bluuebunny/crossref_metadata_2025_split huggingface dataset:
Lipid bodies: cytoplasmic organelles important to arachidonate metabolism in macrophages and mast cells.
Authors: Dvorak A M , Dvorak H F , Peters S P , Shulman E S , MacGlashan D W , Pyne K , Harvey V S , Galli S J , Lichtenstein L M 
Published: December 2022

Abstract
Much has been learned about the biochemical nature and pharmacologic activity of the products of arachidonic acid (AA) oxidation, but relatively little is known about the structures in nucleated cells into which AA is incorporated and from which it is initially mobilized. To address this question, we administered 3H-AA or other 3H-fatty acids in vitro to human lung mast cells and alveolar macrophages as well as to mouse and guinea pig peritoneal macrophages. The subcellular distribution of 3H label was assessed by electron microscopic autoradiography, and the nature of cell-associated 3H-lipids was determined by thin layer chromatography. Autoradiographic analysis of human lung mast cells localized virtually all of the 3H-AA to cytoplasmic lipid bodies. Lipid bodies are roughly spherical, variable osmiophilic, nonmembrane-bound structures that appear in the cytoplasm of a wide variety of cells, but we have found that these lipid bodies occur with increased frequency in granulocytes, macrophages, and mast cells at sites of inflammatory, immunologic, or neoplastic processes. Macrophages also incorporated 3H-AA predominantly into cytoplasmic lipid bodies. In contrast to mast cells, however, macrophages incorporated 3H-AA into the plasma membrane as well. Stimulation of macrophage phagocytosis resulted in striking alterations of the relationships of lipid bodies to intracellular membranes, so that many lipid bodies appeared adjacent to phagolysosomes. In addition, some phagolysosomes contained 3H label, which along with other morphologic evidence suggested that lipid bodies may discharge their contents into these structures. Mast cell and macrophage cytoplasmic lipid bodies appear to represent a major site of intracellular storage and metabolism of products of AA and perhaps other fatty acids taken up from the external milieu. These heretofore neglected organelles may thus influence cellular function in a wide variety of adaptive or pathologic processes.
Chemotactic macrophage subpopulations defined by macrophage chemotactic factors from delayed hypersensitivity reaction sites.
Authors: Honda M , Yoshimura T , Watanabe T , Hayashi H 
Published: December 2022

Abstract
The chemotactic specificity of ia-positive and -negative macrophages was studied by using three macrophage chemotactic factors (MCF), -a, -b, and -c, isolated from delayed hypersensitivity reaction (DHR) skin sites in guinea pigs. Listeria-elicited macrophages migrated toward MCF-a, -b, and -c. The chemotactic responses suggested responsive subpopulations to MCF. The electronic programmable individual cell sorter (EPICS) was used to separate macrophages with anti-la monoclonal antibodies. Ia-positive subpopulations responded to MCF-c, although they did not migrate toward MCF-a and -b. In contrast, Ia-negative subpopulations migrated toward MCF-a and -b, but not toward MCF-c. Furthermore, MCF-c attracted Ia-positive macrophages, whereas MCF-a and -b were Ia-negative in vitro; MCF did not induce Ia-negative macrophages to express surface Ia-antigens in vitro. MCF-c was able to produce massive Ia-positive macrophage accumulations when injected i.p., whereas MCF-a accumulated Ia-negative macrophages. The data suggest that MCF-a and -b, which mediate initial macrophage reactions, attract Ia-negative macrophages, and that MCF-c, which mediates predominant macrophage reactions, attract Ia-positive macrophages in the DHR.
Genetic control of the innate resistance of mice to Salmonella typhimurium: expression of the Ity gene in peritoneal and splenic macrophages isolated in vitro.
Authors: Lissner C R , Swanson R N , O'Brien A D 
Published: December 2022

Abstract
The mouse Chromosome 1 locus Ity regulates the extent to which Salmonella typhimurium replicates within the reticuloendothelial cell system (RES) during the first days of infection. If animals are homozygous for the Itys susceptibility allele, the Gram-negative bacterium undergoes rapid net multiplication, and mice die of a typhoid fever-like disease by day 10 of infection. Animals that are homozygous or heterozygous for the resistance allele, Ityr, control net bacterial replication and survive the first phase of salmonellosis. Indirect studies have implicated the resident macrophage as the effector cell for regulation of early in vivo salmonellae growth. To verify this supposition and to evaluate the phenotypic expression of Ity, we developed an in vitro assay to compare kinetics of S. typhimurium growth within Ityr and Itys macrophages. Resident peritoneal and splenic macrophages were used from inbred Ityr and Itys mice and from Ity congeneic mice. With these mice and through the use of radiolabeled S. typhimurium and an avirulent temperature-sensitive mutant of the bacterium, we found that: phagocytosis of S. typhimurium by Ityr and by Itys macrophages was the same; S. typhimurium grew to a greater extent in Itys peritoneal and splenic macrophages than in Ityr cells; Ityr macrophages killed intracellular salmonellae more efficiently than did Itys macrophages. Thus, we have demonstrated directly that Ity is expressed by the macrophage and have shown for the first time with Ity congeneic mice that the basis for differential net growth of virulent S. typhimurium in Ityr and Itys macrophages is a variation in the degree of bacterial kill.
Selective elimination of a B cell subset having acceptor site(s) for T cell-replacing factor (TRF) with biotinylated antibody to the acceptor site(s) and avidin-ricin A-chain conjugate.
Authors: Hashimoto N , Takatsu K , Masuho Y , Kishida K , Hara T , Hamaoka T 
Published: December 2022

Abstract
A covalent conjugate of avidin with ricin subunit A-chain (avidin-RA) was prepared by using N-succinimidyl 3-(2-pyridyldithio)propionate as a coupling agent. Selective cytotoxic activity after the combined treatment of spleen cells with biotinylated antibody and avidin-RA was demonstrated by the fact that the responsiveness to LPS was selectively abrogated by pretreatment of the cells with biotinylated rabbit anti-mouse immunoglobulin (MIg) antibody, but not with biotinylated anti-Thy-1.2 antibody. Neither the biotinylated antibody alone nor avidin-RA alone was effective in decreasing the responses to mitogens. Moreover, a high anti-DNP PFC response elicited by DNP-KLH-primed BALB/c mouse spleen cells stimulated in vitro with DNP-KLH was mostly abrogated by the pretreatment of the cells with biotinylated anti-MIg antibody and avidin-RA. Again, neither the biotinylated antibody alone nor avidin-RA alone was effective in decreasing the anti-DNP PFC response. This cell-killing method with the use of biotinylated antibody and avidin-RA was applied and evaluated in experimental systems in which the helper action of T cells on B cells was mediated by T cell-replacing factor (TRF) or was performed by the direct interaction of T cells with B cells (cognate interaction). When DNP-KLH-primed splenic B cells, pretreated with biotinylated F(ab')2 fragment of DCF1 male anti-BALB/c-B IgG antibody against acceptor site(s) for TRF followed by treatment with avidin-RA, were stimulated with DNP-OVA in the presence of monoclonal TRF, the anti-DNP PFC response was significantly decreased, whereas the same treated B cells responded well to stimulation with DNP-PPD in the presence of Tbc-primed T cells (cognate interaction). These results indicate that B cells responsible for the cognate interaction and those having TRF acceptor site(s) belong to a distinct subpopulation of B cells, and that the cytocidal action of the noncovalent conjugate of the antibody and RA formed from the biotinylated antibody and avidin-RA via an avidin-biotin complex has immunologic selectivity, eliminating only the latter subset of B cells recognized by the antibody.
Regulation of lymphokine (gamma-interferon) production by corticotropin.
Authors: Johnson H M , Torres B A , Smith E M , Dion L D , Blalock J E 
Published: December 2022

Abstract
We have shown that corticotropin (ACTH), alpha-endorphin, and enkephalins can regulate antibody responses, which suggested a role for neuropeptides in a regulatory circuit between the immune and neuroendocrine systems. ACTH and structurally related peptides were examined here for regulation of mitogen induction of the lymphokine gamma-interferon (IFN gamma) in C57BL/6 mouse spleen cell cultures. Synthetic ACTH1-39 and a porcine pituitary extract containing ACTH activity were potent suppressors of the IFN gamma response. Synthetic ACTH1-39 suppressed the response by approximately 62% at 1 to 3 microM, whereas the porcine extract suppressed by greater than 90% at 1 to 3 microM ACTH. The greater potency of the pituitary extract was shown to be due to the presence of an additional peptide of Mr 2100 that was reactive with antibodies to the N-terminal region of ACTH (ACTH1-13), possessed potent anti-cellular activity against L cells and various transformed cells, but lacked ACTH biologic activity. The anti-cellular peptide suppressed the IFN gamma response by greater than 99% at 0.05 microM. The ACTH1-39 cleavage products, alpha-melanocyte stimulating hormone (alpha MSH; acetylated and amidated ACTH1-13), and corticotropin-like intermediate lobe peptide (CLIP; ACTH18-39) had no effect on IFN gamma production. ACTH1-24, like ACTH1-39, has full steroidogenesis activity but also had no effect on IFN gamma production, which suggests a dissociation of the immunoregulatory and steroidogenic properties of ACTH1-39. ACTH1-39, and possibly also the anti-cellular 2100 Mr peptide, is initially synthesized as the precursor polyprotein pro-opiomelanocortin (POMC). Enzymatic processing of POMC, first to the active ACTH1-39 or the anti-cellular peptide and then to the inactive smaller peptides, probably plays an important role in regulation of lymphokine and antibody production by ACTH and ACTH-related neuropeptides. This is consistent with the recent demonstration of the production of ACTH-like peptides by lymphocytes.
Evidence for extensive polymorphism of RT1 Class II molecules in the rat.
Authors: Sawicki J A , Wettstein P J 
Published: December 2022

Abstract
RT1.B Class II molecules, comparable to I-A and I-E molecules in mice, have been characterized by two-dimensional (2D) gel electrophoresis for seven rat strains expressing different RT1 haplotypes. RT1.B molecules were immunoprecipitated from radiolabeled rat lymphocyte preparations with mouse monoclonal antibodies reactive with mouse I-Ab antigens and I-Ek antigens. For each RT1 haplotype, two I-A-like subunits, alpha and beta, and two I-E-like subunits, gamma and delta, have been identified. 2D gel analysis of RT1.B molecules from different strains in paired combinations reveals that, with a few notable exceptions, the alpha, beta, and delta subunits associated with different RT1 haplotypes are characterized by unique 2D gel spot patterns. In contrast, the gamma subunits of all RT1.B haplotypes appear identical. This evidence confirms and extends our previous analysis of RT1.B molecules by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and suggests a high level of polymorphism for genes in the RT1.B region, with the exception of the RT1.Bc gene encoding gamma. Interestingly, three rat strains appear exceptional in the identity of their alpha, gamma, and delta subunits, which suggests that these strains express closely related RT1 haplotypes derived from a common progenitor.
Rat T lymphocyte antigens comparable with mouse Lyt-1 and Lyt-2,3 antigenic systems: characterization by monoclonal antibodies.
Authors: Matsuura A , Ishii Y , Yuasa H , Narita H , Kon S , Takami T , Kikuchi K 
Published: December 2022

Abstract
Rat T lymphocyte antigens were defined by using two distinct monoclonal antibodies (R1-3B3 and R1-10B5). R1-3B3 antibody, when tested for its reactivity with rat lymphoid cells by immunofluorescence, stained almost all of thymus and T cells but not the majority of B cells and bone marrow cells. The antigen defined by R1-3B3 existed more abundantly on medullary thymocytes and peripheral T cells than on cortical thymocytes. Immunochemical data showed that R1-3B3 antibody recognized a single glycoprotein with a m.w. of 67,000, showing marked electric charge heterogeneity with isoelectric points ranging from 5.4 to 7.3. R1-10B5 antibody, on the other hand, had more restricted reactivity with rat T cells and labeled approximately 85% of thymus cells and 30% of the peripheral T cells but neither B cells nor bone marrow cells. These T cells positive for R1-10B5 appeared to be negative for W3/25 antigen, which has been shown to be the marker for the rat T cell subset associated with helper function. R1-10B5 antibody detected a basic glycoprotein complex consisting of sulfhydryl-linked subunits with 30,000 and 34,000 m.w. Although the antigen defined by R1-3B3 was resistant to trypsin digestion, the one detected by R1-10B5 was much more sensitive to trypsin cleavage. All of these data obtained with either R1-3B3 or R1-10B5 are quite comparable to those reported for mouse Lyt-1 or Lyt-2,3 antigens, and thus suggest that the antigens defined by R1-3B3 and R1-10B5 antibodies represent rat homologues of Lyt-1 and Lyt-2,3 antigens in the murine system, respectively.
Presence of an antigenic determinant common to rat IgE-potentiating factor, IgE-suppressive factor, and Fc epsilon receptors on T and B lymphocytes.
Authors: Huff T F , Yodoi J , Uede T , Ishizaka K 
Published: December 2022

Abstract
Polyclonal antibodies against purified IgE-potentiating factor were prepared in guinea pigs, and mouse monoclonal antibodies were prepared against inactive IgE-binding factor from a T cell hybridoma. The polyclonal antibodies and two of the monoclonal antibodies bound the IgE-potentiating factor, the IgE suppressive factor, and the inactive IgE-binding factor. The results indicate that the three IgE-binding factor molecules share a common antigenic determinant. The polyclonal antibodies and the monoclonal antibody bound intracellular IgE-binding factors that did not have affinity for either lentil lectin or peanut agglutinin, which suggests that the antibodies were directed against the peptide portion of IgE-binding factors. Pretreatment of Fc epsilon R+ T hybridoma cells and Fc epsilon R+ B cells with either the monoclonal or the polyclonal anti-IgE-binding factor (anti-IgE-bF) antibody prevented rosette formation of the cells with IgE-coated erythrocytes, whereas the same treatment failed to affect rosette formation of Fc gamma R+ cells with IgG-coated erythrocytes. Specific binding of the guinea pig anti-IgE-bF antibodies to Fc epsilon R on both B and T cells was confirmed by immunofluorescence. The results indicate that Fc epsilon R on B and T cells share a common antigenic determinant with IgE-binding factors. The F(ab')2 fragments of the guinea pig anti-IgE-bF induced the expression of Fc epsilon R on Fc gamma R+ lymphocytes and the formation of IgE-binding factors. The capacities of not only IgE, but also anti-IgE-bF, to induce both Fc epsilon R expression and IgE-binding factor formation indicate that Fc epsilon R on lymphocytes, rather than IgE, transmit the signal for the formation of IgE-binding molecules.
Leukotrienes: positive signals for regulation of gamma-interferon production.
Authors: Johnson H M , Torres B A 
Published: December 2022

Abstract
Leukotrienes B4, C4, and D4 were capable of replacing the helper cell or interleukin 2 requirement for gamma-interferon (IFN gamma) production by Lyt-1-,2+ cells from C57BL/6 mouse spleen cells at leukotriene concentrations as low as 0.002 microM. An antioxidant inhibitor (butylated hydroxyanisole) of lipoxygenase metabolism of arachidonic acid suppressed IFN gamma production. The suppression was significantly reversed by leukotriene C4, which further suggests that leukotrienes and possibly other substances produced by the lipoxygenase pathway of arachidonic acid metabolism play an important role in the regulation of IFN gamma production. All of these events may be related to activation of guanylate cyclase activity, since cyclic GMP also significantly reversed the suppressor effects of butylated hydroxyanisole in IFN gamma production. The leukotriene help for IFN gamma production was independent of DNA synthesis or cellular proliferation. The data are consistent with the hypothesis that lipxoygenase products of arachidonic acid metabolism may play a role in the mediation of interleukin 2 help in IFN gamma production. Cells that are rich sources of leukotrienes, then, should play important roles in positive regulation of lymphokine production.
In vitro and in vivo studies on protective and inhibitory antibodies against Plasmodium falciparum in the Saimiri monkey.
Authors: Fandeur T , Dubois P , Gysin J , Dedet J P , da Silva L P 
Published: December 2022

Abstract
Immunoglobulins (Ig) were purified from serum or ascitic fluids of Saimiri monkeys infected with Plasmodium falciparum and with differing levels of functional immunity. Their protective activity was assessed in studies of passive transfer of immunity in vivo, and their neutralizing activity was measured in studies of parasite inhibition in vitro in cultures of human or Saimiri RBC. Although protective and inhibitory antibodies were detected in different Ig preparations, the levels of these activities were not directly correlated. Some Ig preparations, showing high protective activity, provide little or no inhibition of the parasite in vitro. Conversely, inhibitory activity was present in Ig preparations unable to confer protection in vivo. These results indicate that protective antibodies are active through a more complex immune mechanism than simple neutralization probably involving cellular immunity.
Role of IgE receptors in effector function of human eosinophils.
Authors: Capron M , Spiegelberg H L , Prin L , Bennich H , Butterworth A E , Pierce R J , Ouaissi M A , Capron A 
Published: December 2022

Abstract
After analysis of the technical parameters of the rosette assay with human IgE-coated erythrocytes, Fc epsilon receptors for IgE (Fc epsilon R) on human peripheral blood eosinophils were compared to Fc epsilon R on lymphocytes and monocytes. Antibodies directed against Fc epsilon R on lymphocytes and monocytes inhibited the IgE rosettes formed by eosinophils from hypereosinophilic patients, which suggests that Fc epsilon R on eosinophils were antigenically related to Fc epsilon R on lymphocytes and monocytes. Fc epsilon R on human eosinophils were shown to participate in the killing effect of Schistosoma mansoni schistosomula in vitro in the presence of purified eosinophils from highly hypereosinophilic patients (blood counts greater than 3000/mm3) and anti-schistosomula IgE antibodies present in S. mansoni-infected patient sera. Similar levels of inhibition of cytotoxicity were obtained after preincubation of eosinophils with aggregated human IgE or with anti-Fc epsilon R antibodies, whereas preincubation with aggregated IgG or with anti-C3b receptor antibodies did not decrease the killing effect for schistosomula targets. This IgE-dependent cytotoxic capacity seemed restricted to eosinophils with an abnormally low density ("hypodense" cells) present only in highly hypereosinophilic patients. These observations might be related to nonparasitic situations in which increased levels of IgE and tissue or blood eosinophils are observed.
Natural killer activity in the rat. III. Characterization of transplantable large granular lymphocyte (LGL) leukemias in the F344 rat.
Authors: Reynolds C W , Bere E W , Ward J M 
Published: December 2022

Abstract
Six transplantable large granular lymphocyte (LGL) tumor lines in F344 rats were examined for natural killer (NK) and antibody-dependent cell-mediated cytotoxicity. Tumor cells from all six lines were highly cytotoxic, even at low effector to target ratios, when tested against NK-susceptible targets, but were unreactive against an NK-resistant target (C58NT)D) and a macrophage-susceptible target (P815). Three lines showed significant levels of lysis against antibody-coated tumor cells. After in vivo transplantation, the levels of cytotoxicity steadily increased in three lines and decreased in one. The cytotoxic activity of one line (RNK-16) remained high through 12 transplant generations. Tumor cells injected i.p. spread via the lymphatics to regional lymph nodes, mediastinal nodes, blood, and eventually the bone marrow. Leukemia occurred concurrently with organ enlargement and increased levels of NK. Studies in (F344 X W/Fu)F1 rats clearly demonstrated that the cytotoxic cells from leukemic animals were the transplanted tumor cells themselves and not merely the activation of normal host LGL. These results demonstrate that naturally occurring, transplantable LGL leukemias are an easily obtainable and excellent source of materials for those studies requiring a large number of functionally active LGL.
Phenotypic modulation of chronic lymphocytic leukemia cells by phorbol ester: induction of IgM secretion and changes in the expression of B cell-associated surface antigens.
Authors: Gordon J , Mellstedt H , Aman P , Biberfeld P , Klein G 
Published: December 2022

Abstract
Freshly explanted neoplastic populations from 22 cases of phenotypically well-characterized chronic type B lymphocytic leukemia were studied for their capacity to respond to the phorbol ester TPA in vitro. In all but four cases the secretion of IgM was either induced or increased, often to a high level. In contrast, the export of free immunoglobulin (Ig) light chains, an almost consistent feature of the B lymphocytic leukemias, remained relatively constant after TPA treatment. Parallel changes in leukemic cell surface phenotype were probed with both "conventional" and monoclonal antibodies, revealing some modulation of markers in every case investigated. A diminution in the level of surface Ig (preferentially IgD) and the accumulation of cytoplasmic Ig observed after phorbol ester treatment were accompanied by a corresponding reduction or loss of the B1 antigen and usually of B2 when present. The most consistent change induced by TPA was the appearance of BB-1, a marker of activated B lymphocytes, which was rarely expressed on fresh leukemic cells. Another marker of activated lymphocytes, LB-1, was also often induced or increased in its expression after exposure of the cells to TPA. The magnitude of the TPA response appeared to relate to the stage of maturation arrest of the individual leukemic clones rather than to any clinical parameter explored. The significance of the findings to normal B cell differentiation and their potential clinical utility are discussed.