Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

Thesis (doctoral)--Lund University, 1997. / Added t.p. with thesis statement inserted.

Endothelin-1 (ET-1) is a potent vasoactive peptide, cleaved from its inactive precursor, big ET-1, by Endothelial Converting Enzyme-1 (ECE-1). ET-1 normally regulates vascular tone via its two receptors ET-A and ET-B. As ET-1 is found to be over-expressed in many tumour models, it has been implicated as having a role in neovascularisation. / Thesis (PhDBiomedicalScience)--University of South Australia, 2005.

Proefschrift Universiteit van Amsterdam. / Met lit.opg. en samenvatting in het Nederlands.

Thesis (M.S.)--Virginia Polytechnic Institute and State University, 1992. / Vita. Abstract. Includes bibliographical references (leaves 76-85). Also available via the Internet.

No description available.

Thesis (M.A.)--University of North Carolina at Chapel Hill, 2005. / On t.p. "alpha" appears as the Greek letter. Includes bibliographical references (leaves 69-71).

Thesis (M.A.)--University of North Carolina at Chapel Hill, 2005. / On t.p. "alpha" appears as the Greek letter. Includes bibliographical references (leaves 69-71). Also available online (PDF file) by a subscription to the set or by purchasing the individual file.

University of Macau / Institute of Chinese Medical Sciences

The activation and effector function of CD4+ T cells are critical points of regulation during an antigen specific T cell response. Dysregulation of these processes can lead to the development of human diseases, encompassing both immunodeficiency and autoimmunity. Members of the TNF superfamily have recently emerged as important regulators of T cell responses, with their overexpression causing autoimmune inflammation in animal models. As overproduction of the novel TNF superfamily ligand BAFF is associated with several autoimmune conditions, we sought to examine the potential role of BAFF as a regulator of T cell activation and effector function. We initially demonstrated BAFF costimulation of T cell activation in vitro. Generation of specific monoclonal antibodies identified BAFF-R as the only BAFF receptor present on T cells, and showed that it was expressed in an activation-dependent and subset-specific manner. Impaired BAFF costimulation in BAFF-R deficient mice indicated that BAFF-R was crucial for mediating BAFF effects in T cells. Analysis of T cell responses in vivo revealed that BAFF transgenic mice have increased T cell priming and recall responses to protein antigens, and showed a corresponding increase in the DTH model of Th1 cell-dependent inflammation. In addition, Th2-dependent allergic airway responses are suppressed in BAFF transgenic mice. Crossing to a B cell deficient background revealed that the proinflammatory effects of BAFF on T cell priming and DTH rely on the presence of B cells, while the suppressive effects during allergic airway inflammation are B cell independent. These data demonstrated that BAFF regulated the outcome of T cell responses in vivo and identified BAFF dependent crosstalk between T and B cells. Stimulation of B cells with BAFF induced the upregulation of MHC class II and ICOS-L both in vitro and in vivo. Induction of these cell surface molecules was associated with an increased capacity to induce T cell proliferation, however this effect was independent of ICOS-L expression. Thus it was demonstrated that BAFF regulated T cell activation and effector function both directly, via stimulation of BAFF-R, and indirectly, by altering the function of B cells. These data suggest that BAFF dependent alterations in T cell function may be an additional causative factor in the association between elevated BAFF levels and the generation of autoimmunity.