Assessment of the long-term shedding pattern of Salmonella serovar choleraesuis following experimental infection of neonatal piglets.
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In the United States, swine salmonellosis is most often attributed to infections by Salmonella serovar choleraesuis. As a host-adapted pathogen rarely found in nonswine sources, S. choleraesuis is thought to be spread primarily via horizontal transmission, with carrier animals playing an important role. Little has been reported regarding infection of neonatal piglets, particularly regarding their potential to become carriers. Evidence reported herein demonstrates that piglets experimentally infected by S. choleraesuis at 2 days of age were capable of shedding the pathogen for up to 85 days postinfection, at which time the study was concluded. This study also presents findings supporting the use of GN-Hajna as a preenrichment medium for the isolation of S. choleraesuis. (+info)
A characterization of human tonsillar lymphocytes after separation from other tonsillar cells in an isokinetic gradient of ficoll in tissue culture medium.
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Purified human tonsillar lymphocytes responded less to mitogentic stimulation than did unseparated tonsillar cells. Their response to mitogens was restored when they were combined with cells from all other gradient fractions. We interpret our data as evidence that the majority of tonsillar lymphocytes require the presence of more rapidly sedimenting cells for a maximum response to the tested mitogens. The purified tonsillar lymphoyctes were 47.0% lymphocytes that have detectable surface immunoglobulin and 29.9% lumphocytes that form rosettes with sheep red blood cells. The predominant cell surface immunoglobulin was IgM. Digestion of the tonsil with trypsin yielded tenfold more plasma cells, more vialbe cells, and a larger proportion of blasts, histiocytes, and binucleated cells than were obtained by mechanical dissociation of the tissue. (+info)
Biologic response of B lymphoma cells to anti-CD20 monoclonal antibody rituximab in vitro: CD55 and CD59 regulate complement-mediated cell lysis.
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The chimeric anti-CD20 MAb rituximab has recently become a treatment of choice for low-grade or follicular non-Hodgkin's lymphomas (FL) with a response rate of about 50%. In this report, we have investigated the mechanism of action of rituximab on 4 FL and 1 Burkitt's lymphoma (BL) cell lines, 3 fresh FL samples and normal B cells in vitro. Rituximab efficiently blocks the proliferation of normal B cells, but not that of the lymphoma lines. We did not detect significant apoptosis of the cell lines in response to rituximab alone. All cell lines were targets of antibody-dependent cellular cytotoxicity (ADCC). On the other hand, human complement-mediated lysis was highly variable between cell lines, ranging from 100% lysis to complete resistance. Investigation of the role of the complement inhibitors CD35, CD46, CD55, and CD59 showed that CD55, and to a lesser extent CD59, are important regulators of complement-mediated cytotoxicity (CDC) in FL cell lines as well as in fresh cases of FL: Blocking CD55 and/or CD59 function with specific antibodies significantly increased CDC in FL cells. We conclude that CDC and ADCC are major mechanisms of action of rituximab on B-cell lymphomas and that a heterogeneous susceptibility of different lymphoma cells to complement may be at least in part responsible for the heterogeneity of the response of different patients to rituximab in vivo. Furthermore, we suggest that the relative levels of CD55 and CD59 may become useful markers to predict the clinical response. (Blood. 2000;95:3900-3908) (+info)
Detection of T-cell lymphoma-associated antigens on cord blood lymphocytes and phytohemagglutinin-stimulated blasts.
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Absorption studies demonstrate that T-cell lymphoma-associated antigens detected by rabbit antisera to human T-lymphoblast cell lines are present in suspensions of cord blood lymphocytes and phytohemagglutinin-stimulated adult blood lymphocytes in amounts similar to those found in T-cell lymphoma tumor cell suspensions. Smaller amounts of antigen activity are found in suspensions of tonsil cells, thymocytes, and unstimulated adult blood lymphocytes. Little or no antigen activity is found in suspensions of lymphoblasts from patients with other types of leukemia or from B-cell lines. T-cell depletion removes antigen activity from suspensions of normal lymphocytes. These findings suggest that T-cell lymphoma-associated antigens may be fetal antigens expressed by activated T-cells. (+info)
Study of human T and B lymphocytes with heterologous antisera. I Preparation, specificity and properties of antisera.
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Heterologous antisera have been raised in the horse and rabbit against human lymphocytes. Appropriate absorptions on either B or T cells were performed to make antisera specific for human T (anti-HTLA) or B (serum 789) lymphocytes respectively. In addition serum 789 was found to react with circulating monocytes. The percentages of T and B cells detected by anti-HTLA and 789 sera in the different lymphoid organs averaged respectively: 78-7 per cent and 14-7 per cent in peripheral blood, 91-4 per cent and 4-0 per cent in thymus, 73-0 per cent and 14-5 per cent in lymph nodes, 53-6 per cent and 30-0 per cent in spleen, 47-1 per cent and 47-6 per cent in tonsils and 17-5 per cent and 13-5 per cent in bone marrow. Anti-HTLA serum appeared to supress E-rosette formation but did not affect binding of C3-coated erythrocytes. Serum 789 did not prevent E-rosette formation and reduced the number of EAC rosettes by 50 per cent. Anti-HTLA serum was found able to suti-lymphocyte serum, and PWM in the presence of complement; it was found highly mitogenic by itself. Serum 789 decreased the proliferative response to phytomitogens in about the proportion of cells killed by the antiserum. These results indicate that the presence of T cells is necessary for the mitogen-induced proliferation to occur, and that B lymphocytes are induced to proliferate in the presence of T cells and phytomitogens. Anti-HTLA serum was found not to inhibit K-cell activity of lymphocytes against antibody-coated chicken erythrocytes. These antisera appear very useful tools for the study of the role of human B and T lymphocytes involved in in vitro immune reactions. (+info)
A subpopulation of human B lymphocytes that rosette with mouse erythrocytes.
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A proportion of human peripheral blood lymphocytes form rosettes with mouse erythrocytes (M-RFC). It is confirmed that the proportion of such rosette-forming cells is high in chronic lymphocytic leukaemia (CLL). Analysis of normal lymphocyte populations revealed that M-RFC belong to the B-lymphocyte subclass exclusively. Analysis of their surface markers showed: (a) complement receptors in 50% as compared to 71% of the total B-cell population; (b) a distribution of surface immunoglobulins G, A, M and E typical of the lymphocyte sources; (c) lack of sheep erythrocyte receptor. No differences in the ratio of M-RFC to total B cells was found between lymphocyte population from tonsils, bone marrow and peripheral blood although a significantly higher ratio was seen in cord blood and in chronic lymphocytic leukaemia. Investigation of the properties of mouse erythrocyte rosette formation revealed the following: (a) incubation of lymphocyte mouse erythrocyte mixtures at 37degreesC before centrifugation inhibited rosette formation when CLL lymphocytes were used; (b) treatment of mouse erythrocytes with neuraminidase or trypsin increased their adhesiveness to lymphocytes; (c) treatment of lymphocytes with neuraminidase promoted M-rosette formation but trypsin treatment had an inhibitory effect; (d) cyanide and fluoride at concentrations which strongly inhibited E-rosette formation had no inhibitory effect on M rosettes; (e) M-rosette formation was inhibited by anti-immunoglobulin serum but not by anti-lymphocyte serum; and (f) M-rosette formation was also inhibited by the presence of staphylococci. E-rosette formation was unaffected. The nature of the bond in mouse rosettes is discussed in the light of these findings. The evidence indicates that the lymphocyte receptor may be a part of an immunoglobulin molecule. (+info)
Engagement of CD153 (CD30 ligand) by CD30+ T cells inhibits class switch DNA recombination and antibody production in human IgD+ IgM+ B cells.
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CD153 (CD30 ligand) is a member of the TNF ligand/cytokine family expressed on the surface of human B cells. Upon exposure to IL-4, a critical Ig class switch-inducing cytokine, Ag-activated T cells express CD30, the CD153 receptor. The observation that dysregulated IgG, IgA, and/or IgE production is often associated with up-regulation of T cell CD30 prompted us to test the hypothesis that engagement of B cell CD153 by T cell CD30 modulates Ig class switching. In this study, we show that IgD+ IgM+ B cells up-regulate CD153 in the presence of CD154 (CD40 ligand), IL-4, and B cell Ag receptor engagement. In these cells, CD153 engagement by an agonistic anti-CD153 mAb or T cell CD30 inhibits S mu-->Sgamma, Smu-->Salpha, and S mu-->Sepsilon class switch DNA recombination (CSR). This inhibition is associated with decreased TNFR-associated factor-2 binding to CD40, decreased NF-kappaB binding to the CD40-responsive element of the Cgamma3 promoter, decreased Igamma3-Cgamma3 germline gene transcription, and decreased expression of Ku70, Ku80, DNA protein kinase, switch-associated protein-70, and Msh2 CSR-associated transcripts. In addition, CD153 engagement inhibits IgG, IgA, and IgE production, and this effect is associated with reduced levels of B lymphocyte maturation protein-1 transcripts, and increased binding of B cell-specific activation protein to the Ig 3' enhancer. These findings suggest that CD30+ T cells modulate CSR as well as IgG, IgA, and IgE production by inducing reverse signaling through B cell CD153. (+info)
BAFF binds to the tumor necrosis factor receptor-like molecule B cell maturation antigen and is important for maintaining the peripheral B cell population.
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The tumor necrosis factor (TNF) family member B cell activating factor (BAFF) binds B cells and enhances B cell receptor-triggered proliferation. We find that B cell maturation antigen (BCMA), a predicted member of the TNF receptor family expressed primarily in mature B cells, is a receptor for BAFF. Although BCMA was previously localized to the Golgi apparatus, BCMA was found to be expressed on the surface of transfected cells and tonsillar B cells. A soluble form of BCMA, which inhibited the binding of BAFF to a B cell line, induced a dramatic decrease in the number of peripheral B cells when administered in vivo. Moreover, culturing splenic cells in the presence of BAFF increased survival of a percentage of the B cells. These results are consistent with a role for BAFF in maintaining homeostasis of the B cell population. (+info)