the Greek letter. Copies of author's previously published articles inserted. Errata pages pasted onto back end-paper. Bibliography: leaves 104-137. Studies milk TGF-[beta] and its receptors in the post-natal gut using a rat model to investigate a link between milk TGF-[beta] and the development of the infant gut and gut mucosal immune system. Finds maternal milk may be a major source of TGF-[beta] to the immature gut and may react with receptors on the cells of the mucosal immune system along the gastro-intestinal tract, modulating infant mucosal immune responses in the transition to the post-natal enteral feeding.

Previous data in our lab demonstrated an inability to induce oral tolerance when using a feeding needle gavage for 14 days. Given that the upper gastrointestinal (GI) tract is the site of antigen introduction, and the interplay between immune cells of the mucosal tissues, we questioned if inflammation in this tissue, induced by physical trauma, would affect oral tolerance induction. We performed studies on Balb/c mice using a needle gavage or syringe feeding method followed by doses of the immunogenic protein ovalbumin (OVA) to induce tolerance. Immunohistochemistry was used to assess inflammation in esophageal tissues and to correlate with an ability or inability to induce tolerance. Non-cellular alterations within the tissue were also assessed using a pathology grading score. Although fluctuations in cell populations were observed in both the syringe and gavage treated mice, the needle gavage caused significant noncellular damage to esophageal mucosal tissue, which is the most likely cause of failed tolerance induction to the OVA. / Department of Biology