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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 31 (1990), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: HLA class II molecules may be induced on non-lymphoid cells by gamma-interferon (IFN-y). We investigated if HLA class II molecules induced by IFN-y on the HT29 colonic carcinoma cell line are functional, i.e, if they may be recognized by allogeneic T cells. We found that IFN-y-treated HT29 (HT29IFN) cells could not induce primary proliferative responses of peripheral blood T lymphocytes, nor were they able to induce proliferation in T-lymphocytc clones (TLC) specific for HLA class II molecules found on HT29IFN. However, in the presence of exogenous interleukin 2 (lL-2). 1 of 5 DQw8-specific TLC proliferated when restimulated with HT29IFN, and 3 of these 5 TLC could very effectively inhibit the growth of HT29IFN, probably due to a cytoloxic effect. Both the proliferative response and the cytotoxicity were inhibited by anti-DQ MoAb. We conclude that T cells may recognize HLA-DQ molecules on non-lymphoid cells, which may be of relevance for autoimmune diseases, graft-versus-host disease, and possibly for the recognition of malignant cells.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We studied the expression of the Tac antigen, the transferrin receptor (Tfr-R), HLA class II antigens (DR, DQ, DP), CD30, and Act 1 on purified CD4+ and CD8+ cells isolated from synovial fluid (SF), synovial tissue (ST), and peripheral blood (PB) of patients with rheumatoid arthritis (RA) and with non-RA inflammatory arthritides (not ST). Subfractionated T cells of PB from healthy individuals served as controls. SF CD4+ cells from RA and non-RA arthritides expressed the Tac antigen much more frequently than corresponding CD8+ cells (54 and 58% versus 16 and 17%). In contrast, SF CD8+ cells of both patient groups expressed the HLA class II antigens rather more frequently than the corresponding CD4+ cells (88 and 68% versus 72 and 40%), Tfr-R expression was low on CD4+ and CD8+ SF T cells from both patient groups SF T cells did not express CD30, and their expression of Act 1 did not differ from that of normal PB T cells. The RA ST findings were similar to those of RA SF. The overall expression of activation markers on PBT cells of patients was slightly higher than on those of normal controls, and the RA group was slightly higher than the non-RA group. The results show that intra-articular T cells in arthritis are activated and that CD4+ and CD8+ subsets differ in their expression of Tac antigen and HLA class II antigens. There were also similar patterns of activation markers on both CD4+ and CD8+ SF cells from RA and non-RA arthritis patients, suggesting that several types of arthritis display a similar immunopathogenesis in the joints.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 26 (1987), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We studied the requirements for secondary activation signals in pure CD4+ and CD8+ T cells after stimulation with anti-CD3 antibodies. Stimuluion or CD4+ or CD8+ cells with anti-CD3 monoclonal antibodies (MoAb) bound to polyptyene monosized particles never resulted in a proliferative response. However, DNA synthtsis was observed when recombinant interietikin 2 (IL-2) or other secondary signals, such as those provided by phorbol myristate acetate (PMA) or autologous accessory cells (AC), were also added. These secondary signals were not in themselves capable of inducing DNA synthesis in the absence of particle-bound anti-CD3. We also found that the signals provided by AC may be dependent on the activation state of these cells. Thus, the effects of accessory cells were enhanceed by a factor present in fetal calf serum (FCS), must likely endotoxin or lipopolysaccharide (LPS), which alone, however, were not able to activate T cells, even in the presence of particle-bound anti-CD3. Recombinant lL-1 over a broad dose range was unable to replace PMA or activated AC after slimulation with particle-bound anti-CD3. Purified CD4+ and CDS+ T cells behaved idenlically in all the experiments, indicating that the basic mechanisms for activation in the two T-cell subsets are idenlical.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 25 (1987), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The colonic carcinoma cell line HT-29 had no constitutive expression of HLA class II molecules. Gamma interferon (IFN-γ) induced expression of HLA class II molecules in a dosedependent manner with 100 U/ml as an optimal dose. The expression of HLA-DR, HLA-DP, and HLA-DQ molecules seemed to follow different kinetics. While DR and DP molecules were maximally induced after 2 days, DQ molecules appeared later with maximum percentage positive cells after 8 days. Treatment with a prostaglandin synthesis inhibitor (indomethacin) neither induced class II expression nor altered the dose-response curve for IFN-γ; this indicated that possible endogenous production of prostaglandins iin this cell line did not interfere with its class II expression. The lectins phytohaemagglutinin (PHA), concanavalin A (Con A), pokeweed mitogen (PWM), and wheat germ agglutinin (WGA) did not induce class II expression.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 17 (1983), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: We have earlier shown that coculture of macrophages and cells from a methylcholanthiene-induced sarcoma (MCI M-AA) in vitro resulted in macrophage activation and production of type II (gamma) interferon. When ascites fluid from the MCIM-AA sarcoma (shown previously to activate macrophages in vitro) was added to spleen cell populations from semisyngeneic C3D2 mice in vitro. NK activity was markedly enhanced. After intraperitoneal injection of MCI M-AA cells or ascites fluid, 4- to 12-fold increased NK cell activity with a peak at 3–5 days could be measured in the spleen cell population and in the non-adherent peritoneal exudate cell population. The mice injected with tumour cells or ascites fluid developed a pronounced splenomegaly, and maximum spleen size coincided with peak NK activity. Injection of tumour cells or tumour ascites fluid resulted in marked changes in the T-cell, B-cell, macrophage, and ‘null’ cell content of ihe peritoneal exudate.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 18 (1983), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The natural killer (NK) activity of spleen cells from C57B1/10 mice subjected to standardized stress conditions was reduced when compared with that of untreated controls. Both the total number of nucleated spleen cells and their cytotoxic activity against an NK-sensitive target were reduced. The reduction appeared after induction of stress, and the NK activity was reduced throughout an 8-day stress period.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 11 (1980), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Prior immunization of BALB/c mice with free light chains from myeloma proein 315 (VL315) and its variable domain (VL3l5) inhibited the growth of subcutaneously injected MOPC315 tumour cells. The growth suppression observed after immunization with L315 was equivalant to that which resulted from immunization with the complete M315. VL315 and non-polymerized L315 did not elicit specific antibodies. Polymerized L315; induced both suppression of MOPC315 growth and antibodies specific for free L315; however, these anybodies did not rect with the complete M315, nor were they absorbed by MOPC315 tumour cells. the data indicated that the suppression of tumour growth was mediated by specifically sensitized cells acting in the absence of antibodies against M3l5 or L315. Immunization with the variable domain of the heavy chain from M315 (VH315) had no effect on the growth of MOPC315, the M315 fragment and subunits that induced growth suppression were thus identical with those capable of inducing T helper cells in BALB/c mice.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 30 (1989), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Many CD4+ human T lymphocyte clones (TLC) are found not to proliferate against appropriate stimulating cells, and many lose this capacity during culture. This may be due, not to a defect in the recognition of the antigen, but to an inability to produce sufficient amounts of interleukin 2 (IL-2) for autocrine growth, since specific HLA-restricted proliferative responses could be induced in ‘non-proliferative’ clones by the addition of exogenous IL-2 or phorbol myristate acetate (PMA). Of various factors tested during expansion procedures of the clones, the proliferative capacity could only be restored by changing the stimulatory cells from B lymphoblastoid cell lines (B-LCL) to peripheral blood mononuclear cells (PBM). The cytotoxicity of the TLC was found to be independent of its proliferative capacity. After restoration of the proliferative capacity, a mouse B lymphoma cell line transfected with the appropriate HLA DQA and DQB genes was still not able to induce proliferation in the absence of exogenous IL-2. We conclude that (1) ‘non-proliferative’ TLC may recognize their targets, but fail to proliferate due to temporary lack of IL-2 production, and (2) even ‘proliferative’ T cells may fail to respond to certain target cells carrying the specific antigen, such as a murine transfectant, in the absence of exogenous IL-2.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 28 (1988), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The activation signals necessary for interleukin-2 (IL-2) receptor induction, IL-2 production, and DNA synthesis in resting T cells were investigated. IL-2 receptors were induced after activation via CD2 or CD3 alone, while IL-2 production in both CD4+ and CD8+ T cells required activation via both CD3 and CD2. The sequence of activation signals via CD3 and CD2 was shown to be important since DNA synthesis was induced when the primary activation signal was delivered via CD3, and the CD2 signal within 8h. In contrast, no DNA synthesis was demonstrated when the primary activation signal was delivered via CD2 and the CD3 signal later. Ciclosporin A (CyA) inhibited T-cell DNA synthesis after activation via CD2 and CD3. The inhibition seemed to be due to the prevention of IL-2 synthesis.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Scandinavian journal of immunology 29 (1989), S. 0 
    ISSN: 1365-3083
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: T-cell receptor (TcR)-γδ-bearing lymphocytes were isolated from the peripheral blood of two healthy donors by immunomagnetic separation and subsequent cultured. The cell lines generated showed two distinct patterns of cytotoxicity. One TcR-γδ+ cell line (HG.D) lysed K562 and U937 target cells, three TcR-γδ+ cell lines lysed Daudi cells, and one TcR-γδ+ cell line showed a shift from the former to the latter specificity during culture Cold target inhibition experiments showed that the HG.D effector cells which were cytotoxic against 119.17 cells also lysed K562 cells. The cytotoxicity against Daudi cells was strongly inhibited by monoclonal antibodies (MoAb) against the CD3 complex, whereas the cytotoxicity of the HG.D cell line against K562 and U937 was unaffected by such antibodies. The cytotoxicity against Daudi cells was also strongly inhibited in the presence of anti-TcR-γδ MoAb. However, in two of the Daudi-specific cell lines, strong cytotoxicity against K562 cells was induced by Anti-TcR-γδ MoAb. Anti-LFA-1 MoAb caused only a partial inhibition of cytotoxicity, while anli-CD2and anti-TcR-αβ MoAb were found to have no effect. The results indicate that human γδ receptor-bearing T cells demonstrate a certain degree of target cell specificity, and that recognition of some target cells may be mediated through the TcR-γδ.
    Type of Medium: Electronic Resource
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