scholarly journals MECHANISMS OF RECOVERY FROM A GENERALIZED VIRAL INFECTION: MOUSEPOX

1971 ◽  
Vol 133 (5) ◽  
pp. 1074-1089 ◽  
Author(s):  
R. V. Blanden
Keyword(s):  
Antiviral Activity ◽  
Immune Serum ◽  
Mononuclear Phagocytes ◽  
Host Responses ◽  
Spleen Cells ◽  
Hyperimmune Serum ◽  
Recovery Mechanisms ◽  
Interferon Responses ◽  
Immune Spleen Cells

The following passive transfer experiments evaluated the contributions of the various host responses in recovery from mousepox. (a) Immune spleen cells transferred highly efficient antiviral activity, but preinfected recipients of these cells made no detectable splenic interferon or antibody in the 24 hr interval after cell transfer. (b) Passively administered interferon was ineffective. (c) Recipients of hyperimmune serum had much more antibody than recipients of immune spleen cells but significantly less antiviral activity. (d) Immune spleen cell populations with antiviral activity contained mediators of CMI to virus antigens. (e) The antiviral activity of immune spleen cells was specific; it was inhibited by in vitro treatment with ATS, anti-light chain serum, and anti-theta ascitic fluid, but not by removal of mononuclear phagocytes from the immune population. These results are interpreted to mean that recovery mechanisms conferred by immune spleen cells were triggered by specifically sensitized, thymus-derived lymphocytes, and that antibody and interferon responses were of less importance. A radiosensitive recipient component was necessary for the full expression of the antiviral activity of both immune cells and immune serum. It seemed likely that this component was the blood monocyte.

scholarly journals Monoclonal antibody to murine gamma interferon inhibits lymphokine-induced antiviral and macrophage tumoricidal activities.

1984 ◽  
Vol 159 (5) ◽  
pp. 1560-1565 ◽  
Author(s):  
G L Spitalny ◽  
E A Havell
Keyword(s):  
Monoclonal Antibody ◽  
Antiviral Activity ◽  
Recombinant Dna ◽  
Gamma Interferon ◽  
Spleen Cells ◽  
Tumoricidal Activity ◽  
Antiviral Activities ◽  
Immune Spleen Cells ◽  
Mouse Myeloma

Fusion of rat immune spleen cells with mouse myeloma cells resulted in the formation of a stable hybridoma that secretes monoclonal antibody (MAb) directed against murine gamma interferon ( MuIFN -gamma). This MAb specifically neutralized the antiviral activity of a variety of MuIFN -gamma preparations, including a sample produced by recombinant DNA technologies. In contrast, the antiviral activities of a mixture of MuIFN -alpha plus MuIFN -beta, as well as those of rat or human IFN-gamma, were not neutralized by this antibody. The ability of the MAb to inhibit lymphokine-induced macrophage activation was also tested. It was found that in relation to the quantity of antibody needed to completely neutralize antiviral activity, much higher concentrations of MAb were required to abolish the capacity of lymphokine preparations to induce macrophage tumoricidal activity in vitro. The MAb was also coupled to cyanogen bromide-activated Sepharose beads and used as an immunoadsorbent. By reacting lymphokines with MAb coupled to an insoluble matrix, it was possible to show that this immobilized antibody completely and specifically removed from the lymphokine preparations the ability both to invoke macrophage tumoricidal activity and to mediate antiviral activity.

scholarly journals HETEROGENEITY OF THE EFFECTOR CELLS IN THE CYTOTOXIC REACTION AGAINST ALLOGENEIC LYMPHOMA CELLS

1973 ◽  
Vol 137 (2) ◽  
pp. 369-386 ◽  
Author(s):  
James Forman ◽  
Sven Britton
Keyword(s):  
Immune Cells ◽  
Host Response ◽  
Marked Reduction ◽  
Cytotoxic Effect ◽  
Immune Serum ◽  
Spleen Cells ◽  
Effector Cells ◽  
Normal Spleen ◽  
Peak Phase

The cytotoxic effect of spleen cells from H-2 allogeneic mice was tested in vitro against an A strain leukemia (YAC) labeled with [125I]iododeoxyuridine. After the mice were primed with tumor cells, significant and specific H-2 immunity was detected on day 3 and peak cytotoxicity was observed between 7 and 14 days after priming. Two effector cells appear to be involved in the host response, because spleens taken from mice soon after priming were not sensitive to antitheta sera and complement while those taken during the peak stages of the response showed a marked reduction in cytotoxicity after treatment. Macrophages were not involved, since removal of these cells by the carbonyl iron method did not result in any reduction in cytotoxicity. Immune serum that was capable of inducing cell-mediated cytotoxicity in normal spleen cell populations also augmented cytotoxicity of spleen cells taken from mice primed 3 days previously. However, when spleen cells were taken from mice during the peak phase of the immune response, the same serum at the same dilutions inhibited the preexisting cytotoxicity. A difference was also detected in the killing efficiencies between early and late immune cells.

scholarly journals Antigen-specific suppressor T-cell activity in genetically restricted immune spleen cells.

1978 ◽  
Vol 148 (5) ◽  
pp. 1271-1281 ◽  
Author(s):  
C W Pierce ◽  
J A Kapp
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Activity ◽  
Antibody Responses ◽  
Spleen Cells ◽  
Suppressor T Cells ◽  
Specific Suppressor T Cells ◽  
Immune Spleen Cells

Virgin spleen cells develop comparable primary antibody responses in vitro to syngeneic or allogeneic macrophages (Mphi) bearing the terpolymer L-glutamic acid60-L-alanine30-L-tyrosine10 (GAT), whereas immune spleen cells primed with syngeneic or allogeneic GAT-Mphi develop secondary responses preferentially when stimulated with GAT-Mphi syngeneic to the GAT-Mphi used for priming in vivo. These restrictions are mediated by products of the I-A subregion of the H-2 complex and are operative at the level of the GAT-Mphi-immune helper T-cell interactions. To investigate why these immune spleen cells fail to develop a significant antibody response to GAT-Mphi other than those used for in vivo immunization and determine the mechanism by which the restriction is maintained, spleen cells from virgin and syngeneic or allogeneic GAT-Mphi-primed mice were co-cultured in the presence of GAT-Mphi of various haplotypes. Antibody responses to GAT developed only in the presence of GAT-Mphi syngeneic to the Mphi used for in vivo priming; responses in cultures with GAT-Mphi allogeneic to the priming Mphi, whether these Mphi were syngeneic or allogeneic with respect to the responding spleen cells, were suppressed. The suppression was mediated by GAT-specific radiosensitive T cells. Thus, development of GAT-specific suppressor T cells appears to be a natural consequence of the immune response to GAT in responder as well as nonresponder mice. The implications of stimulation of genetically restricted immune helper T cells, and antigen-specific, but unrestricted, suppressor T cells after immunization with GAT-Mphi in vivo are discussed in the context of regulatory mechanisms in antibody responses.

scholarly journals THE EFFECT OF ANTIBODY ON INTRACELLULAR PARASITISM OF SALMONELLA TYPHIMURIUM IN MONONUCLEAR PHAGOCYTES IN VITRO

1959 ◽  
Vol 110 (5) ◽  
pp. 715-730 ◽  
Author(s):  
Justus Gelzer ◽  
Emanuel Suter
Keyword(s):  
Salmonella Typhimurium ◽  
Gamma Globulin ◽  
Fluorescent Antibody ◽  
Immune Serum ◽  
Mononuclear Phagocytes ◽  
Fluorescent Antibody Technique ◽  
Antibody Technique ◽  
Long Time ◽  
Infected Cells

The effect of antibody on the fate of Salmonella typhimurium within mononuclear phagocytes (MN) of rabbits was studied in vitro. Monocytes and bacteria were incubated either in absence or presence of antibody. After 45 minutes during which phagocytosis occurred infected cells were washed to remove extracellular bacilli and free antibody. The cells were then reincubated in a medium without addition of antibody, and the interaction between the MN and bacteria was followed, correlating bacterial viability and the morphology of the mixture. The following results were obtained. The anti-Salmonella antibody was not bactericidal even in presence of complement and did not enhance phagocytosis. Regardless of whether antibody was present or absent during phagocytosis, the bacteria appeared to multiply within the cells. When no antibody was present during phagocytosis the infected cells were severely damaged within a few hours of incubation, and extensive extracellular multiplication was dominating. When antibody was present during phagocytosis MN packed with bacteria persisted for a long time. Little or no extracellular growth occurred. It was possible to demonstrate the presence of the antibody within the infected MN, using the fluorescent antibody technique. The antibody appeared as a coat around the bacteria. Antibody entered the cells only during phagocytosis, presumably attached to the bacteria. The active factor of the immune serum was found in the gamma globulin fraction and reacted specifically with the somatic antigen of Salmonella typhimurium. The antiflagellar portion of the antiserum was not involved in the phenomenon described. It is concluded that this antibody protects monocytes against the effect of intracellularly located Salmonella.

Antigenicity of a Spontaneous Murine Mammary Adenocarcinoma during in Vitro Cultivation

1977 ◽  
Vol 63 (5) ◽  
pp. 415-427 ◽  
Author(s):  
Anwar A. Hakim
Keyword(s):  
Extracellular Protease ◽  
Mammary Adenocarcinoma ◽  
In Vitro Cultivation ◽  
Membrane Glycoproteins ◽  
Spleen Cells ◽  
Alpha 1 Antitrypsin ◽  
Immunogenic Properties ◽  
Cells Cultured ◽  
Immune Spleen Cells

The present study reports on the transplantability and immunogenic properties of a murine spontaneous mammary adenocarcinoma (AdCa) cultured under various conditions. When cultured under standard conditions for 300 days, AdCa cells became nononcogenic, and 74 % survived the effects of immune spleen cells. Cell cultures grown in presence of the « extracellular protease » retained their transplantability, and only 25 % survived the effects of immune spleen cells. In cotton-stoppered bottles without HEPES, the cells retained their transplantability and survived after incubation with immune spleen cells, whereas AdCa cells cultured in presence of human alpha-1-antitrypsin became less oncogenic and remained sensitive to the killing effects of immune spleen cells. When treated with serum of mice or rabbits immunized with AdCa cells, the cells cultured under standard conditions or grown in presence of the human antitrypsin became non-transplantable, whereas cells grown in cotton-stoppered glass bottles or in presence of the « extracellular protease » retained their oncogenicity. When cultured AdCa cells were incubated with cAMP and then used to immunize syngeneic hosts, tumors arising from a challenging dose of untreated AdCa cells grew faster in mice immunized with cAMP-treated cells than in mice immunized with untreated cells. On the other hand, immunization with AdCa cells treated with EDTA, iodoacetate, or heparin reduced the transplantability of the challenging AdCa cells. Treatment with vibrio cholera neuraminidase (VCN) at pH 5.6 increased the immunogenicity of AdCa cells: immunization with VCN-treated AdCa cells protected syngeneic hosts against challenge with untreated AdCa cells, whereas formalin-or glutaraldehydeflxed untreated AdCa cells gave a transient protection. Rabbit and mouse antisera raised against VCN-treated AdCa cells and against membrane glycoproteins of untreated AdCa cells showed definite though variable cytotoxic activity against cultured untreated AdCa cells.

Cell-mediated immunity during the infection of CBA mice with Trypanosoma musculi

1974 ◽  
Vol 20 (1) ◽  
pp. 105-106 ◽  
Author(s):  
Pierre Viens ◽  
Pierre Pouliot ◽  
G. A. T. Targett
Keyword(s):  
Subcutaneous Administration ◽  
Immune Serum ◽  
Cell Mediated Immunity ◽  
Spleen Cells ◽  
Cba Mice ◽  
Serum Transfer ◽  
Immune Spleen Cells

CBA/J mice were infected with Trypanosoma musculi. On the 10th day of infection, when the parasitemia had become stabilized and parasites consisted only of adult (non-dividing) trypomastigotes, non-adherent spleen cells from immune donors were injected intravenously, with or without simultaneous subcutaneous administration of immune serum. The immune spleen cells accelerated the termination of infection whilst immune serum transfer had no effect on the course of the parasitemia.

scholarly journals Vaccinia Virus-Mediated Inhibition of Type I Interferon Responses Is a Multifactorial Process Involving the Soluble Type I Interferon Receptor B18 and Intracellular Components

2008 ◽  
Vol 83 (4) ◽  
pp. 1563-1571 ◽  
Author(s):  
Zoe Waibler ◽  
Martina Anzaghe ◽  
Theresa Frenz ◽  
Astrid Schwantes ◽  
Christopher Pöhlmann ◽  
...  
Keyword(s):  
Vaccinia Virus ◽  
Type I Interferon ◽  
Poly I:C ◽  
Host Responses ◽  
Type I ◽  
Immune Modulators ◽  
Modified Vaccinia Virus Ankara ◽  
Multistep Process ◽  
Interferon Responses

ABSTRACT Poxviruses such as virulent vaccinia virus (VACV) strain Western Reserve encode a broad range of immune modulators that interfere with host responses to infection. Upon more than 570 in vitro passages in chicken embryo fibroblasts (CEF), chorioallantois VACV Ankara (CVA) accumulated mutations that resulted in highly attenuated modified vaccinia virus Ankara (MVA). MVA infection of mice and of dendritic cells (DC) induced significant type I interferon (IFN) responses, whereas infection with VACV alone or in combination with MVA did not. These results implied that VACV expressed an IFN inhibitor(s) that was functionally deleted in MVA. To further characterize the IFN inhibitor(s), infection experiments were carried out with CVA strains isolated after 152 (CVA152) and 386 CEF passages (CVA386). Interestingly, neither CVA152 nor CVA386 induced IFN-α, whereas the latter variant did induce IFN-β. This pattern suggested a consecutive loss of inhibitors during MVA attenuation. Similar to supernatants of VACV- and CVA152-infected DC cultures, recombinantly expressed soluble IFN decoy receptor B18, which is encoded in the VACV genome, inhibited MVA-induced IFN-α but not IFN-β. In the same direction, a B18R-deficient VACV variant triggered only IFN-α, confirming B18 as the soluble IFN-α inhibitor. Interestingly, VACV infection inhibited IFN responses induced by a multitude of different stimuli, including oligodeoxynucleotides containing CpG motifs, poly(I:C), and vesicular stomatitis virus. Collectively, the data presented show that VACV-mediated IFN inhibition is a multistep process involving secreted factors such as B18 plus intracellular components that cooperate to efficiently shut off systemic IFN-α and IFN-β responses.

scholarly journals Production of auto-anti-idiotypic antibody during the normal immune response to TNP-ficoll. II. Hapten-reversible inhibition of anti-TNP plaque-forming cells by immune serum as an assay for auto-anti-idiotypic antibody

1979 ◽  
Vol 150 (1) ◽  
pp. 154-165 ◽  
Author(s):  
EA Goidl ◽  
AF Shrater ◽  
GW Siskind ◽  
GJ Thorbecke
Keyword(s):  
Immune Response ◽  
Caproic Acid ◽  
Immune Serum ◽  
Plaque Formation ◽  
Antibody Activity ◽  
Spleen Cells ◽  
Reversible Inhibition ◽  
Idiotypic Antibody ◽  
Normal Immune Response

Sera taken from AKR/J mice 7 d after the intravenous injection of 2,4,6-trinitrophenyl-lys-Ficoll (TNP-F) caused a specific inhibition of anti- trinitrophenol (TNP) plaque-forming cells (PFC) in vitro. This inhibition was reversed by the incorporation of 10(-8)-10(-7) M 2,4,6-trinitrophenyl- ε-amino-n-caproic acid (TNP-EACA) into the agar during the PFC assay. The factor responsible for the hapten-reversible PFC inhibition was removed from serum by passage through an anti-immunoglobulin column or through a 2,4,-dinitrophenyl-human-serum-albumin-bromoacetylcellulose plus anti-TNP- antibody column, but not by DNP-HSA-BAC alone. It was concluded that this immunoglobulin-like substance, lacking anti-TNP activity but reacting with anti-TNP antibody of AKR/J origin, was most likely an auto-anti-idiotypie antibody that had been produced during the normal course of the response of AKR/J mice to TNP-F. Pools of anti-idiotypic-antibody-containing antisera inhibited anti-TNP plaque formation to varying degrees when tested on d-4 PFC from different mice of the same inbred strain, suggesting a variability in idiotype expression. 4 d after transfer of immune (7 d after 10 μg TNP-F, administered intravenously) AKR/J spleen cells plus 10 μg TNP-F into syngeneic mice, the number of PFC detectable in the recipients' spleens could be markedly augmented by the inclusion of TNP-EACA in the agar during the PFC assay. Incubation of spleen cells containing such hapten-augmentable PFC with TNP- EACA yielded a factor in the supernate that caused a specific, in vitro, hapten-reversible inhibition of anti-TNP PFC. Studies with immunoadsorbents indicated that this PFC-inhibiting factor was antigenically immunoglobulin- like, lacked anti-TNP-antibody activity, but reacted with anti-TNP antibody of AKR/J origin. The results are consistent with the view that this PFC inhibitor is auto-anti-idiotypic antibody that is involved in the normal regulation of the immune response. It is proposed that hapten-reversible inhibition of plaque formation can be employed as an assay for anti-idiotypic antibody and the conditions for such an assay are described. It is further proposed that the detection of hapten-augmentable PFC suggests the presence of auto-anti-idiotypic antibody.

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