bluuebunny/crossref_metadata_2025_split huggingface dataset:
The ability of lymphokine and lipopolysaccharide to induce procoagulant activity in mouse macrophage cell lines.
Authors: Farram E , Geczy C L , Moon D K , Hopper K 
Published: December 2022

Abstract
A comparison was made of the abilities of mouse macrophage cell lines and cultured bone marrow-derived macrophages to respond to lymphokine and lipopolysaccharide (LPS) in the macrophage procoagulant assay (MPCA). Mouse macrophage cell lines PU5 and WEHI 265 responded to low concentrations of lymphokine and LPS by increased procoagulant activity; the activity of PU5 cells was comparable to that of TG-PEC. Approximately one-half of the MPCA induced by lymphokine after 20 hr culture was detectable after 2 hr with either cell line. J774 was unresponsive to LPS but responded weakly to lymphokine, and P388D1 and WEHI 274 were unresponsive to both stimuli as determined by the MPCA test. Addition of purified T cells (five T cells to one macrophage) to the unresponsive cell lines induced procoagulant activity in the presence of either stimulus, which suggests that cell contact is necessary in some cases. Only J774 cells responded to lymphocyte-derived chemotactic factor (LDCF) or endotoxin-activated mouse serum (EAMS) in chemotaxis assays. Immature bone marrow cells responded to chemotactic stimuli, and procoagulant activity was induced with lymphokine after 4 days in culture. Cells cultured for 7 days had about twice as much MPCA, but further culturing did not result in cells with enhanced activity. The procoagulant responsiveness of different macrophage cell lines to lymphokine or LPS may reflect differences in the maturation and differentiation states of these cells.
Two surface antigens expressed on proliferating mouse T lymphocytes defined by rat monoclonal antibodies.
Authors: Takei F 
Published: December 2022

Abstract
A hybrid cell line resulting from the fusion of a Con A-activated normal mouse spleen cell and a transformed mouse T cell (EL-4BU) has been used to prepare and select rat monoclonal antibodies reactive with molecules expressed on the surface of proliferating, as opposed to resting, mouse T cells. In this report, the characterization of two such antigens identified in this way is described. One antigen is a membrane component common to mitogen-activated T and B cells, some bone marrow cells, and various transformed cell lines but is not detectable on either normal thymocytes or the majority of spleen cells by radioimmunoassay or FACS analysis. It has a m.w. of approximately 200,000 daltons under nonreducing conditions and 100,000 daltons under reducing conditions. Antibodies to this antigen precipitate cell-bound transferrin but do not react directly with transferrin itself. It would thus appear that the antigen is the transferrin receptor molecule. The second antigen is not detectable on normal thymocytes, spleen cells, bone marrow cells, or mitogen-stimulated spleen cells but is expressed at high levels on some transformed T cell lines. It, too, appears to be a dimer, with a m.w. of 95,000 daltons under nonreducing conditions, decreasing to 50,000 daltons under reducing conditions. Although the function of the 95,000-dalton antigen is not yet known, its lack of expression on adult T cell populations both before and after activation suggests either a short-lived role at a very early stage of T cell development and/or an association with T cell transformation.
Decreased C5b67-inhibitor activity in two families with hereditary functional deficiency of the eighth component of complement.
Authors: Zeitz H J , Zeff R A , Gewurz H , Lint T F 
Published: December 2022

Abstract
In addition to its role in hemolysis and host defense against Neisseria infection, the eighth component of human complement (C8) is one of several plasma proteins that are C5b67-inhibitors (C5b67-INH). The recent identification in our laboratory of two new families with hereditary deficiency of C8 provided an opportunity to study further the role of C8 as a C5b67-INH. Based on mixing and reconstitution experiments, the deficiency of C8 seemed to be due to a selective lack of the C8 beta-chain in one family and the C8 alpha-gamma subunit in the other family. Sera from individuals homozygous for the C8 abnormality were substantially deficient in C5b67-INH activity as well as totally deficient in hemolytic activity. Sera from control individuals possessed approximately 2500 C5b67-INH U/ml, whereas sera from the C8-deficient individuals had markedly depressed C5b67-INH activity, with a mean of only 428 U/ml. C5b67-INH activity was completely reconstituted in C8-deficient serum by the addition of purified human C8. We conclude that C8 constitutes the substantial majority of the C5b67-INH activity of normal human serum.
Cell-bound C4b resists reduction by reducing agents: analysis by chain structure and by hemolytic activity.
Authors: Ejzemberg R , Brown E J , Ohanian S H , Hammer C H , Borsos T 
Published: December 2022

Abstract
EA3H-C4hu treated with 2-mercaptoethanol (MSH) or dithiothreitol (DTT) were analyzed for residual chains and hemolytic activity. MSH treatment resulted in no loss of the chains of C4b and no loss of reactivity with a polyclonal anti-human C4 rabbit antibody, and the cells did not lose their ability to generate SAC4b2a. DTT-treated cells lost about 70% of the gamma-chain and over 95% of C4b activity; there was no loss of alpha' and beta chains or the ability to react with anti-C4 antibody. Kinetic studies indicated that the remaining 30% of the gamma-chains could not be removed by prolonged incubation with DTT, implying heterogeneity of cell bound C4b. The data also imply that the gamma-chain is important in the generation of SAC4b2a.
Characterization of mast cell precursors by physical means: dissociation from T cells and T cell precursors.
Authors: Yung Y P , Wang S Y , Moore M A 
Published: December 2022

Abstract
Murine bone marrow precursors (MCP) differentiate into mast cells and proliferate in response to mast cell growth factor (MCGF). An assay system based on the incorporation of [3']thymidine by proliferating mast cells in response to substantially purified MCGF was used to titrate MCP. Murine bone marrow was separated into fractions by Percoll density gradient centrifugation or velocity sedimentation at unit gravity. Individual fractions were analyzed to determine the relative concentrations of MCP. To determine if mast cells were derived from precursors different from those for T lymphocytes and granulocytes and macrophages, separated cells were also analyzed for responsiveness to interleukin 2 (IL 2) in standard [3H] thymidine incorporation assays and to granulocyte-macrophage colony stimulating factors (CSF) in agar cloning (CFU-GM) assays. Cultured marrow cells from Dexter type long-term marrow cultures (LMC) were included as a source of marrow cells devoid of mature T cells, so as to dissociate MCP from pre-T cells. MCP were readily dissociable from T cells and/or pre-T cells present in fresh, as well as cultured, marrow cells by either density or velocity of sedimentation separation techniques. MCP were, however, not readily separable from CFU-GM. Nevertheless, MCP appeared not to share a common precursor with pure macrophage type colony-forming cells (CFU-M phi). The implications of the findings on the lineage origin of mast cells were discussed.
The malaria merozoite surface: a 140,000 m.w. protein antigenically unrelated to other surface components on Plasmodium knowlesi merozoites.
Authors: Hudson D E , Miller L H , Richards R L , David P H , Alving C R , Gitler C 
Published: December 2022

Abstract
We previously identified three proteins on the surface of merozoites (140,000, 105,000 and 75,000 m.w.). To determine if 140,000 m.w. protein was related to other surface proteins, we immunized mice with liposomes containing merozoite proteins from the 140,000 m.w. region of the polyacrylamide gel. The immune sera reacted with the surface of viable merozoites and acetone-fixed schizonts by immunofluorescence. The sera immunoprecipitated only the 140,000 m.w. protein from surface-labeled merozoites. We demonstrated that monoclonal antibody 13C11 immunoprecipitated a 250,000 m.w. protein from metabolically labeled schizonts and bound to the merozoite surface. This monoclonal antibody immunoprecipitated the 75,000 and lower m.w. proteins from surface-labeled merozoites but did not bring down the 140,000 m.w. protein. Because the mouse immune sera did not immunoprecipitate the 250,000 m.w. protein from metabolically labeled schizonts or proteins other than the 140,000 m.w. protein from surface-labeled merozoites, we conclude that the 140,000 m.w. protein is unrelated to other merozoite surface antigens identified to date. The mouse immune sera against the 140,000 m.w. protein on the merozoite surface did not immunoprecipitate a 140,000 m.w. protein from metabolically labeled schizonts. Instead, the major protein immunoprecipitated had a m.w. of 144,000. By analogy to the 250,000 m.w. protein and its cleavage products, we propose that the 140,000 m.w. protein on the merozoite surface is a cleavage product of the higher m.w. protein.
A unique antigen expressed on myeloid cells and acute leukemia blast cells defined by a monoclonal antibody.
Authors: Ball E D , Graziano R F , Fanger M W 
Published: December 2022

Abstract
A murine hybridoma-derived monoclonal antibody, PM-81, was obtained from a fusion of cells of the NS-1 myeloma cell line with cells from a mouse immunized with the HL-60 promyelocytic leukemia cell line. This cytotoxic IgM monoclonal antibody was specific for myeloid cells. Employing indirect immunofluorescence and flow cytometry, we determined that this antibody reacts strongly with normal human granulocytes, eosinophils, and monocytes but not lymphocytes (including phytohemagglutinin-activated lymphocytes), null cells, red blood cells, or platelets. Moreover, the PM-81 antibody reacts with leukemia cells from 19 of 22 patients with acute myelocytic leukemia of all FAB subclasses, three of three patients with common acute lymphocytic leukemia, four of four patients with chronic myelocytic leukemia (CML) in myeloid blast crisis (terminal transferase (TdT)-negative) but did not react with cells from two patients with CML in lymphoid blast crisis (TdT-positive) or five patients with chronic lymphocytic leukemia. The myeloid cell lines HL-60, K562, KG-1, and U937 were all reactive with PM-81. The lymphoid lines CCRF-CEM and Daudi did not express PM-81 but HSB-2 was positive. The PM-81 antigen was absent on myeloid and erythroid progenitor cells as determined by their insusceptibility to complement-dependent lysis. In addition, only PM-81-unreactive cells were capable of colony formation. Furthermore, the PM-81 antibody does not appear to induce modulation of the antigen to which it binds. Thus, this monoclonal antibody appears to fulfill several criteria for clinical utility in the diagnosis and treatment of both acute myelocytic and acute lymphocytic leukemia.
Characterization of cloned cytotoxic lymphocytes with NK-like activity.
Authors: Acha-Orbea H , Groscurth P , Lang R , Stitz L , Hengartner H 
Published: December 2022

Abstract
Cloned H-2b-restricted male antigen-specific cytotoxic T cells were kept in culture in the presence of IL 2 for over 2 yr. During this time, they lost their antigenic specificity and now exhibit high NK-like activity. Three separate clones HY 1, HY 2, and HY 3 and their subclones, when tested on a panel of NK-sensitive and NK-insensitive target cells, showed typical lysis patterns of NK cells. Three cytotoxicity-loss mutants were obtained by subcloning. At least one of these cytotoxicity-loss mutants still exhibited binding to NK-sensitive target cells. The various HY clones were compared with cloned alloreactive cytotoxic T cells of B10 anti-B10.D2 specificity with respect to surface markers, target specificity, kinetics of lysis, morphology, and influence of monoclonal antibodies and chemicals on cytotoxicity. Only one major difference between cloned NK-like and alloreactive T cells was detected: monoclonal anti-Lyt-2 antibodies inhibited cytotoxic activity of alloreactive T cells but not of NK-like cells, although both expressed Lyt-2 on their surface. Morphologically, HY cells were characterized by numerous lysosomal granules in their cytoplasm. Clones with NK-like activity differed from cytotoxicity-loss mutants by both ultrastructural appearance and enzyme histochemistry of lysosomes. Interaction of NK-like cells with YAC-1 cells induced membrane lesions of variable size in target cells. Effects of chemicals influencing lysosomal pathways such as monensin, NH4Cl, and chloroquine on cytotoxicity were investigated. Monensin as well as NH4Cl inhibited cytotoxicity of NK as well as alloreactive clones, whereas chloroquine did not. Spleen cells from acutely virus-infected mice with high NK reactivity showed the same behavior except for chloroquine, which was slightly inhibitory. The addition of monensin to the cells resulted in morphologic changes in the lysosomal granules. These data strongly suggest that NK-like killing is triggered by unknown substance(s) released from lysosomes of effector cells. Cloning of antigen-specific cytotoxic T cells under conditions of limiting dilution and continuous growing in medium containing Con A supernatant but not the relevant antigen often leads to loss of specificity and appearance of NK-like activity. The results presented are representative of a great amount of work in this and probably many other laboratories attempting to clone cytotoxic effector T cells.
Studies on the mechanism of natural killer cytotoxicity. III. Activation of NK cells by interferon augments the lytic activity of released natural killer cytotoxic factors (NKCF).
Authors: Wright S C , Bonavida B 
Published: December 2022

Abstract
The mechanism by which interferon (IFN) pretreatment of effector cells augments natural killer (NK) cell-mediated cytotoxicity (CMC) was examined by determining whether IFN has any effect on the production of natural killer cytotoxic factors (NKCF). NKCF are released into the supernatant of co-cultures of murine spleen cells and YAC-1 stimulator cells, and their lytic activity is measured against YAC-1 target cells. It was demonstrated that pretreatment of effector cells with murine fibroblast IFN or polyinosinic-polycytidylic acid (pIC) resulted in the release of NKCF with augmented lytic activity. Evidence indicated that the IFN-induced augmentation of NKCF activity required protein synthesis during the IFN pretreatment period, because concurrent pretreatment with both IFN and cycloheximide abrogated the IFN effect. Protein synthesis, however, is not required for the production of base levels of NKCF because emetine pretreatment of normal spleen cells did not result in a decrease in NKCF production. Furthermore, substantial levels of NKCF activity could be detected in freeze-thaw lysates of freshly isolated spleen cells. Cell populations enriched for NK effector cells, such as nylon wool-nonadherent nude mouse spleen cells, produced lysates with high levels of NKCF activity, whereas lysates of CBA thymocytes were devoid of NKCF activity. Pretreatment of spleen cells with either IFN or pIC resulted in an augmentation of the NKCF activity present in their cell lysates. Taken altogether, these findings suggest that freshly isolated NK cells contain preformed pools of NKCF. Pretreatment of these cells with IFN causes de novo synthesis of additional NKCF and/or activation of preexisting NKCF. According to our model for the mechanism of NK CMC, target cell lysis is ultimately the result of transfer of NKCF from the effector cell to the target cell. The evidence presented here suggests that the IFN-induced augmentation of NK activity could be accounted for by an increase in the synthesis, activation, and/or release of NKCF.
Alterations in lymphocyte homing patterns within mice exposed to ultraviolet radiation.
Authors: Spangrude G J , Bernhard E J , Ajioka R S , Daynes R A 
Published: December 2022

Abstract
This report presents the results of an investigation designed to establish whether exposure of mice to ultraviolet radiation (UVR) is capable of influencing the factors that control the distribution of lymphoid cells in vivo. We found that such exposure resulted in a dramatic and long-lasting increase in the tropism of peripheral lymph nodes for circulating lymphoid cells. Termination of UVR exposure did not result in a reversal of this phenomenon. Since an increase in lymphocyte migration into the lymph nodes of UVR-exposed mice was apparent within 2 hr of infusion of the radiolabeled cells, we conclude that the homing assay data reflect a relatively increased binding of circulating lymphocytes to high endothelial venules (HEV) within the lymph nodes of irradiated animals. A histologic analysis of skin from UVR-exposed mice established that the dermal microvasculature had expanded in terms of size and number of vessels, a condition that also does not completely reverse after the termination of treatments. In spite of the increase in dermal microvasculature, very few inflammatory cells were detected in the irradiated skin site. These observations support our conclusion that the enhanced traffic of lymphocytes into peripheral lymph nodes of UVR-exposed mice occurs primarily via lymphocyte-HEV interactions rather than afferent drainage of the irradiated skin.
Augmentation of syngeneic tumor-specific immunity by semiallogeneic cell hybrids.
Authors: Toffaletti D L , Darrow T L , Scott D W 
Published: December 2022

Abstract
Hybrid cell lines were established from fusions between lipopolysaccharide- (LPS) stimulated C57BL/6J spleen cells and MPC-11 tumor cells (45.6TG1.7, abbreviated M45), and were tested for their ability to immunize semiallogeneic mice against a parental tumor challenge. These hybrids were tumorigenic in syngeneic (BALB/c X C57BL/6J) F1 (CB6F1) mice but did not grow in semiallogeneic (BALB/c X A/J) F1 (CAF1) mice. All hybrids express both parental major histocompatibility antigens (H-2b and H-2d) as detected by indirect immunofluorescence and by their ability to function as either stimulators or targets for allogeneic cytotoxic lymphocytes (CTL). M45 tumor-associated antigens (TAA) were expressed on the hybrid surface as shown by their ability to act as either stimulators or targets for syngeneic CTL specific for M45 TAA. Immunization of semiallogeneic CAF1 mice with the hybrids i.p. followed by a challenge with M45 tumor cells resulted in extended survival when compared to untreated mice or animals immunized i.p. with M45 tumor cells. This immunity was specific and was not due to an allogeneic effect; immunization with an unrelated H-2bd tumor, 70Z/3, or H-2bd B6D2F1 spleen cells or with semiallogeneic spleen cells plus M45 did not protect mice from M45 challenge. Interestingly, prophylactic priming with semiallogeneic hybrid tumor cells or parental myeloma cells led to M45-specific CTL and "help" for an in vitro CTL response; however, the degree of CTL priming by hybrid tumors was not augmented when compared to the level of CTL achieved with parental tumor alone. Hence, stimulation of CTL activity per se by hybrid tumor cells cannot explain the protective effect of hybrid tumor immunization. These studies nevertheless confirm that semiallogeneic hybrids, which we show express TAA and alloantigens, can be used to immunize mice against a lethal syngeneic myeloma tumor challenge.
Parenteral immunization causes antigen-specific cell-mediated suppression of an intestinal IgA response.
Authors: Koster F T , Pierce N F 
Published: December 2022

Abstract
Rats immunized s.c. with cholera toxin (CT) or toxoid (CTd) show antigen-specific suppression of the jejunal IgA anti-CT response to subsequent enteric doses of CT. We determined whether this effect was partly cell-mediated and studied the suppressor cell response involved. Spleen cells from s.c.-immunized rats suppressed the jejunal anti-CT response in adoptive recipients when cell transfer was at, or 4 days before, intraduodenal priming with CT. Transferred suppression was antigen-specific, and the suppressor cells were nylon wool-nonadherent. Increasing the s.c. dose of CT from 0.1 to 40 micrograms, and the interval between immunization and cell harvest from 2 to 16 wk, each increased the suppressive effect of a constant spleen cell inoculum. After s.c. immunization, suppressor cells were present in the spleen within 1 to 2 wk, among TDL within 4 to 8 wk, and in Peyer's patches and thymus within 8 to 16 wk; this sequence suggested they arose in the spleen and later migrated to mucosae and the thymus. Prior splenectomy did not alter the suppressive effect of s.c. CT, however, nor did it prevent suppressor cell appearance among TDL, indicating that suppressor cells also arose from nonsplenic sites. Transferred suppressor cells acted by interfering with the development of specific immunologic memory within Peyer's patches during enteric priming; transfer of suppressor cells at the time of enteric boosting had no effect upon the secondary mucosal anti-CT response. We conclude that the suppressive effect of s.c. immunization on a specific mucosal IgA response is due largely to the action of systemically derived suppressor cells upon the primary mucosal immune response within Peyer's patches. This sequence resembles the mirror image of oral tolerance, which involves the suppression of systemic IgG and IgM responses by suppressor cells that arise in Peyer's patches and migrate to the spleen after antigen feeding.
Polyvalent epitope inhibits but added with anti-idiotype antibody enhances idiotype suppression.
Authors: Kim B S , Massey P B 
Published: December 2022

Abstract
When BALB/c spleen cell cultures were preincubated with polyvalent PC-antigens, regardless of their immunogenicity, cultures became resistant to id suppression induced by subsequent treatment with anti-id antibody and immunogenic PC-antigen. In addition, incubation with both anti-id and any of these antigens assisted the induction of rapid, irreversible B cell tolerance. These results suggest that B cells bearing receptors for an epitope undergo an initial triggering in response to polyvalent epitope regardless of the T dependence and/or immunogenicity of the antigen. An additional signal must then facilitate the differentiation of the partially activated B cells to produce antibody. Therefore, a nonimmunogenic polyvalent epitope-bearing molecule can deliver either an initial triggering signal or a tolerogenic signal, depending on the presence of anti-id antibody, and it is as efficient as a complete immunogen.