bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction of antigen-specific antibody response in human peripheral blood lymphocytes in vitro by a dog kidney cell vaccine against rabies virus (DKCV).
Authors: Uytdehaag F G , Osterhaus A D , Loggen H G , Bakker R H , van Asten J A , Kreeftenberg J G , van der Marel P , van Steenis B 
Published: December 2022

Abstract
In the present report an in vitro method for obtaining a secondary human antibody response to a dog kidney cell vaccine against rabies virus (DKCV) is described. Cultures of peripheral blood mononuclear cells from normal rabies-immune and nonimmune donors were stimulated in vitro by DKCV. The production of virus-specific antibody in supernatant fluids was monitored by ELISA. Antibody was produced by lymphocytes from rabies-immune individuals, whereas those of nonimmune subjects consistently failed to produce anti-rabies antibodies after in vitro stimulation with DKCV. The generation of the anti-rabies virus antibody response of lymphocytes stimulated with DKCV was shown to be an antigen-dependent, as well as an antigen-specific process. Optimal antigen-specific responses were observed at relatively low concentrations of antigen (10(-1) to 10(-2) micrograms/culture). At increasing concentrations of antigen in culture (greater than 1 microgram/culture), the anti-rabies virus response was suppressed. Antibody produced upon stimulation was capable of neutralizing rabies virus. The response to rabies virus requires T cell help because lymphocytes depleted of SE rosetting cells did not respond to an antigenic stimulus. Studies in which the same individuals were followed over time showed a sequential development of circulating B cell subsets. The system may provide a model for the study of human B cell differentiation in vivo and in vitro and may be valuable for testing the potency of rabies vaccines in vitro.
Anti-idiotype as a probe in the analysis of autoimmune tubulointerstitial nephritis in the Brown Norway rat.
Authors: Zanetti M , Mampaso F , Wilson C B 
Published: December 2022

Abstract
Rabbit antibodies specific for the idiotype (Id) of autoantibodies to tubular basement membrane (TBM) eluted from kidneys of Brown Norway rats with tubulointerstitial nephritis (TIN) were used to analyze the immune response to TBM antigens at the humoral and cellular levels. These antibodies appeared to recognize Id determinants associated with the antigen combining site on the anti-TBM Id as well as on splenic lymphocytes. However, efforts to detect Id-positive cells in the interstitial infiltrates of kidneys with TIN failed. In contrast, in vivo injection of anti-Id serum before immunization with TBM resulted in a) significant selective suppression of antibodies to the autologous collagenase-solubilized TBM moiety but not to antigenic determinants of the intact TBM nor to those of heterologous TBM, and b) a corresponding decrease of TIN. These results suggest that anti-Id antibodies of this type can be useful as a probe for further dissecting the pathogenetic mechanisms underlying these complex autoimmune responses.
Comparative analysis of the influences of human gamma, alpha and beta interferons on human multipotential (CFU-GEMM), erythroid (BFU-E) and granulocyte-macrophage (CFU-GM) progenitor cells.
Authors: Broxmeyer H E , Lu L , Platzer E , Feit C , Juliano L , Rubin B Y 
Published: December 2022

Abstract
Preparations of human interferon (HuIFN) immune (gamma) (2 X 10(7) units/mg protein), HuIFN leukocyte (alpha) (1.4 X 10(8) units/mg protein) and HuIFN fibroblasts (beta) (10(6) U/mg protein) were assessed for their influence on colony formation of human hematopoietic progenitor cells: colony forming unit-granulocyte, erythroid, macrophage, megakaryocyte (CFU-GEMM), burst forming unit-erythroid (BFU-E), day 7 colony forming unit granulocyte-macrophage (CFU-GM) and day 14 CFU-GM. Colony formation by CFU-GEMM and BFU-E was suppressed equally by the three preparations of HuIFN, but colony formation by CFU-GM was suppressed differentially. CFU-GM were, on the whole, more responsive to HuIFN gamma than HuIFN alpha, and HuIFN beta was least effective. HuIFN alpha, but not HuIFN gamma or HuIFN beta, suppressed colony formation from CFU-GM without also suppressing the total number of colonies plus clusters. This was due to an increase in the numbers of clusters formed in the presence of HuIFN alpha. The suppressive influence on colonies from CFU-GM by the preparations of HuIFN and the enhancement of clusters by HuIFN alpha was apparently equal for colonies and clusters of neutrophils, eosinophils, macrophages and neutrophils plus macrophages. The suppressive effects of HuIFN gamma were inactivated by a monoclonal antibody to HuIFN gamma and the suppressive and enhancing effects of HuIFN alpha were inactivated with a heteroantiserum to HuIFN alpha. Depletion of monocytes, T lymphocytes and B lymphocytes from the target bone marrow cells had no influence on the effects of the preparations of HuIFN. These results demonstrate that the effects of HuIFN gamma and HuIFN alpha are due to the HuIFN themselves and that these actions on the hematopoietic progenitor cells are probably not mediated through monocytes and/or lymphocytes.
Human B cell differentiation. IV. Effect of monoclonal anti-immunoglobulin M and D antibodies on B cell proliferation and differentiation induced by T cell factors.
Authors: Kuritani T , Cooper M D 
Published: December 2022

Abstract
Monoclonal anti-mu and anti-delta antibodies and mixed lymphocyte reaction-derived T cell factors (MLR-TF) were examined alone and in combination for their effects on proliferation and differentiation of human B cells. MLR-TF induced proliferation and subsequent plasma cell differentiation of blood B cells without additional stimulation. The monoclonal anti-mu and anti-delta antibodies alone did not induce proliferation, but each was capable of augmenting B cell proliferation induced by MLR-TF. In contrast, the anti-mu antibody inhibited the MLR-TF induction of IgM plasma cell differentiation but did not affect the differentiation of IgG and IgA plasma cells. The anti-delta antibody had no effect on MLR-TF-induced plasma cell differentiation. Studies using density gradient separation of B cell subpopulations suggest that MLR-TF induce low-density B cells to proliferate and differentiate into plasma cells but that by themselves MLR-TF have little effect on B cells of relatively high density. The latter subpopulation of small resting B cells responded with proliferation to MLR-TF when combined with either the anti-mu or the anti-delta antibody, but these stimuli were insufficient for induction of terminal plasma cell differentiation.
Identification and characterization of gp TFA-1, a guinea pig T cell surface antigen associated with T cell function.
Authors: Burger R , Reske K , Mauer U , von Steldern D , Husmann M 
Published: December 2022

Abstract
Monoclonal antibodies (Ab) were produced that specifically recognized guinea pig T cells. FACS analysis revealed that Ab 188 bound to the majority of peripheral T lymphocytes of strain 2 and strain 13 guinea pigs and to a minor population of thymocytes. It failed to react with the Ia-bearing guinea pig B cell leukemia line EN-L2C, with macrophages, bone marrow cells, erythrocytes, or thrombocytes. Treatment of T cells with Ab 188 and complement prevented T cell activation. Culturing primed T cells with antigen- or mitogen-pulsed syngeneic or with allogeneic macrophages in the continuous presence of Ab 188 produced a marked, dose-dependent inhibition of T cell proliferation. The antigen defined by Ab 188 was therefore designated guinea pig T lymphocyte function-associated antigen-1, gp TFA-1. The magnitude of inhibition by Ab 188 varied between 65 and 85% whereas three other antibodies to guinea pig T cells had no inhibitory effect on T cell proliferation. Time course experiments revealed that gp TFA-1 is critically involved in an early phase of T cell activation. Maximal inhibition was achieved only if the antibody was present from the beginning of the cell culture; the addition of antibody after 24 hr of culture no longer had an inhibitory effect. Ab 188 did not induce T cell mitogenesis. Two-dimensional analysis (one-dimensional, IEF; two-dimensional, SDS-PAGE) of immunoprecipitates obtained from NP40 lysates of [35S]methionine-labeled T cell blasts indicated that a molecule was specifically precipitated that consisted of two noncovalently associated polypeptide chains with apparent m.w. of 43,000 and 38,000. Both subunits displayed extensive charge heterogeneity focusing at an average isoelectric point of 5.0 and 6.5, respectively. The gp TFA-1 molecule exhibits striking similarities in its functional and structural properties to recently described clonotypically expressed T cell glycoproteins, which were shown to be involved in antigen recognition by T cells in the murine and human systems.
Lymphocyte recognition of lymph node high endothelium. V. Isolation of adhesion molecules from lysates of rat lymphocytes.
Authors: Chin Y H , Carey G D , Woodruff J J 
Published: December 2022

Abstract
Lymphocytes migrate from blood into lymph nodes (LN) of rats specifically at segments of venules lined by high endothelium (HEV). Investigation of lymphocyte surface molecules mediating this interaction has been carried out using an in vitro assay in which lymphocytes adhere selectively to HEV when overlaid onto sections of peripheral LN. Using this assay we have previously isolated a thoracic duct lymph component termed High Endothelial Binding Factor (HEBF), which is detected by its ability to block HEV sites where lymphocytes attach. In the current study, we present evidence that anti-HEBF antibody recognizes surface molecules of lymphocytes involved in adhesion to high endothelium. Rabbit antibody was produced against HEBF isolated from lymph by sequential ion exchange [diethylaminoethyl (DEAE)-cellulose and carboxymethyl (CM)-Sepharose] and Sephacryl S-200 gel filtration. Anti-HEBF F(ab')2 bound to 60 to 70% thoracic duct lymphocytes (TDL), spleen, and LN cells but to only 2 to 9% thymus and bone marrow cells (indirect immunofluorescence). In addition, biologically active HEBF was isolated from lymph and detergent lysates of lymphocytes by antibody affinity chromatography. Comparable amounts of the factor were isolated from lysates of TDL, LN, and spleen cells whereas little or no HEBF was detected in lysates of thymus or bone marrow cells or in serum. HEBF obtained from TDL appeared to be a glycoprotein because it was trypsin sensitive, bound to lentil lectin, and was eluted with alpha-methyl-D-mannoside. The finding that HEBF was not recovered from lysates of trypsinized TDL indicates that the activity was mediated by components expressed on cell surface membranes. Immunoprecipitation studies revealed that anti-HEBF antibody recognized radioiodinated surface membrane proteins of TDL and TDL-derived T cells and B cells that resolved on sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) autoradiography into three major bands with m.v. of 230,000, 210,000, and 92,000 (nonreduced) and one major band with m.w. of 70,000 and two minor bands with m.w. of 92,000 and 45,000 (reduced). These observations indicate that HEBF is a surface membrane component that is not class-specific. It is suggested that lymphocyte surface HEBF is composed of high endothelial adhesion molecules that mediate cell-cell interactions involved in entry of lymphocytes from blood into peripheral lymph nodes.
Selective inhibition of platelet activation by the amyloid P-component of serum.
Authors: Fiedel B A , Ku C S , Izzi J M , Gewurz H 
Published: December 2022

Abstract
One component of amyloid, protein AP, has a characteristic pentameric structure and is identical with a 9.5s serum alpha 1-globulin designated serum amyloid P-component or SAP. Another pentameric molecule, the acute-phase reactant C-reactive protein (CRP), shares major amino acid sequence homology with SAP although, in man, SAP is not an acute-phase reactant. Recently, we demonstrated that heat-aggregated CRP (H-CRP), like heat-aggregated IgG, activates platelets to reactions of aggregation, secretion, and generation of thromboxane A2. We report here that physiologic concentrations of SAP inhibit platelet aggregation stimulated by H-CRP. SAP must be present before platelet challenge with H-CRP to be effective. Native (unaggregated) CRP does not inhibit platelet activation induced by H-CRP, and the platelet inhibitory effect of SAP is restricted because platelet responses to each heat-aggregated IgG, acid-soluble collagen, DNA, ADP, and thrombin remain unaltered in the presence of SAP. Thus, human SAP seems to selectively modulate platelet reactivity to modified CRP, and as such to down-regulate at least one aspect of the biologic capacity of its acute-phase homologue.
Degradation of the heparin matrix of mast cell granules by cultured fibroblasts.
Authors: Atkins F M , Metcalfe D D 
Published: December 2022

Abstract
The ability of cultured rat fibroblasts to phagocytose rat peritoneal mast cell granules has been previously demonstrated by light and electron microscopy. To determine if the heparin matrix of ingested granules could be degraded by fibroblasts after phagocytosis, the heparin within peritoneal mast cells was labeled with [35S]sulfate in vivo. The 35S-labeled rat peritoneal mast cells were purified and their granules were isolated and shown to contain [35S]heparin proteoglycan. Incubation of [35S]heparin proteoglycan-containing granules with cultured rat fibroblasts revealed internalization of radioactivity by the fibroblasts over the first 24 hr consistent with phagocytosis of the granules by these fibroblasts. The [35S]heparin proteoglycan internalized by the fibroblasts was shown to decrease in size over 72 hr indicating that the fibroblasts were capable of degrading the heparin within the ingested granules. Degradation of [35S]heparin proteoglycan within the fibroblast was accompanied by the appearance of free [35S]sulfate in the extracellular compartment. Similar findings were obtained using cultured human fibroblasts. These data demonstrate for the first time that both rat and human fibroblasts are not only capable of ingesting mast cell granules but also of degrading mast cell granule heparin proteoglycan. This ingestion and degradation of mast cell granules by fibroblasts may represent an important mechanism in the regulation of the biologic expression of heparin and other granule-associated mediators in immediate hypersensitivity reactions.
Studies on the induction and expression of T cell-mediated immunity. XIV. Antigen-nonspecific oxidation-dependent cellular cytotoxicity (ODCC) mediated by sodium periodate oxidation of cytotoxic T lymphocytes.
Authors: Fan J , Bonavida B 
Published: December 2022

Abstract
Alloimmune murine thymus-derived cytotoxic lymphocytes (CTL) generated in vivo or in vitro are shown to lyse antigen-nonspecific target cells (tumor cells, Con A, and LPS blasts) following treatment of CTL with an oxidizing agent, sodium periodate (NaIO4). It has been shown that NaIO4 oxidizes terminal sialic acid residues of cell surface macromolecules. The presence of reactive aldehyde groups, generated by NaIO4 modification, is required for the expression of antigen-nonspecific cytotoxicity because treatment of modified cells with a reducing agent such as potassium borohydride (KBH4) resulted in the abrogation of cytotoxicity. However, KBH4 treatment of unmodified or NaIO4-modified CTL has no effect on antigen-specific cytotoxicity. The modification of CTL by NaIO4 is sufficient to lead to the formation of lymphocyte-target cell conjugates and lysis of bound targets. Monoclonal antibodies directed against the Lyt-2 antigens of CTL, but not Lyt-1 antigens, in the absence of complement inhibited the nonspecific cytotoxicity resulting from NaIO4 modification of effector lymphocytes. These findings suggest that the mere interaction with or perturbation of appropriate cell surface molecule(s) of effector lymphocytes such as Lyt antigens by receptor-ligand interaction in SCMC or by NaIO4 modification in ODCC may lead to the expression of cytotoxicity. The present studies demonstrate a functional role of surface carbohydrates on CTL in cell-to-cell recognition and interactions. Furthermore, the results suggest that target cell modification is not a requisite for recognition and lysis in an antigen-nonspecific cytotoxic system such as ODCC. However, partial blocking of ODCC by alloantibodies directed against the H-2 of unmodified target cells suggests that NaIO4-modified CTL recognize unrelated target H-2 antigens. The implication of these findings on the molecular mechanism of cell-mediated cytotoxicity is discussed.
Mechanisms of protective immunity against Schistosoma mansoni infection in mice vaccinated with irradiated cercariae. IV. Analysis of the role of IgE antibodies and mast cells.
Authors: Sher A , Correa-Oliveira R , Hieny S , Hussain R 
Published: December 2022

Abstract
Mice resistant to challenge infection with Schistosoma mansoni by vaccination with highly irradiated cercariae were examined for the presence of circulating IgE antibodies and peritoneal mast cells sensitized against schistosome antigens. Significant levels of SWAP- or CAP-specific IgE antibodies could not be detected by solid phase radioimmunoassay in the sera of C57BL/6 mice during the first 6 wk after vaccination. Similarly, heatlabile antibodies capable of passively sensitizing normal mast cells for degranulation in response to SWAP could not be identified in the same sera. In contrast, peritoneal mast cells harvested from C57BL/6 mice 2 wk or later after vaccination gave strong degranulation responses when challenged with SWAP or CAP. Thus, vaccination with irradiated cercariae induces an unusual form of immediate-type hypersensitivity in which mast cells become sensitized in the absence of detectable circulating IgE antibodies. Mice deficient in mast cells (W/Wv mutant strain) were observed to develop the same resistance to challenge infection after vaccination with irradiated cercariae as nondeficient littermates. Similarly, vaccinated SJL/J mice were found to mount an extremely weak IgE response as measured by mast cell degranulation yet displayed the same level of resistance to challenge infection as other inbred mice developing potent mast cell responses. These findings argue that IgE antibodies and mast cells are not essential components in the effector mechanism of irradiated vaccine-induced immunity against schistosome infection.
Interleukin 2 deficiency in murine Leishmaniasis donovani and its relationship to depressed spleen cell responses to phytohemagglutinin.
Authors: Reiner N E , Finke J H 
Published: December 2022

Abstract
This study examined the kinetics and mechanisms of depressed spleen cell responses to phytohemagglutinin (PHA) that occur during Leishmania donovani infection of BALB/c mice. In co-culture experiments, neither spleen cells from infected animals nor parasite-infected macrophages suppressed PHA responses of normal spleen cells. In addition, parasite-mediated suppression of PHA-stimulated spleen cell proliferation could not be demonstrated. Mice with 2 wk of infection did manifest an impairment in spleen cell production of interleukin 2 (IL 2) and by 8 wk IL 2 activity in supernatants from these cells was reduced by approximately 95%. This finding was not explained by an alteration in the kinetics of IL 2 production. Furthermore, diminished IL 2 activity in supernatants of PHA-activated spleen cells from infected animals was not caused by suppressive factors in these fluids as shown by their inability to suppress IL 2 stimulation of IL 2-dependent T cells. When spleen cells from mice with 8 wk of infection were cultured with PHA and supplemented with exogenous IL 2, there was an approximately 48% increase in mitogenesis. These data indicate that abnormal PHA-induced spleen cell activation in BALB/c mice with L. donovani infection is associated with impaired production of IL 2. In addition, the observation that supplementation of spleen cells from infected mice with IL 2 resulted in partial reconstitution of the PHA response is consistent with a defect in IL 2 responsiveness.
Lack of general immunosuppression during visceral Leishmania tropica infection in BALB/c mice: augmented antibody response to thymus-independent antigens and polyclonal activation.
Authors: Colle J H , Truffa-Bachi P , Chedid L , Modabber F 
Published: December 2022

Abstract
Leishmania tropica causes a lethal visceral disease in highly susceptible BALB/c mice, with many immunopathologic features resembling those in human kala-azar. The responses to thymus-independent antigens of Type 1 and 2 (TI-1, TI-2) were compared in infected mice of susceptible BALB/c and resistant C57BL/6 strains at various times after infection. The infected BALB/c mice had an augmented response to both types of antigens at 45 days after infection. Later (day 76), the response to trinitrophenylated lipopolysaccharide (TNP-LPS, a TI-1 antigen) was diminished but that to dinitrophenylated Ficoll (DNP-Ficoll, a TI-2 antigen) remained statistically above the response of uninfected mice. The response of the resistant strain to either antigen was not modified as a result of the infection. Both strains showed significant polyclonal activation, which was considerably greater in the BALB/c than in the C57BL/6 mice. The observations presented here are in contrast to the widely held belief that a generalized nonspecific immunosuppression occurs in L. tropica infected BALB/c mice.
Effects of neonatal spleen cell products on the multiplication of toxoplasma in rat peritoneal macrophages.
Authors: Sakurai H , Igarashi I , Omata Y , Saito A , Suzuki N 
Published: December 2022

Abstract
We studied the resistance of newborn rats to infection with T. gondii. Neonates of chronically infected rats were significantly more resistant to infection with Toxoplasma than were the newborn of normal, uninfected rats. Neonatal athymic rats (nu/nu) from immune mothers were susceptible to infection, whereas normal littermates (nu/+) were very resistant. Rat peritoneal macrophage monolayers did not exhibit enhanced toxoplasmacidal activity after the addition of immune serum to the culture medium. However, inhibition of Toxoplasma multiplication was observed when the parasites were exposed to immune serum just before the infection of macrophages. The effects of spleen cell products from neonates of chronically infected mothers on the multiplication of Toxoplasma in rat peritoneal macrophages were examined. A significant inhibition of Toxoplasma multiplication occurred in macrophages incubated with the supernatants of spleen cell cultures obtained from immune newborn rats, with added lysate antigen. The ability to be induced to make an inhibitory supernatant disappeared by the third week after birth. Also examined were supernatants of spleen cells sensitized in vitro by incubation with a Toxoplasma lysate antigen; when these were added to macrophage monolayers, inhibition of Toxoplasma multiplication was observed only if the antigen was accompanied by supernatant of immune spleen cells.