Transduction of the gene coding for a human G-protein coupled receptor FPRL1 in mouse tumor cells increases host anti-tumor immunity
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Formyl peptide receptor
Antigenicity
This chapter describes antigens in terms of immune responses. To induce an immune response, the substance must be perceived as foreign to the body by the immune mechanism of the reacting organism. The meaning of the concept foreign is a basic problem of immunology. According to accepted terminology, the substance is called an immunogen when it provokes a specific immune response. The words antigen and antigenicity are frequently used to describe the capacity of the substance to react in a specific manner with the effect or mechanisms of the immune response, that is, the antibodies or the antigen-reactive cells. Antibodies are directed against small structures on the surface of the antigen. Exactly which fine structures are perceived as foreign and, thus, give rise to antibody production is genetically determined and vary between various species and between individuals of the same species. The immune apparatus displays a significant disinclination to produce antibodies against the body's own substances. An immune response registering genetic differences in macromolecules from different individuals within the same species is called alloimmunity, and the immunogens are called alloantigens. There is a minimum time requirement for the immunogen to remain in the body for an immune response to be initiated. Substances that are rapidly cleared from the blood or are catabolized through enzymatic breakdown are, thus, often weak immunogens.
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Immunoglobulin A
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After immunization of rats with heterophilic antigen (boiled homogenates of guinea-pig kidney), their immune responses to sheep red cells were consistently depressed, whereas those to heterophilic antigen were increased, as compared with controls. The suppression of immune responses to sheep red cells in rats immunized with heterophilic antigen may represent an animal model paralleling the interference with Rh immunization of ABO incompatibility in man. Experiments intended to elucidate the mechanism of this interference included simultaneous administration of sheep red cells and heterophilic antigen; comparison of antibody formation in intact and splenectomized rats; and passive immunization with isophilic and/or heterophilic antibodies prior to challenge with sheep red cells. On the basis of the experimental observations, a hypothesis was proposed according to which cellular diversion of antigen may be responsible for these inhibitions of immune responses.
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In this study, stable high-five insect cell line constitutively expressing rotavirus (RV) VP2 was co-transfected with VP6 and VP7-recombinant plasmids. The presence of RV proteins in stably transfected high-five cells was verified by molecular and protein analyses. To yield self-assembled triple-layered RV-like particles (tlRLPs), a stable insect high-five cell line was generated to produce RV VP6 and VP7 besides VP2. Self-assembled tlRLPs were observed by transmission electron microscopy (TEM), and enzyme-linked immunosorbent assay (ELISA) was used to assess their antigenicity in vivo. The results suggest that the stable transfected high-five cells are able to generate tlRLPs with the efficient antigenicity. J. Med. Virol. 87: 102–111, 2015. © 2014 Wiley Periodicals, Inc.
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Isolation and characterisation of Plasmodium falciparum (Welch, 1897) soluble antigens from infected patient plasma, Western blotting, thermal stability and ELISA assays using hyperimmune IgG-antimalaria antibodies was the main objective of this work. A circulating antigen of approximately Mr 33-35 kDa with good specificity and antigenicity, in the plasma of malarial patients was shown. Heating at 100 degrees C did not destroy its antigenicity. When fractions highly enriched in the 33-35 kDa proteins were used in ELISAs, a seroreactivity in plasma obtained from primary-infected individuals was found. Controls from normal patients were always negative. The antigenic characteristics suggest that it may be included within the group of new described Plasmodium soluble antigens.
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Specific immune complexes, prepared at different ratios of antibody to antigen, were examined for their effects on the antibody response of BALB/c mice to the cell wall polysaccharide antigen (PnC) extracted from Streptococcus pneumonia R36a. Mice immunized with complexes formed in antigen excess developed a PnC-specific antibody response that was equivalent to that in mice injected with free antigen. On the other hand, mice injected with complexes formed in antibody excess developed very little PnC-specific antibody. Furthermore, administration of immune complexes (formed in antibody excess) resulted in suppression of the response to an immunogenic dose of PnC given concurrently or 1 day after injection of immune complexes but not when the antigen was given 1 day before injection of the immune complexes. Injections of free antibody (TEPC-15) also resulted in suppression of the response to antigenic challenge; however, suppression was greatest when the antibody was injected concurrently with the antigen, suggesting that the suppression was mediated through the formation of immune complexes in vivo. The suppression appears to be specific for the antigen (PnC), since in mice injected with TEPC-15/PnC complexes (formed in antibody excess) and challenged with PnC coupled to sheep RBC, only the response to PnC was suppressed.
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To characterize the development and evolution of cellular immune responsiveness in individuals infected with the parasite Schistosoma mansoni, we studied fifteen patients with acute, subacute and chronic schistosomiasis. Lymphocytes from the three acutely infected patients responded vigorously to schistosome antigens in an in vitro blastogenic assay. By contrast, cells from nine chronically infected individuals were essentially unreactive to these same antigens. Patients infected for an intermediate period of time (9 months) generated responses between those of acute and chronic patients. The diminished responsiveness of chronically infected individuals was specific for schistosome antigens and did not extend to humoral immune responses. Following treatment of the infection with niridazole, these patients temporarily regained responsiveness to schistosome antigens. From these data we speculate that during the course of this parasitic helminth infection there develops a progressive and specific modulation of antigen recognition and proliferation by lymphocytes to schistosome antigens, and that such diminished immune reactivity may be important in maintaining the unique biological relationship which exists between a host and its parasites.
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