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To investigate their importance in non-Hodgkin’s lymphoma (NHL), I enumerated Treg cells in peripheral blood mononuclear cells (PBMC) and involved tissues from 30 newly diagnosed patients CD25+FoxP3+CD127^lowCD4+ Treg cells were increased markedly in PBMC (median=20.4% CD4 T cells, n=20) versus healthy controls (median=3.2%, n=13:<i> p</i>&lt;0.001, rank sum test) and correlated with serum lactate dehydrogenase (n=14; R_s=0.79, <i>p</i>&lt;0.001) and disease stage. I documented poor proliferation of T cells with mitogen ConA and almost none with recall antigens PPD and DPT in both PBMC and involved tissue samples (n=9). T cell hyporesponsiveness was reversed by depleting CD25+ cells (n=4), or by adding anti-CDLA-4 (n=3), supporting the view that Treg cells explain the systemic immunosuppression seen in NHL. As a high percentage of Treg cells were also present in involved tissues (patients’ involved tissues median=38.8% of CD4 T cells (n=15) vs. reactive nodes median=11.6% of CD4 T cells (n=2); <i>p</i>=0.02, rank sum test), I determined if tumour cells could induce a T regulatory phenotype. I incubated CD25+ depleted PBMC with tumour cells <i>in vitro</i> for five days. A dose and time dependent T regulatory phenotype induction from CD25+ depleted PBMC fractions were seen (n=6, maximum induction of 86.7%). Partial induction was seen when these fractions were separated with transwells. These ‘induced Treg cells’ were FACS sorted and suppressed effector T cells proliferation. I conclude that NHL cells are powerful inducers of Treg cells. These cells circulate systemically and induce active immune tolerance both systematically and within tumour microenvironment, thus representing a new therapeutic target in NHL.

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Thesis (Ph.D.)--University of Nebraska-Lincoln, 2006. / Title from title screen (site viewed on Feb. 6, 2007). PDF text: vi, 218 p. : ill. UMI publication number: AAT 3218217. Includes bibliographical references. Also available in microfilm and microfiche format.

This study evaluates the efficiency of albendazole against different stages of Angiostrongylus cantonensis in Sprague-Dawley rats. Using a single oral dose of albendazole of 10 mg/kg at 0 or 1 or 2 or 3 weeks post-infection (PI) showed that the drug in 0 or 1 weeks PI was more effective in the larval infection. Compared to those in non-treated control, the rats treated 0 or 1 weeks PI showed significant reductions not only in the relative wet weight of heart and lungs (g/100 g body weight), but also in the mean number of adults recovered. With regard to single oral doses of 10 or 50 or 100 mg/kg at weekly intervals from 6 weeks PI, the rats treated 100 mg/kg in 2 weeks post-treatment (PT) showed significant reduction in the L1 in its feces and the amounts were lastingly few. In the rats treated 10 or 50 mg/kg, larval output reappeared from 4 weeks PT. The histomorphology of granuloma formation was also investigated in the lungs of SD rats infected with A. cantonensis¡@by paraffin section. It was observed that granulomatous fibros was strongly associated with the number of L1 in the lungs. IgG and IgE antibodies specific for antigens from L1, L5, male worms or female adults of A. cantonensis were respectively measured by an enzyme-linked immunosorbent assay (ELISA). The specific IgE response to antigens from L1 or female adults of A. cantonensis in the serum reached the maximum at 1 and 5 weeks PI. Similarly, the eosinophil response also revealed remarkable peaks at 1 and 5 weeks PI. These results might prove that the increases of IgE titer and eosinophil are related to antibody-dependent cell mediated cytotoxicity (ADCC).