bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of T- and B Lymphocyte Responses to Mitogens by Tumor-Associated Macrophages: The Dependency on the Stage of Tumor Growth
Authors: Evans Robert 
Published: January 2018

Abstract
This preliminary investigation was concerned with the hypothesis that macrophages associated with tumors induced to regress temporarily by the action of cyclophosphamide (CY) have the capacity to suppress local T- or B lymphocyte responses which otherwise might cause permanent regression. Cultures of adherent cells, predominantly tumor-associated macrophages (TAMs), isolated from two C57BL/6J (B6) sarcomas, MCA/76-9 and 76-64, after various periods of tumor growth or after CY injection (240 mg/kg) were shown to suppress or enhance the response of 106 B6 normal spleen cells to stimulation by concanavalin-A (Con A) or lipopolysaccharide (LPS). At any given time point, the extent of suppression or enhancement induced by adherent cells isolated from tumors after CY injection was similar to that induced by cells from progressing tumors and appeared to be more dependent on the time after the initial injection of tumor cells than on drug treatment per se. Thus, adherent cells suppressed Con A and LPS responses when they were isolated either from small (0.5 g) or large (&gt;1.5 g) progressing tumors or from tumors 4–9 days after CY injection. However, during the logarithmic phase of tumor growth or within 4 days of injecting CY, adherent cells enhanced spleen cell mitogenic responses, particularly to LPS stimulation. The cultures of putative TAMs isolated at the various time points were seen to contain varying proportions of polymorphonuclear cells (PMNs), the proportions coinciding with the period of reduced spleen cell mitogenic responses. Cultures prepared from small or large progressing tumors contained about 10% or 20–30% PMNs, respectively, while those from tumors tested during the log phase contained less than 5% PMNs. Cultures from tumors removed within 4 days of injecting CY contained less than 5% PMNs while those prepared from tumors tested at later times contained as high as 25% PMNs by 9 days after CY injection. A comparison of peritoneal PMNs and macrophages from non-tumor-bearing mice in terms of their ability to influence mitogenesis indicated that PMNs at high ratios (1 PMN:2 spleen cells) could suppress responses directly. Lower ratios had either small suppressive effects or no effects but in no case was enhancement of responses seen. Peritoneal macrophages suppressed responses at a ratio of 1 macrophage:10 spleen cells but enhanced responses at ratios of 1 macrophage:100 or 1,000 spleen cells. The overall data indicated that the microenvironment of the tumor site may modulate the functional activity of macrophages, or their subpopulations, during their potential regulation of T- and B-cell responses. In addition, the presence of PMNs in large numbers at these inflammatory sites may also contribute to the regulation of lymphocyte function.
Evidence That X-Irradiation and 4-Hydroperoxycyclophosphamide Affects Different Lymphocytes That Respond to Specific Antigen In Vitro
Authors: Clark Connie , LaSota Irene , Borch Richard F 
Published: January 2018

Abstract
The present study examined the effect of pulse treatment with the in vitro active synthetic derivative of cyclophosphamide (CY),4-hydroperoxycyclophos- phamide (4-HPCY), and exposure to X-irradiation on the in vitro Concanavalin A (ConA), lipopolysaccharide (LPS), and antigen-specific blastogenic responses of in vivo-primed lymph node cells. Primed lymph node cells from CY- pretreated, aggregated (A) human IgG-complete Freund's adjuvant (AHGG- CFA)-immunized mice were untreated, exposed to various doses of irradiation, or pulse treated with different concentrations of 4-HPCY before being cultured in medium alone or in medium containing HGG, ConA, or LPS. The results show that HGG-responding and LPS-responding cells exhibited similar dose- inactivation profiles following exposure to irradiation or pulse treatment with 4- HPCY. More than 75% of reactivity was eliminated by exposure to 100 rads or pulse treatment with 20 4-HPCY. In contrast to preculture pulse treatment with 4-HPCY, however, when primed lymph node cells were cultured in medium containing 4-HPCY (culture treatment) LPS-responding cells were shown to be more sensitive to inactivation than HGG-responding cells. The data further show that the effect of low-dose irradiation and of culture treatment with 4-HPCY on the HGG-specific response of primed lymph node cells was additive, suggesting that these agents inactivate different cell subtypes that contribute to the HGG-specific response in vitro.
Receptor-Mediated Entry of Peroxidases Into the Parasitophorous Vacuoles of Macrophages Infected With Leishmania Mexicana Amazonensis
Authors: Rabinovitch Michel , Topper Gail , Cristello Paul , Rich Abby 
Published: January 2018

Abstract
Leishmania amastigotes, obligatory parasites of macrophages, lodge and multiply within long-lived phagolysosomelike “parasitophorous vacuoles” (PV). The glycoprotein horseradish peroxidase (HRP) was shown, by light and electron microscopic cytochemistry, to enter the PVs of rat in vitro-derived bone marrow macrophages infected with Leishmania mexicana amazonensis. Uptake was obtained both in preinfected macrophages incubated with HRP and in macrophages pulsed with HRP, infected, and futher incubated in ligand-free medium. Peroxidase positive and negative PVs could coexist in the same macrophages. Infected macrophages commonly displayed fewer labeled secondary lysosomes than noninfected cells. Lactoperoxidase (LP) was also shown, by light microscopy, to enter the PVs of rat macrophages. Uptake of HRP and of LP was blocked by mannan, supporting the mannose receptor mediated recognition of these ligands. Transfer of HRP to PVs was much less efficient in resident mouse peritoneal macrophages, even at 50 × higher ligand concentrations. Such macrophages expressed negligible mannose receptor function. The efficient mannan-inhibitable uptake of HRP by rat marrow macrophages was confirmed biochemically. Bulk HRP uptake in infected and noninfected cultures was found to be similar. Peroxidases should be useful in further studies of endocytosis by Leishmania-infected macrophages and in the development of lysosomotropic macrophage-targeted drug carriers.
Monitoring Human Neutrophil Granule Secretion by Flow Cytometry: Secretion and Membrane Potential Changes Assessed by Light Scatter and a Fluorescent Probe of Membrane Potential
Authors: Fletcher Mark P , Seligmann Bruce E 
Published: January 2018

Abstract
Purified human peripheral blood polymorphonuclear neutrophils (PMN) were incubated at 37°C with the fluorescent membrane potential sensitive cyanine dye di-O-C(5)(3) and exposed to a number of stimulatory agents (N- formylmethionylleucylphenylalanine (FMLP), cytochalasin B (cyto B) + FMLP, phorbol myristate acetate (PMA). Flow cytometry was utilized to measure changes in forward light scatter (FS), orthogonal light scatter (90°-SC), and fluorescence intensity of individual cells over time. A saturating (10 −6 M) dose of FMLP lead to a significant increase in the cells' FS without a change in 90°- SC as well as a heterogeneous loss of di-O-C(5)(3) fluorescence. PMA (100 ng/ ml) also caused an increase in FS but a uniform loss of dye fluorescence by all cells (apparent depolarization). Cyto B + FMLP produced an increase in FS, a marked loss of 90°-SC, and a uniform loss of fluorescence. Secretion experiments under identical incubation conditions indicated a significantly positive relationship between loss of enzyme markers or cell granularity and orthogonal light scatter (r = 0.959, 0.998f and 0.989 for loss of 90°-SC vs lysozyme, 0- glucuronidase, and granularity index, respectively). Sequential exposure of PMN to PMA and then cyto B + FMLP produced a stepwise shift in scatter parameters (increased FS then loss of 90°-SC). Normalization of membrane potential dye fluorescence changes for the changes in light scatter did not abrogate the heterogeneous fluorescence response of cells to stimulus, indicating that stimulus-induced scatter changes were not responsible for such fluorescence shifts. The data demonstrate that loss of 90°-SC relates closely to secretion of primary granules while changes in FS reflect alterations in cell shape and/or surface/volume ratios that accompany cell activation. Flow cytometric light scatter measurements may yield important information on the extent of prior cell degranulation or activation.
The Strain of Mouse and Assay Conditions Influence Whether MulFN- γ Primes or Activates Macrophages for Tumor Cell Killing
Authors: Pace Judith L , Varesio Luigi , Russell Stephen W , Blasi Elisabetta 
Published: January 2018

Abstract
Investigators from two different laboratories have compared several variables in the short-term macrophage-mediated cytotoxicity assays used by each group to study the role of MulFN- γin macrophage activation. The findings suggest that the capacity of MulFN- γto activate macrophages without the need for a second triggering stimulus is related to assay conditions and, most especially, the strain of mouse used to provide the macrophages.
Natural Antitumor Defense System of the Murine Liver
Authors: Cohen Stefan A , Salazar Daniel , von Muenchhausen Wittiches , Werner-Wasik Maria , Nolan James P 
Published: January 2018

Abstract
Murine nonparenchymal liver cells from various genetic strains isolated by collagenase digestion and differential sedimentation contain both lymphocytes and macrophages. Nonparenchymal liver cells as well as spleen cells, mononuclear blood cells, and peritoneal exudate cells from C3HeB/FeJ mice were tested for natural cytotoxicity against YAC-1 (sensitive to NK cells) and P815 (resistant to NK cells) tumor cell lines. Resident peritoneal exudate cells exerted no cytotoxicity against either tumor cell, whereas spleen and mononuclear blood cells lysed only YAC-1. In contrast, nonparenchymal liver cells lysed both YAC-1 (4 h) and P815 (18 h) tumor cells. Treatment of nonparenchymal liver cells with anti-asialo GM1 and complement abolished the antitumor activity against both tumor cell lines but not the phagocytic activity. Nonadherent nonparenchymal liver cells exerted greater cytotoxicity against YAC-1 tumor cells but little cytotoxicity against P815 tumor cells when compared with unfractionated cells. Adherent nonparenchymal liver cells (macrophages) from untreated mice exerted no antitumor activity against either tumor cell. In contrast, adherent nonparenchymal liver cells from Coryn- ebacterium parvum treated mice were directly cytotoxic to P815 tumor cells. Spleen cells that are normally not cytotoxic to P815 tumor cells (18 h) became cytotoxic when mixed with adherent nonparenchymal liver cells from untreated mice. These results indicate that the tumoricidal effector cell in nonparenchymal liver cells from untreated mice appears to be the NK cell. Apparently, murine liver marophages from untreated mice do not have tumoricidal activity per se but can “activate” NK cells to kill tumor cells normally resistant to NK cells.
Cultured Human Alveolar Macrophages From Smokers With Lung Cancer: Resolution of Factors That Stimulate Fibroblast Proliferation, Production of Collagenase, or Prostaglandin E2
Authors: Dayer J-M , Sundstrm L , Polla B S , Junod A F 
Published: January 2018

Abstract
Marked connective tissue remodelling involves both destruction and repair in inflammatory lung diseases. Throughout the remodelling event, it was reasoned that alveolar macrophages may release substances similar to those produced by blood monocyte-macrophages that affect fibroblast functions, ie, the interleukin 1 family of monokines (or cytokines). We have examined human alveolar macrophage cultures obtained after bronchoalveolar lavage of freshly excised lungs from heavy smokers with bronchial carcinoma. Crude culture media contained fibroblast proliferative activity and collagenase- and PGE2- production-stimulating activity. The main peak of these biological activities was located around - I8 kilodaltons (kD) on gel filtration chromatography. Resolution of this peak by high performance liquid chromatography showed the presence of three distinct peaks, with quantitative and qualitative differences in biological activities. This suggests the presence of heterogeneous factors.
Modulation of Neutrophil-Reduced Pyridine Nucleotide Content Following Stimulation With Phorbol Myristate Acetate and Chemotactic Factors
Authors: Van Epps Dennis E , Bender James G , Steinkamp John A , Chenoweth Dennis E 
Published: January 2018

Abstract
Modulation of NAD(P)H in human neutrophils (PMN) following stimulation with phorbol myristate acetate (PMA) or chemotactic factors was determined by flow cytometry. Stimulation of PMN with 1 μg/ml of PMA results in a time-dependent decrease in fluorescence, attributable to the oxidation of NAD(P)H. The decrease in fluorescence did not occur with PMN from a patient with chronic granulomatous disease (CGD) and was observed in only half of PMN from the mother of the patient. Loss of fluorescence in normal PMN was maximal following 7–15 min of stimulation with PMA. Simultaneous measurement of PMA-stimulated NAD(P)H oxidation and H2O2 production showed that NAD(P)H oxidation occurred as an all-or-none response while H2O2 production showed a graded response.
These data suggest that with PMA stimulation, a threshold exists beyond which constitutive NAD(P)+ reduction is suppressed and complete oxidation of NAD(P)H occurs, while H2O2 production is proportional to the concentration of PMA. PMA-stimulated oxidation of NAD(P)H was reversible, and fluorescence returned to the initial level or higher after 40–60 min. Oxidation of NAD(P)H also occurred when cytochalasin B-treated PMN were stimulated with 25 nM C5a or 100 nM formyl-methionyl-leucyl-phenylalanine (f-MLP), but occurred more rapidly, peaking at 1 to 3 min. Fluorescence also returned by 5–6 min. This response to C5a and f-MLP was graded and proportional to the concentration of chemotactic factor used. Comparative studies showed that the cytochalasin-B treatment was essential for measurement of NAD(P)H oxidation, in response to C5a and F-MLP.
Selective Recognition of Rat Follicular Dendritic Cells (Dendritic Reticulum Cells) by a New Monoclonal Antibody Ki-M4R In Vitro and In Vivo
Authors: Wacker H H , Radzun H J , Mielke V , Parwaresch M R 
Published: January 2018

Abstract
Using unstimulated rat peritoneal cells as immunogen a new monoclonal antibody KiM4R was produced. Ki-M4R recognizes follicular dendritic cells (dendritic reticulum cells) in germinal centers of lymphoid follicles in lymphatic tissue. In addition, sinus lining cells, endothelia of postcapillary venules, as well as mesangial cells of the renal glomerula immunoreact with Ki-M4R in vitro as well as in vivo. This antibody might be useful for studying the interaction of follicular dendritic cells and B-cell immune response.
Expression of Granulocyte Colony-Stimulating Factor by Human Cell Lines
Authors: Devlin James J , Devlin Patricia E , Myambo Kenneth , Lilly Michael B , Rado Thomas A , Warren M Kim 
Published: January 2018

Abstract
We have isolated and expressed a cDNA clone that encodes a human granulocyte colony-stimulating factor from the MIA PaCa-2 cell line. A genomic clone of this factor has been isolated from the CHU-2 cell line and is reported to encode two alternative transcripts [The EMBO J. 5,575, 1986]; one transcript predicts an amino acid sequence identical to that predicted by our MIA PaCa-2 cDNA clone; the other transcript predicts a similar protein containing a three amino acid residue insertion. To investigate which types of this colony-stimulating factor are produced by other cell lines, we used specific oligonucleotides to determine which types of transcripts were present in MIA PaCa-2, 5637, and LD-1 cells, all of which have been reported to produce a factor that can stimulate the growth of predominantly granulocyte colonies in human bone marrow cell cultures. Northern analysis with these probes revealed MIA PaCa-2-like transcripts in all of these cell lines and failed to detect transcripts that would encode the colony-stimulating factor that contained the three-amino-acid-residue insertion.
Independent Regulation of Leukotriene B4-Elicited Polymorphonuclear Leukocyte Exocytosis and Superoxide Generation by a Serum Factor
Authors: Mandell Brian F 
Published: January 2018

Abstract
Serum from a patient with inactive systemic lupus erythematosus (SLE) and ibuprofen-induced transient neutropenia was used as a probe to define further the control of human polymorphonuclear leukocyte (PMN) exocytosis and superoxide (O-2) generation. Thirty-minute preincubation of normal PMNs with 10-50H v/v of this serum, followed by washing, produced a specific dose-related suppression of leukotriene B4 (LTB4)-elicited β-glucuronidase and lysozyme release of up to 45% and 30% respectively. If cells were not washed, the inhibition increased to 60% and 40%. Superoxide production stimulated by LTB4 was unaffected. The serum had no effect on formyl-met-leu-phe (FMLP) or phorbol myristate acetate-stimulated O2- or exocytosis. O2- and β-glucuronidase release elicited by zymosan-treated serum (ZTS) were both decreased by 15%, but there was no increased inhibition seen if cells were not washed, or if the time of preincubation was increased from 7 to 30 min. In contradistinction, the serum inhibition of LTB4 exocytosis did show time dependence. Serum obtained when the patient was not leukopenic and sera from 6 normal controls, 2 patients with inactive SLE, 1 patient with SLE and chronic leukopenia, and 2 controls taking Ibuprofen did not influence any PMN function. The serum inhibition of ZTS-induced functions was qualitatively similar to that observed when PMNs were preincubated and desensitized with ZTS in vitro. Selective inhibition of LTB4 exocytosis was not seen when PMNs were desensitized with LTB4 in vitro. These observations indicate that LTB4-elicfted O2- and exocytosis can be independently and specifically regulated. The cellular site at which this serum factor acts is not clear, but the current studies strongly suggest that this inhibition is not due to in vitro deactivation by LTB4 activity.
Induction of Tissue Transglutaminase in Human Peripheral Blood Monocytes by Intracellular Delivery of Retinoids
Authors: Mehta Kapil , Turpin Jim , Lopez-Berestein Gabriel 
Published: January 2018

Abstract
Human peripheral blood monocytes (HPBM) from normal donors, isolated by counter-current centrifugal elutriation into two subpopulations, showed no significant difference in their ability to differentiate in vitro into macrophages as determined by induction of a protein cross-linking enzyme tissue transglutaminase (TGase). The two subpopulations were equally responsive to the augmenting effect of recombinant interferon-γ (riFN-γ) on expression of tissue TGase. In vitro maturation and treatment with rlFN-γ of HPBM were associated with increased binding of tritlated retinol. Intracellular delivery of retinol rendered this hormone active in inducing the differentiation of HPBM. The retinoid-induced expression of tissue TGase was the result of increased accumulation of the enzyme peptide and not activation of preexisting enzyme. We propose, therefore, that maturation of HPBM, induced by in vitro culture or treatment with rlFN-γ, is associated with acquisition of cell surface receptors for serum retinol-binding protein.
Requirements for Immunoglobulin Synthesis in Leukocyte Cultures Exposed to Human Cytomegalovirus
Authors: Beeler Barbara A , Hutt-Fletcher Lindsey M 
Published: January 2018

Abstract
T cell-depleted leukocytes from normal healthy donors lacking antibody to cytomegalovirus (CMV) were induced to secrete immunoglobulin (Ig) by exposure to inactivated CMV. The responses to two virus strains were compared. One strain had been reported to require specific T cell help to induce Ig synthesis, and the other had been reported to induce Ig synthesis in the presence of only very few cells. Both viruses induced T cell-depleted leukocytes from one group of seronegative donors to secrete Ig. However, both viruses failed to induce leukocytes from a second group of donors to secrete Ig unless B cell growth factor was added as a source of T cell help. These findings suggest that certain individuals are hyperresponsive to CMV and raise the possibility that this group may be most likely to develop mononucleosis after primary infection with CMV.
Proposal for Classification of Leukocyte-Associated Cytolytic Molecules: Denver, Colorado, September 28, 1986
Authors: Koren H , Goldfarb R , Henkart P , Bleackley C , Bonavida B , Granger G , Palladino M , Podack E , Reynolds C , Ruddle N , Ziegler-Heitbrock H W L 
Published: January 2018

Abstract
The continuous increase of newly described cytolytic factors and the lack of a nomenclature system to accommodate these molecules prompted the nomenclature committee of the Reticuloendothelial Society (RES) to sponsor a dry workshop focusing on this topic preceding the Annual RES Meeting, September 28, 1986, in Denver, Colorado. Similar attempts to establish a nomenclature system in other areas of immunology have been quite successful in the past. These include the HLA system, the interleukin system, B-cell stimulating factors, and the CD nomenclature for monoclonal antibodies. The workshop was attended by about 100 scientists mainly from the U.S., although representatives of other countries were present as well.
Expression of an Activation Antigen, Mo3e, Associated With the Cellular Response to Migration Inhibitory Factor by HL-60 Promyelocytes Undergoing Monocyte-Macrophage Differentiation
Authors: Todd Robert F , Bury Martin J , Liu David Y 
Published: January 2018

Abstract
HL-60 promyelocytic cells acquire the surface expression of the Mo3e antigenic determinant after exposure to PMA or compounds that raise intracellular concentrations of cyclic AMP (dibutyryl cyclic AMP or a combination of cholera toxin and IBMX). The expression of Mo3e by these stimulated HL-60 cells coincides with the development of features of monocyte-macrophage differentiation (characteristic morphology, nonspecific esterase activity, and respiratory burst activity). During in vitro monocyte-macrophage differentiation, HL-60 cells become responsive to migration inhibitory factor (MIF); the MIF responsiveness of differentiated HL-60 cells is blocked by anti-Mo3e monoclonal antibody. These findings further support the relationship between the expression of Mo3e and the cellular response to MIF.