bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies on the Mechanism of T Cell-Mediated Lysis at the Single Effector Cell Level
Authors: Zagury Daniel , Bernard Jacky , Jeannesson Pierre , Thiernesse Noëlle , Cerottini Jean-Charles 
Published: December 2022

Abstract
A procedure has been previously developed to allow kinetic analysis of target cell lysis in individual conjugates formed between murine alloimmune peritoneal exudate lymphocytes (PEL) and relevant tumor cells in suspension. Under the conditions used in the present work, 60% of the conjugates consisted of one lymphocyte bound to one target cell, whereas the remaining were multicellular, i.e., contained one lymphocyte bound to either two (24%), three (12%), or four (4%) target cells. Both ultrastructural studies and micromanipulation experiments with individual multicellular conjugates indicated differences in the degree of target cell binding to the same PEL. In more than 80% of the multicellular conjugates, lysis of all conjugated target cells occurred within a 3-hr incubation period at 37°C. Kinetic analysis of target cell lysis, however, showed that the time required for target cell death was quite variable, both within the same multicellular conjugate and between different conjugates, ranging from a few minutes to 3 hr after conjugation. By comparing the elapsed time necessary for lysis of 50% of the target cells in conjugates containing one lymphocyte bound to three target cells, it could be estimated that, on the average, lysis of the first, second, and third target cells occurred after 30, 60, and 90 min, respectively.
The time required for lethal hit of each conjugated target cell was measured by adding EDTA to the incubation medium of individual multicellular conjugates at various time intervals. Evidence could be obtained that a CTL induced irreversible lesions in only one of the conjugated target cells at a time, i.e., lethal hits were given sequentially rather than simultaneously.
Glucocorticoid-Induced Inhibition of T Cell Growth Factor Production
Authors: Gillis Steven , Crabtree Gerald R. , Smith Kendall A. 
Published: December 2022

Abstract
Although it has been clearly established that glucocorticoids inhibit mitogen- or antigen-induced lymphocyte proliferation, the mechanism underlying this effect has remained ill-defined. Recently, it has become evident that T cell proliferation is mediated by a soluble T cell growth factor (TCGF) released by mitogen/antigen stimulated T cells. Therefore it seemed probable that the inhibitory effects of glucocorticoids were manifested either at the level of TCGF production or at the level of the activated T lymphocyte. We found that differentiated cytolytic T lymphocytes harvested from TCGF-dependent long-term culture were only mildly sensitive to inhibitory effects (25 to 30% inhibition) of glucocorticoids as measured by decreased cellular proliferation and the incorporation of tritiated thymidine. The degree of inhibition observed was most probably mediated through glucocorticoid receptors in that the half maximal inhibitory glucocorticoid concentration correlated with half-maximal glucocorticoid receptor saturation. In contrast, we found that mitogen-induced TCGF production and T cell proliferation were completely inhibited by pharmacologic concentrations of dexamethasone (10-6 M). Finally, the TCGF supplementation of mitogen-stimulated cultures treated with maximal inhibitory concentrations of dexamethasone resulted in complete amelioration of glucocorticoid suppression. These results indicate that a major mechanism of glucocorticoid-mediated immunosuppression may occur at the level of the TCGF-producing cell, resulting in the control of clonal expansion of activated T cells via inhibition of TCGF production.
Signal Requirements for T Lymphocyte Activation
Authors: Rosenstreich David L. , Mizel Steven B. 
Published: December 2022

Abstract
Purified guinea pig T lymphocytes cannot be induced to proliferate by plant lectins in vitro unless they are reconstituted with either macrophages or a macrophagederived soluble factor. The effects of phorbol myristic acetate (PMA) on the activation of this purified T lymphocyte population were studied. Although PMA by itself was nonmitogenic for guinea pig T cells, at very low concentrations (10-5 µg/ml) it enabled purified T cells to respond to the lectins, PHA or Con A. However, it could not induce primed T cells to respond to a soluble antigen in the absence of macrophages. On the basis of several criteria, PMA appeared to be acting independently of macrophages. Its effect was unrelated to the number of macrophages in a lymphocyte preparation and it did not increase the accessory capability of additional macrophages.
Analysis of the kinetics of the interaction between PMA, lectins, and T cells revealed that these compounds could be added to the T cells independently and in any order and still induce activation. However, maximal T cell proliferation required that PMA and lectin be added within the first 4 hr of culture. In addition, both agents were capable of exerting their effects after a brief (1 hr) exposure. The results of this study indicate that PMA can replace macrophages as a source of the second signal that is required to induce T cell proliferation in vitro. This agent may prove to be extremely valuable in the analysis of both the biochemical alterations involved in the process of T cell activation, and the mechanism by which macrophages induce these alterations.
Direct suppression of lymphocyte induction by the immunoregulatory human serum low density lipoprotein, LDL-In.
Authors: Fujii D K , Edgington T S 
Published: December 2022

Abstract
Preparations of LDL-In, an immunosuppressive lipoprotein subfraction, were analyzed for the capacity to directly suppress the response of human lymphocytes to the representative stimulant PHA vis-a-vis indirect mechanisms mediated by soluble factors or cell:cell interactions. Serum lipoprotein subfraction enriched in LDL-In induced a suppressed state in lymphocytes during 18-hr induction cultures. These lymphocytes, whether partially or completely suppressed, when added to fresh responder lymphocytes in the presence of PHA did not suppress the response of the responder lymphocytes. In contrast, the major low density lipoprotein (LDL) did not suppress lymphocytes at equivalent concentration in the induction culture, nor did LDL-exposed lymphocytes suppress responder lymphocytes. The supernatant medium from LDL-In-suppressed lymphocytes did not contain a newly synthesized or released suppressive factor. Finally, LDL-In-suppressed lymphocytes were not rescued by normal lymphocytes. Each of these observations, and previous evidence that adherent cells do not mediate the biologic effects of LDL-In, support the hypothesis that the biologic manifestations of LDL-In suppression of lymphocyte function result from a direct effect on the lymphocyte that is exposed to this lipoprotein, possibly via the previously demonstrated LDL-In receptor.
Human granulocyte-specific nuclear antigen(s). II. Detection of antigens in human proliferative syndromes.
Authors: Briggs R C , Forbes J T , Hnilica L S , Montiel M M , Thor D E 
Published: December 2022

Abstract
Antisera raised to dehistonized chromatin from isolated normal human granulocytes revealed the presence of chromatin-associated antigens specific for the human neutrophils that appear during late stages of myeloid cellular differentiation. Immunological specificity was demonstrated by C fixation, immunodiffusion, and immunocytochemical reactions. Chromatin prepared from both normal granulocytes and specimens of myeloid leukemia showed immunologic reactivity. Although the normal antigens were detected in a specimen of CML, the position of immunodiffusion precipitin lines was different from that obtained with normal granulocyte chromatin. In addition, chromatin prepared from the myeloid leukemic cell line HL-60 expressed only one of the three precipitin bands normally found in immunodiffusion. The immunocytochemical staining reaction was confined to the nucleus of mature neutrophils in normal peripheral blood smears. Greater than 90% of cells in peripheral blood specimens of CML showed positive immunocytochemical nuclear staining. In other types of leukaemia, the normal mature granulocyte reacted with antiserum, but the nonmyeloid leukemic cells in these specimens did not. The specificity of immunologic reactions described here suggests the usefulness of nuclear antigens as cell markers.
Allogeneic radiation chimeras respond to TNP-modified donor and host targets.
Authors: Lattime E C , Gershon H E , Stutman O 
Published: December 2022

Abstract
Tolerance to major histocompatibility antigens as well as the ability to mount a cytotoxic response to hapten-modified cells of bone marrow donor and host origin was studied in allogeneic radiation chimeras. Lethally irradiated (C57BL/6 X DBA/2)F1 hosts reconstituted with anti-Thy 1.2 + C-treated bone marrow from (C57BL/6 X CBA)F1 mice showed tolerance to the MHC antigens of the three parental strains as measured by MLC and CML assay. The chimeras responded normally to unrelated allogeneic cells. Chimeric animals generated a cytotoxic response to hapten-modified cells of both donor (CBA) and host (DBA/2) haplotypes, as well as to C57BL/6, demonstrating that tolerance to the hapten-presenting host haplotype is sufficient to allow a cytotoxic antihapten response, and that processing through a semiallogeneic host environment does not affect the ability to generate a response to hapten in conjunction with self-determinants. Chimeras failed to mount a cytotoxic response to hapten presented on nontolerated allogeneic spleen cells.
Mechanisms of recovery from viral infections: destruction of infected cells by neutrophils and complement.
Authors: Grewal A S , Rouse B T , Babiuk L A 
Published: December 2022

Abstract
Highly enriched populations of bovine neutrophils (PMN) were able to destroy herpesvirus-infected cells when in the presence of C. This mechanism of cytotoxicity was termed C-dependent neutrophil-mediated cytotoxicity (CDNC). To demonstrate CDNC required viable PMN, an active source of C, and a target cell expressing viral antigens. Noninfected cells were not susceptible to lysis. Several approaches were used to exclude the presence of antibody as an explanation for the cytotoxicity observed. In a comparison of the effectiveness of different cell types at mediating CDNC, PMN were more effective than macrophages, and lymphocytes were without activity. The results was discussed in terms of the possible in vivo significance of the neutrophil as a cell type capable of mediating recovery from infection, since if a mechanism similar to CDNC occurs in vivo, this could play a role in defense before the time when protective levels of antibody and immune cells are generated.
Neonatal susceptibility to MHV3 infection in mice. II. Role of natural effector marrow cells in transfer of resistance.
Authors: Tardieu M , Héry C , Dupuy J M 
Published: December 2022

Abstract
Protection of newborn mice against MHV3 infection requires the transfer of several cell populations originating from adult syngeneic donors: adherent spleen cells, T lymphocytes, and a third population present in the nonadherent spleen cell fraction, in peritoneal exudates, and in bone marrow cells (M cells). M cells were found to be sensitive to short-term incubation at 37 degrees C and to preincubation with anti-bone marrow antiserum, mitomycin C, puromycin, and aggregated Ig, the latter suggesting the presence of Fc receptors. They were resistant to silica particles but were sensitive to irradiation with x-rays as well as with 89Strontium. Nonadherent spleen cells, however, behaved differently from M cells toward x-irradiation since they were radio-resistant, suggesting that M cells are precursors that require further differentiation or division to participate in MHV3 resistance. Effector M cells responsible for MHV3 resistance display, therefore, some similarities with natural killing cells. They might belong to a group of effector cells operative in regulatory processes or anti-tumor surveillance but also may be defense mechanisms against infectious diseases.
Antibody gene linkage studies in (NZB X C58) recombinant-inbred lines.
Authors: Riblet R , Claflin L , Gibson D M , Mathieson B J , Weigert M 
Published: December 2022

Abstract
A set of recombinant inbred mouse strains has been constructed from the cross of NZB by C58. These strains provide new tools for the analysis of antibody heavy and light chain genes and NZB autoimmunity. Typing of heavy chain genes confirmed the allotype linkage of the dextran response locus Igh-Dex. One strain has fixed a recombinant chromosome carrying NZB allotype genes and the Dex+ variable region gene from C58. Two kappa-light chain variable region genes, Igk-Pc and Igk-Ef1, co-segregated with the Lyt-2 lymphocyte alloantigen locus. This confirms the tight linkage of these loci and decreases the maximum estimate of the recombination frequency between them to 1.7%.
Bactericidal activity of eosinophil peroxidase.
Authors: Jong E C , Henderson W R , Klebanoff S J 
Published: December 2022

Abstract
A partially purified preparation of guinea pig eosinophil peroxidase was found to be bactericidal when combined with H2O2 and either iodide, bromide, chloride, or thiocyanate ions. The EPO-H2O2-halide bactericidal system had an acid pH optimum and was inhibited by the proteins albumin and gelatin and by the hemeprotein inhibitors azide, cyanide, and aminotriazole. When the EPO concentration of the reaction mixture was lowered, the bactericidal effect at pH 7.0 was lost first with chloride, then with bromide, and finally with iodide as the halide. Activity with physiologic concentrations of chloride was favored by a relatively high EPO level, a decrease in pH below neutrality and an absence of extraneous protein. These findings are discussed in relation to the potential role of the peroxidase system in the intracellular and extracellular toxic reactions of eosinophils.
Specific enhancement of immune responses by BCG: isolation of extracellular DNA from supernatants of specifically stimulated BCG-primed lymphoid cells.
Authors: Alaba O 
Published: December 2022

Abstract
When lymphocytes obtained from W/Fu rats primed with BCG are cultured in the presence of PPD, they elaborate a factor that is capable of potentiating the specific in vitro generation of cytotoxic lymphocytes to syngeneic (C58NT)D lymphoma cells and to BN alloantigen. Purification of the factor, achieved by gel filtration on Sephadex G-100, was facilitated by using a serum-free culture condition and the removal of the specific stimulating antigen, PPD, after an initial incubation period. The factor isolated contains DNA by its absorption spectrum, resistance to trypsin and RNase, but complete susceptibility to DNAase, and by the presence of ethidium bromide-positive material in the purified sample. It displays a 260/280 nm absorption ratio of 1.6 and a m.w. estimate of 10,000 to 30,000. Electrophoresis of the purified factor on agarose gel yielded three ethidium bromide reactive bands. Data obtained following the slicing and elution of these bands, and then testing for potentiating activity indicated that two of the three bands contained potentiating activity.
OKT3: a monoclonal anti-human T lymphocyte antibody with potent mitogenic properties.
Authors: Van Wauwe J P , De Mey J R , Goossens J G 
Published: December 2022

Abstract
OKT3, a monoclonal anti-human T cell antibody (IgG2), was found to induce DNA synthesis in human peripheral lymphocyte cultures. OKT3 induced maximal mitogenesis at a concentration of 10 to 20 ng/ml and was about 20-fold more potent than PHA as a mitogen. No high-dose inhibition of thymidine incorporation was noticed at concentrations up to 2.5 microgram OKT3/ml. The monovalent Fab fragment of OKT3 was also mitogenic but about 100 times less potent than the parent IgG. OKT3 appeared to be a T lymphocyte mitogen as only sheep red blood cell rosetting lymphocytes were responsive. Quantitative studies on the binding of 125I-labeled Fab fragment of OKT3 to human lymphocytes showed an average of 5.1 x 10(4) receptor sites/cell with an association of about 10(8) M-1 at 37 degrees C, with no heterogeneity of the cell binding sites. These data suggest a strong interaction of the monoclonal OKT3 with a limited number of identical T cell membrane receptors. As this interaction can trigger mitogenesis, the cell membrane determinant recognized by OKT3 could be described as a "T cell stimulation receptor." The mitogenecity of the lymphocytes is not solely dependent on cross-linking of these receptors.
Structural polymorphism of murine C4 and its linkage to H-2.
Authors: Natsuume-Sakai S , Kaidoh T , Nonaka M , Takahashi M 
Published: December 2022

Abstract
Heretofore unrecognized structural polymorphism of murine C4(Ss) was demonstrated by using two different techniques: immunofixation electrophoresis and immunofixation isoelectric focusing. By these methods C4 was demonstrated as a broad protein band in freshly bled EDTA-plasma of inbred strains and wild mouse lines. Seven variants of C4(Ss) were identified among a large number of mice tested:C4-v (pI 7.7) exemplified by strain SM/J, C4-B(pI 7.5) exemplified by B10, C4-k (pI 7.3) exemplified by C3H/He, C4-bactrianus (pI 7.2) exemplified by Mus m.bacterianus, C4-d.s(pI 7.0) exemplified by DBA/2 and SJL/J, C4-castaneus (pI 6.6) exemplified by Mus m.castaneus, and C4-NC(pI 6.3) exemplified by NC. F1 hybrid exhibited two C4 bands, each of which corresponds to C4 of a parent. The possibility that the observed polymorphism represents variation of Slp was ruled out because an identical C4 pattern was always observed between male and female mice. The observed structural variation of murine C4 is controlled by a single codominant locus localized within or in the proximity of the S subregion of H-2. This was shown by phenotyping several intra-H-2 recombinant strains and backcross progeny, (B10 X NC)F1 X B10 and (B10 X NC)F1 X NC. An alloantiserum specific for one of the C4 variants (C4-NC) was successfully produced in C3H/He mice by repeated injection of purified C4 of NC mouse. This finding suggests that observed C4 variants or at least some of them represent antigenically distinguishable allotypes of murine C4.
Demonstration of a chemotactic factor receptor on macrophages.
Authors: Snyderman R , Fudman E J 
Published: December 2022

Abstract
Certain synthetic N-formylated peptides are potent chemotactic agents for phagocytic cells. We have identified a specific, high affinity receptor for the chemotactic peptide fMet-Leu-[3H]Phe on inflammatory as well as on resident guinea pig peritoneal macrophages. The receptor on inflammatory macrophages has an equilibrium dissociation constant (KD) of 11 nM at room temperature, and there are approximately 10,000 binding sites per cell. The receptor on resident peritoneal macrophages has a KD of 7 nM with approximately 12,000 sites per cell. The increased chemotactic responsiveness of inflammatory macrophages as compared to resident macrophages is probably not due to differences in the fMet-Leu-[3h]phe receptor since the number of binding sites per cell and the KD are quite similar. The specificity of the binding site on both cell types for a series of N-formylated peptides correlates well with the ability of the peptides to initiate macrophage chemotaxis. These studies suggest that the chemotactic response of guinea pig peritoneal macrophages to N-formylated peptides is initiated by the binding of the peptides to a specific cell-surface receptor.
Identification of a major serum DNA-binding protein as factor B of the alternative complement pathway.
Authors: Gardner W D , Haselby J A , Hoch S O 
Published: December 2022

Abstract
One of the major proteins in human serum capable of binding DNA has been shown to be factor B of the alternative pathway of complement activation. This protein, designated DNA-binding protein-2 (DBP-2), is recognized by antisera directed against both factor B and its activated form, fragment Bb. Its m.w., charge microheterogeneity, and amino acid composition correspond closely with reported values for those properties of factor B. A radioimmunoassay was used to estimate the serum concentration of DBP-2 at 266 +/- 83 microgram/ml, which also corresponds with the level of factor B normally present in the serum. DBP-2 functions as factor B in the activation of factor B-depleted serum. Limited proteolytic treatment of DBP-2 produced a fragment pattern resembling that of factor B both in the m.w. of the fragments and their electrophoretic mobilities. By means of DNA affinity chromatography of the fragments produced by trypsinization, the DNA-binding domain of DBP-2 was localized.
Monogamous bivalency of IgG antibodies. I. Deficiency of branched ABHI-active oligosaccharide chains on red cells of infants causes the weak antiglobulin reactions in hemolytic disease of the newborn due to ABO incompatibility.
Authors: Romans D G , Tilley C A , Dorrington K J 
Published: December 2022

Abstract
This study shows that monogamous bivalency of human IgG anti-A and anti-B is necessary to maintain sensitization of red cells in the antiglobulin test. On red cells of infants and of adults of i phenotype, the known deficiency of branched ABHI-active oligosaccharide chains limits monogamous bivalency, and these accounts for the relatively weak direct antiglobulin reactions in hemolytic disease of the newborn due to ABO incompatbility. One corollary of this finding is that there is strong biologic selection against the transition on fetal red cells from the straight-chain i phenotype to branched-chain I phenotype, since such branching of cell-surface oligosaccharide chains would compromise ABO-incompatible pregnancies.
Evidence for the influence of the initial complement components on the assembly and activity of the membrane attack complex.
Authors: Boyle M D , Ohanian S H 
Published: December 2022

Abstract
The failure of functionally purified C5gp to reconstitute the hemolytic complement (C) activity of C5-deficient human serum was studied. The lack of hemolytic activity of C5gp in this system could not be correlated with the failure of EAC1-3hu to bind and activate C5gp, but was related to the failure of EAC1-3hu5gp6hu to efficiently bind C7hu in a form that would lead to lysis when HuC8 and HuC9 were added. This failure was not observed with EAC1-3gp5gp6hu or EAC1-3hu5hu6hu, which could be lysed with any combination of human or guinea pig C7 through C9. The implications of these findings on the control of the lytic C attack mechanism by the initial components in the C cascade are discussed.