No description available.

A mouse testis cDNA library was screened with an oligonucleotide probe corresponding to a sequence in the 5$ sp prime$ region of mouse N-cadherin cDNA. A composite clone containing three individual cDNAs was isolated. These included a 711 bp cDNA encoding part of mouse testicular N-cadherin, an unidentified 392 bp cDNA, and a 1500 bp cDNA encoding the mouse homologue of a human breast tumor autoantigen. / The cadherins, the influenza strain A hemagglutinins, and the fibroblast growth factor receptors are three different families of integral membrane glycoproteins that harbour the amino acid motif histidine-alanine-valine (HAV) in regions involved in protein-protein interactions. In order to identify other proteins that possess the HAV motif in functionally important regions, the SwissProt database was searched using a consensus sequence derived from the cadherins, influenza strain A hemagglutinins, and fibroblast growth factor receptors. This search identified the $ alpha$ chains of the HLA class I histocompatibility antigens as a fourth family of integral membrane glycoproteins with an HAV-containing region that is involved in a protein-protein interaction. (Abstract shortened by UMI.)

Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.

When injected with live P815 tumour cells, DBA/2 mice developed cytotoxic cells reactive to the tumour. In addition, T helper cells from tumour-bearing mice enhanced the iri vitro generation of cytotoxic cells from normal DBA/2 spleen cells. The helper cells had the following properties (1) expression of the Thy-1.2 antigen; (2) resistance to y-radiation; (3) specific enhancement of the cytotoxic response to P815; (4) detectability in P815-bearing mice at the peak of cytotoxic cell activity; (5) activity in the early phase of cytotoxic cell activation. In parallel to the development of helper cell activity, suppressor cells were generated which suppressed the cytotoxic response to P815. These suppressor cells were removed by pre-treating mice with low doses of cyclophosphamide. High doses of cyclophosphamide reduced the cytotoxic response to both P815 and C57B1/6 alloantigens. Cyclophosphamide treatment reduced the frequency of cytotoxic precursor cells directed against P815, and an antigen-reactive helper cell involved in interleukin 2 production. Both interleukin 2 and thymocytes from P815-primed mice, restored the cytotoxic response against P815, to normal levels. Twenty six percent of animals primed with tumour cells cleared a challenge dose of P815 faster than unprimed control mice. Of these, 88% survived longer than the control animals. Eighteen percent of the recipients of cells from tumour-primed mice, cleared a challenge dose of P815 faster than mice injected with normal cells. Of these 53% survived significantly longer than control groups given either normal cells or no cells at all. Cells from mice primed to PPD showed significantly enhanced proliferative responses to soluble and P815-bound PPD, when compared with unprimed animals. However, cells from only a few PPD-primed mice showed enhanced cytotoxicity against P815 tumour cells, and PPD-primed cells either did not alter, or suppressed, the cytotoxic response of normal DBA/2 spleen cells, when stimulated with PPD-coated P815. / Science, Faculty of / Microbiology and Immunology, Department of / Graduate

Cancer is the second leading cause of death in the United States. The risk of cancer development and subsequent death from the disease increases sharply in the population over 55 years of age(1). Coagulation problems also increase with age and have been implicated in increasing the metastatic spread of cancer. Although cancer treatment has improved constantly it still remains quite toxic and improvement are needed Mouse mammary tumor is a common form of cancer used for experimental animal study. This investigation was designed to study the nature of leukocytic response to mouse mammary tumor implants in C3H/HeJ mice with and without anticoagulants. The main thrust of the research was in three areas: first, to develop a background in light microscope morphology of spontaneous mouse mammary tumor and its change with first and second passage into normal mice; second, to analyze change in leukocytic response in sham operated, tumor- and liver-implanted mice; and third, to analyze changes in leukocytic response to tumor implants with and without anticoagulation.

No description available.

Prostaglandin E2 (PGE2) is an immunosuppressive factor secreted by the murine Lewis lung carcinoma (LLC). This factor can help to insure the survival of a tumor by suppressing the functions of lymphocytes and macrophages in their defense against tumors.Four weekly assays of macrophage tumoristatic activity from tumor-bearing mice were performed during the course of tumor development. Macrophages from the peritoneal cavity were cultured with LLC cells and after 48 hours the LLC growth was measured.The results of this study showed that macrophages from tumorbearing mice were suppressed in their ability to halt LLC growth in vitro. This suppression could be prevented by the use of indomethacin, a prostaglandin synthesis inhibitor. Indomethacin administration to tumor-free mice also enhanced their macrophage tumoristatic activities suggesting that the tumor was not the exclusive source of prostaglandin which suppressed anti-tumor immunity. Finally, indomethacin-fed tumor-bearing mice had smaller tumors than did mice not fed indomethacin.Ball State UniversityMuncie, IN 47306

[Truncated abstract] A paradox exists in tumour immunology whereby progressive tumour growth exists in parallel with an anti-tumour T cell response. This defective T cell response is thought to result from the induction of T cell tolerance and/or tumour induced immunosuppression, which act to inhibit the activation, differentiation and function of tumour-specific CD8+ T cells. Dendritic cells (DCs) are professional antigen presenting cells (APCs) that are critical to the generation of effective CTL; however their function and phenotype is often defective or altered in tumour-bearing hosts, which may limit their capacity to mount an effective tumour specific T cell response. In this thesis, the role of DCs in the cross-presentation of tumour antigen was assessed in terms of their APC function, migration and location. In doing so the intention was to gain insight into the early processes that potentially contribute to the development of an ineffective anti-tumour immune response. This study examined cross-presentation of the nominal tumour antigen, influenza A hemagglutinin (HA) expressed by the murine malignant mesothelioma cell line, AB1-HA. Cross-presentation was predominantly restricted to the local draining lymph nodes throughout tumour growth and was mediated by CD8a+ and CD8a- DCs. This results in an ineffective CTL response due to the lack of DC activation and the presence of potentially immunosuppressive B7 molecules. However, the capacity of the CD8a- DC subset to cross-present antigen suggested a role for migratory tumour-resident DCs in this process. Analysis of tumour infiltrating DCs showed that they were paralysed in their capacity to cross-present tumour antigen and were immobilised at the tumour site. Conversely, cross-presentation of tumour antigen in the local draining lymph node was dependent on the continuous traffic of antigen from the tumour microenvironment. In this vein, small numbers of metastatic tumour cells were detected in the draining lymph nodes, however their isolation was dependent on the removal of DCs and T cells, suggesting immune control of metastatic spread. Thus, tumour cells may be the source of antigen for cross-presentation by DCs in the tumour draining lymph nodes. .... In conclusion, the results presented in this thesis support a role for DCs in the generation of tumour-specific T cell responses that fail to control tumour growth. In addition the results provide a basis for further investigation into the effects of chemotherapy on the source and form of tumour antigen for cross-presentation by specific DC subsets in the tumour bearing host. These findings may have important implications for the development of future anti-cancer immune therapies targeting DCs.

Thesis (Ph. D.)--University of Missouri-Columbia, 2002. / Typescript. Vita. Includes bibliographical references (leaves 233-247). Also available on the Internet.

Thesis (Ph. D.)--University of Missouri-Columbia, 2002. / Typescript. Vita. Includes bibliographical references (leaves 233-247). Also available on the Internet.