bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cellular origins of human polymeric and monomeric IgA: intracellular and secreted forms of IgA.
Authors: Moldoveanu Z , Egan M L , Mestecky J 
Published: January 2023

Abstract
Intracellular and secreted IgA from pokeweed mitogen (PWM)-stimulated normal peripheral blood lymphocytes, from 12-O-tetradecanoylphorbol-13-acetate (TPA)-stimulated peripheral blood lymphocytes of a patient with chronic lymphocytic leukemia (CLL), or from an IgA-producing human Epstein Barr virus (EBV)-transformed lymphoblastoid cell line were analyzed by molecular-sieve chromatography, electrophoresis in sodium dodecyl sulfate, and sucrose density ultracentrifugation. Fluorochrome-labeled anti-human IgA and secretory component (SC) were used as probes for the detection of polymeric IgA in individual cells. These methods demonstrated that the majority of intracellular IgA occurred in monomeric form, even when the predominant form of secreted IgA was polymeric. Sequential analyses of the IgA secreted by PWM-stimulated normal peripheral blood lymphocytes revealed that the proportion of polymeric IgA increased with the time of culture and that polymers represented the prevalent form of secreted IgA from the fifth day of culture. Although approximately one-half of TPA-stimulated CLL cells bound fluorochrome-labeled SC, only trace amounts of extracellular and intracellular polymeric IgA were detected in both culture supernatants and lysates. Culture supernatants of an IgA-secreting EBV-transformed cell line contained predominantly polymeric IgA. However, intracellular IgA was largely represented by monomers. The predominance of intracellular monomers in polymeric IgA-secreting cells suggested that the pathway of the assembly of human IgA molecules is analogous to that described for mouse IgA synthesis.
The adjuvant activity of nonionic block polymer surfactants. II. Antibody formation and inflammation related to the structure of triblock and octablock copolymers.
Authors: Hunter R L , Bennett B 
Published: January 2023

Abstract
We tested the ability of 17 surface-active agents to enhance antibody formation and inflammation. The surfactants were all block copolymers of hydrophilic polyoxyethylene (POE) and hydrophobic polyoxypropylene (POP), which differed in m.w. and mode of linkage of POP to POE. Mice were injected in each rear footpad with 1.25 mg of each surfactant with 25 micrograms of bovine serum albumin in an oil-in-water emulsion. Each agent produced a distinct pattern of immune response and inflammation. Preparations that are large and insoluble with the POE chains flanking the POP chains were very effective adjuvants for increasing antibody formation. They also activated complement and induced the release of chemotactic factors from serum. Increasing the percent of POE decreased adjuvant activity and inflammation. Decreasing the m.w. of the molecules while maintaining the proportions of POP and POE decreased the adjuvant activity and increased inflammation. Preparations synthesized in the reverse order, with the POP flanking POE, tended to induce granulomas instead of antibody. These data demonstrate that block copolymer surfactants have a spectrum of biologic activities that depend on the size and arrangement of their constituent parts. We suggest that much of the activity of these agents derives from their ability to form adsorptive surfaces similar to those of a mycobacterial glycolipid, quartz, and monosodium urate.
The structure-function relationship of I-A molecules: correlation of serologic and functional phenotypes of four I-Ak mutant cell lines.
Authors: Beck B N , Glimcher L H , Nilson A E , Pierres M , McKean D J 
Published: January 2023

Abstract
We have isolated and characterized four mutant I-Ak-expressing cell lines derived from the B cell-B lymphoma hybrid antigen-presenting cell line TA3. The mutants were isolated by first selecting against expression of one Ak epitope by treatment with a monoclonal antibody in the presence of complement and then selecting for retention of a second Ak epitope by electronic cell-sorting of cells stained for fluorescence with a second monoclonal antibody. The serologic and functional phenotypes of the mutants were characterized by using panels of I-Ak-specific monoclonal antibodies and I-Ak-restricted T hybridomas. We obtained one Ak alpha mutant (J4) that no longer reacts with any Ak alpha-specific antibody and also is incapable of stimulating any I-Ak-restricted T hybridoma. We obtained three Ak beta mutants (LD3, K5, G1) that express a wide range of serologic and functional phenotypes. Correlation of the serologic and functional phenotypes reveals that the serologic epitope Ia.1 may overlap with a major site of T cell recognition, whereas the Ia.17 serologic epitope appears to be only a minor site for T cell recognition.
Coexpression of the human HLA-A2 or HLA-B7 heavy chain gene and human beta 2-microglobulin gene in L cells.
Authors: Bernabeu C , Maziarz R , Spits H , de Vries J , Burakoff S J , Terhorst C 
Published: January 2023

Abstract
L cells expressing human HLA-A2 or HLA-B7 class I antigen heavy chains are not recognized by human cytotoxic T lymphocytes directed at HLA-A2 or HLA-B7 antigens. To test whether the absence of human beta 2-m was the cause of the lack of recognition by the human cytotoxic T lymphocytes, coexpression of the human beta 2-m gene and the HLA-A2 or HLA-B7 heavy chain in L cells ("double transfectants") was obtained. In addition, L cells expressing HLA-A2 or HLA-B7 antigens in association with human beta 2-m were obtained by an exchange reaction, in which human beta 2-m from serum replaced the endogenous murine beta 2-m. Both types of transfectant cells were used in 51Cr-release assays and cold target inhibition assays for human cytotoxic T cell clones which were directed at HLA-A2 or HLA-B7. Neither human CTL clones nor a mixture of CTL specific for HLA-A2 and HLA-B7 were able to recognize these cells. Several alternative explanations for these observations are discussed.
Identification of the MT3 molecule from HLA-DR4, 7, and w9 homozygous cell lines.
Authors: Mukai R , Suzuki M , Yabe T , Hamaguchi H , Maeda H 
Published: January 2023

Abstract
Human B lymphoblastoid cell lines are known to express several class II antigens. The MT3 specificity defined by alloantisera is in linkage disequilibrium with DR4, DR7, and DRw9, and is called a "supertypic" specificity. To identify the MT3 molecule, immunoprecipitates of HLA-DR and MT3 antigens from extracts of three metabolically labeled HLA-DR homozygous cell lines (Wa;DR4, L-Pi-tot;DR7, L-KT12;DRw9) were analyzed by two-dimensional gel electrophoresis. The light chains of the MT3 antigens from DR4, DR7, and DRw9 homozygous cell lines were indistinguishable from one another in charge and m.w. The light chains of the MT3 antigens differed from those of DR4, DR7, and DRw9 antigens, whereas the heavy chains of the MT3 and DR antigens were indistinguishable. The MT3 antigen appears to share the same heavy chain as the DR antigens. However, this antigen would constitute a new human class II molecule distinct from the DR antigen. These data also raised the possibility that the light chains of the MT3 molecules may be the products of a new locus different from the DR locus.
Macrophage processing of peptide antigens: identification of an antigenic complex.
Authors: Nairn R , Spengler M L , Hoffman M D , Solvay M J , Thomas D W 
Published: January 2023

Abstract
In this report, we present data from our examination of the fate of the octapeptide antigen angiotensin II (AII) after processing by guinea pig macrophages. Macrophages were cultured with [125I]-AII or [3H]-AII for various times, and the AII products in the culture supernatant fluid and solubilized cell lysate (macrophage-associated AII) were analyzed by chromatography on Sephadex G-25. With [3H]-AII, both the cell-associated and cellfree AII was catabolized to three distinct peptide fragments: Peak B, containing seven to eight amino acids; Peak B1, with five to six amino acids; and Peak C, containing four to five amino acids. Surprisingly, in the cells another major form of AII was obtained, Peak A, which showed an m.w. of 50,000 to 70,000. Formation of Peak A was blocked by inclusion of non-radiolabeled AII into the incubation mixture, and could be formed by repulsing fresh macrophages with isolated Peaks B and B1, and to only a minor extent with Peak C. Peak A was formed within an hour of culture of macrophages with [3H]-AII, and remained stably cell-associated through a day of culture. In a pulse-chase type of experiment, it was shown that macrophages rapidly exocytose cell-associated Peaks B and C, and Peak B1 less rapidly, whereas Peak A is retained and is the predominant cell-associated form of AII after a day in culture. Incubation of [3H]-AII with isolated macrophage plasma membranes also resulted in Peak A formation, showing that the complex can be formed by a membrane event not requiring cellular uptake of peptide. The complex of AII in Peak A was acid-stable, and approximately 20% of Peak A was recovered after boiling in SDS. Because Peak A is the primary form of AII retained by macrophages, it was important to determine if this complex was antigenic for T cells. AII-immune T cells cultured with Peak A showed significant proliferation that was specific for AII. Thus, Peak A appears to represent a stable complex of AII with macrophage membrane structures that provide an immunologically relevant form of the antigen. These results are discussed with respect to a pathway for macrophage processing of peptide antigens to form a stable membrane-bound complex that is important for T cell responses.
Inhibition by somatostatin of the release of mediators from human basophils and rat leukemic basophils.
Authors: Goetzl E J , Payan D G 
Published: January 2023

Abstract
The release of mediators from unpurified human basophils challenged with anti-human myeloma IgE serum was suppressed significantly by somatostatin at respective concentrations of 3 x 10(-13) M to 10(-9) M for histamine and 10(-13) M to 10(-11) M for leukotriene D4, which had no effect on release elicited by ionophore A23187. A direct effect of picomole-nanomole concentrations of somatostatin on basophils predominated, as shown by the significant inhibition of immunologically stimulated mediator release from monocyte-free human basophils of 15 to 32% purity and from rat basophil leukemia cells. The dependence of basophil inhibition on the conformation of somatostatin was suggested by the lower potency of reduced and alkylated somatostatin and the lack of inhibitory activity of [D-Trp8] somatostatin. Somatostatin thus may mediate suppressive effects of sensory nerves in some basophil-dependent hypersensitivity reactions.
Thrombin-induced degranulation of cultured bone marrow-derived mast cells.
Authors: Razin E , Marx G 
Published: January 2023

Abstract
This study was undertaken to determine if a plasma protease such as thrombin, a highly specific procoagulant enzyme that has numerous effects on platelets, endothelial cells, and smooth muscle cells, could mediate mast cell activation processes. Our results indicate that at near physiologic levels, thrombin can rapidly trigger mast cell degranulation without activating the 5-lipoxygenase system.
Blood clearance by anti-phosphocholine antibodies as a mechanism of protection in experimental pneumococcal bacteremia.
Authors: McDaniel L S , Benjamin W H , Forman C , Briles D E 
Published: January 2023

Abstract
Previous studies have demonstrated that monoclonal IgG and IgM antibodies to phosphocholine (PC), a determinant in the cell wall of Streptococcus pneumoniae, can protect mice from fatal infection with S. pneumoniae. In this study we demonstrate that both passive and naturally occurring anti-PC antibodies promote the clearance of S. pneumoniae from the blood. The bulk of the cleared pneumococci are apparently killed, because they fail to accumulate in reticuloendothelial tissues. These findings suggest that their protective effect is probably dependent on their ability to promote phagocytosis. We have found that on a weight basis IgG antibody is more effective at promoting blood clearance than IgM antibody. This observation fits with our earlier findings that IgG anti-PC antibody is more protective against i.v. infection than IgM anti-PC antibody. We have also demonstrated that anti-PC antibodies are protective against S. pneumoniae infection when given as late as 24 hr postinfection. This finding makes it unlikely that the ability to protect against pneumococcal infection with anti-PC antibody is dependent on an artifact associated with either their in vitro growth or the harvesting procedure.
Role of inflammatory cells in Chagas' disease. II. Interactions of mouse macrophages and human monocytes with intracellular forms of Trypanosoma cruzi: uptake and mechanism of destruction.
Authors: Villalta F , Kierszenbaum F 
Published: January 2023

Abstract
In this study we examined the kinetics of interaction between mouse peritoneal macrophages (MPH) or human blood monocytes (HBM) with intracellular (amastigote [AMA]) forms of Trypanosoma cruzi. In electron microscopy studies, AMA were seen bound to the surface of unelicited MPH after 5 min of interaction, i.e., when the first observations were made. Internalization was visible after 8 min, and the AMA were never seen outside of phagocytic vacuoles. Signs of AMA damage were first seen after 4 hr. Amastigote disintegration was commonly observed 12 hr after their initial contact with MPH. Similar results were obtained with HBM. These kinetic patterns of AMA uptake and destruction were in agreement with the results of quantitative assays in which the number of AMA contained by 200 MPH and the percentage of infected MPH were measured. The extent of the release of 3H-labeled materials from MPH that had phagocytosed [3H]AMA was approximately 10, 90, and 99% of the total ingested radioactivity after 4, 12, and 24 hr of incubation, respectively. A comparison of the kinetic patterns of MPH interaction with noninvasive AMA and invasive trypomastigote (TRY) forms showed that, after internalization, both the percentage of AMA-containing MPH and the number of AMA per 200 MPH declined dramatically over a 70-hr incubation period, whereas the percentage of MPH infected by the TRY remained virtually constant and the number of organisms per 200 cells increased markedly. This contrast indicated that the AMA had been destroyed, whereas the TRY had managed to survive, transform into AMA, and multiply within MPH. AMA killing by MPH involved H2O2 but not other intermediates of oxygen reduction, because it was inhibited by catalase but not by scavengers of O2, OH ., and 1O2. AMA lost their viability when incubated with glucose and glucose oxidase, confirming their sensitivity to H2O2. Thus, MPH and HBM have the potential for participating in the clearance of T. cruzi AMA from chagasic tissue lesions.
Cell contact-mediated macrophage activation for antileishmanial defense. II. Identification of effector cell phenotype and genetic restriction.
Authors: Sypek J P , Panosian C B , Wyler D J 
Published: January 2023

Abstract
Host defense in cutaneous leishmaniasis, due to Leishmania tropica, is largely--if not exclusively--cell mediated. We observed in vitro that draining lymph node lymphocytes from L. tropica-infected C57BL/6 mice activate L. tropica-infected macrophages to kill the intracellular parasites (leishmanicidal effect). Because direct cell contact between lymphocytes and infected macrophages is required to achieve a maximum leishmanicidal effect, this effect cannot be attributed solely to lymphokines. Furthermore, because effector lymphocytes induced no detectable damage to infected macrophages, the effect also differs from conventional lymphocyte-mediated cytotoxicity. The present study identifies the phenotype of the effector lymphocyte and assesses the genetic restriction of the lymphocyte-macrophage interaction. Nylon wool column-enriched T lymphocytes from infected mice activate macrophages for antileishmanial effects; treatment of lymphocytes with anti-Thy-1.2 antibody plus complement abolishes this capacity. Furthermore, treatment with anti-Lyt-1 antibody plus complement (but not with anti-Lyt-2 plus complement) likewise abolishes the effector capacity of the lymphocytes. Parallel studies reveal that the percentage of Lyt-1+2- cells present in draining lymph nodes increases during the course of infection and reaches a peak with the onset of spontaneous resolution of the infection. Syngeneic, but not allogeneic, combinations of lymphocytes and infected macrophages result in macrophage activation. Furthermore, treatment of cells with appropriate anti-Ia monoclonal antibody abrogates the antileishmanial effects. These results indicate that Lyt-1+2- lymphocytes obtained from mice with spontaneously healing L. tropica infections can exert antileishmanial effects in vitro. This effect is genetically restricted--most likely to the I region of the MHC--and requires direct cell contact. The temporal relationship between the appearance of these effector lymphocytes in mice and the onset of disease resolution argues that they may also exert these antileishmanial effects in vivo.
Cell contact-mediated macrophage activation for antileishmanial defense. I. Lymphocyte effector mechanism that is contact dependent and noncytotoxic.
Authors: Panosian C B , Sypek J P , Wyler D J 
Published: January 2023

Abstract
Leishmania are obligate intracellular protozoa in mammalian hosts. They infect and replicate within macrophages. Antileishmanial host defense is largely cell mediated. We conducted studies in vitro to investigate the ability of lymphocytes to activate macrophages for antileishmanial effects. Draining lymph node lymphocytes from C57BL/6 mice with cutaneous Leishmania tropica major infection were co-cultured in suspension with syngeneic, starch-elicited peritoneal macrophages infected in vitro with homologous parasites. In the presence of these effector lymphocytes, parasite replication was inhibited, and in some cases intracellular parasites were destroyed. In contrast, control lymphocytes from complete Freund's adjuvant-treated or Listeria-infected mice exerted no antileishmanial effects. Antileishmanial effects were greatest when Leishmania-sensitized lymphocytes were in direct contact with parasitized macrophages. Effector lymphocytes did not cause detectable damage to infected macrophages. Lymphocytes that induced the most profound antileishmanial effects in vitro were those obtained from mice entering a phase of spontaneous clinical resolution of their infections. We conclude that macrophages can be activated for microbicidal effects by direct contact with appropriately sensitized lymphocytes. This antigen-specific, contact-mediated lymphocyte effector mechanism may be important in host defense against certain intracellular microorganisms such as Leishmania.
The induction of Leu-1 antigen expression in human malignant and normal B cells by phorbol myristic acetate (PMA).
Authors: Miller R A , Gralow J 
Published: January 2023

Abstract
Malignant cells from five patients with B cell leukemia or lymphoma were cultured with phorbol myristic acetate (PMA). PMA was found to induce cell surface expression of the Leu-1 antigen in cells from three of the five patients. Using one- and two-color immunofluorescence staining and flow cytometry, we have shown simultaneous expression of the Leu-1 antigen with other B cell markers. Induction of Leu-1 antigen expression was not related to histologic subtype, in vitro secretion of immunoglobulin, or other clinical features. Biosynthetic labeling experiments showed that synthesis of Leu-1 antigen occurred and preceded expression of the antigen on the cell surface. PMA also induced the appearance of Leu-1 antigen-positive B cells in cultures of normal peripheral blood mononuclear cells. We propose that the Leu-1 antigen is expressed transiently during the differentiation of some B cells.
Inhibition of growth of MOPC 104E cells in immunosuppressed mice.
Authors: Hiramoto R N , Cox P J , Hiramoto N S , Ghanta V K 
Published: January 2023

Abstract
In this report we provide evidence that suggests that MOPC 104E may come under regulation in highly immunosuppressed hosts depleted of T cells. Mice that are adult thymectomized, total body irradiated, and transplanted with bone marrow cells were able to resist the growth of MOPC 104E cells. Spleen cells from such animals had low NK activity and no cytotoxicity against MOPC 104E, and poor response to Con A, PHA, and LPS. The animals were deficient in Lyt-1+ and Lyt-2+ cells. The growth of MOPC 104E cells was measured by using the circulating level of MOPC 104E IgM in vivo in mice treated by different modalities. We observed that inhibition of tumor growth in vivo varied with the treatment of the host. Growth was inhibited in the host in the following order: ATXBM greater than XBM greater than NORMAL greater than ATx mice.
Target cell lysis: ultrastructural and cytoskeletal alterations.
Authors: Leopardi E , Friend D S , Rosenau W 
Published: January 2023

Abstract
The cytoskeleton, with particular emphasis on filamentous actin (f-actin), was studied in target L cells treated with the cytotoxic lymphokine, alpha-lymphotoxin (LT), or with cytotoxic T lymphocytes. The f-actin distribution was also examined in cytotoxic T cells interacting with targets. LT-treated targets retracted their processes, rounded up, and subsequently underwent lysis. These changes were accompanied by loss of stress fibers and rearrangement of f-actin, although there was no appreciable change of total cytoskeletal protein or f-actin content. Thus, the arrangement of f-actin was altered, but not its cellular concentration. Similar morphologic changes were seen at the light microscopic level in targets affected by T cells. T lymphocytes interacting with targets showed marked polarization of f-actin adjacent to the effector target interface; some f-actin rearrangement was also noted in the underlying target cell cytoplasm. Ultrastructurally, the LT-affected targets showed a decrease of f-actin organization within microvilli and underneath the plasma membrane associated with loss of villi and cytoplasmic bleb formation. Furthermore, prominent bundles of intermediate filaments were apparent and clusters of vesicles were noted which may be an expression of plasma membrane repair. These findings suggest that target cell cytoskeletal changes may lead to the morphologic changes in LT- and T cell-mediated cytotoxicity and lysis.