bluuebunny/crossref_metadata_2025_split huggingface dataset:
Simultaneous assay for oxidative metabolism and adhesion of human neutrophils: evidence for correlations and dissociations of the two responses
Authors: Bellavite P , Chirumbolo S , Mansoldo C , Gandini G , Dri P 
Published: January 2018

Abstract
An assay method for the simultaneous evaluation of the oxidative metabolism and adherence of human neutrophils is described, together with certain specific applications. Incubations were performed in serum-coated microtiter plates, where oxidative metabolism was measured as O−2 release and, after washing out the nonadherent cells, the adhesion was measured as activity of acid phosphatase. Three agonists tested in this system –- opsonized zymosan, concanavalin A, and N-formyl-methionyl-leucyl-phenylalanine –- induced both activation of O−2 release and cell adhesion, but the two functions had time course and dose dependence patterns that varied depending on the stimulant. Particularly with concanavalin A, O−2 release and adhesion response were markedly dissociated; this lectin at low doses increased neutrophil adherence without triggering any O−2 production, whereas at high doses it increased both O−2 production and adherence. Anti-integrin monoclonal antibodies did not affect adhesion induced by low-dose concanavalin A but inhibited the adhesion induced by the other tested agonists. Adhesion and O−2 production were also found to be differentially affected by the NADPH oxidase inhibitor diphenylene iodonium, the sulfhydryl reagent N-ethylmaleimide and the A2 agonist adenosine, indicating that these neutrophil responses have various transductional pathways that also depend on the type of stimulus.
A monoclonal antibody specific for immunoglobulin A receptor triggers polymorphonuclear neutrophil superoxide release
Authors: Shen Li 
Published: January 2018

Abstract
An immunoglobulin M (IgM) monoclonal antibody, My43, specific for IgA Fc receptor (FcαR) on human monocytes, bound to human polymorphonuclear neutrophils (PMNs) and inhibited their ability to bind IgA but not IgG. It was observed that the PMN oxidative burst was induced by both polymeric IgA and aggregated IgG, whereas IgM was without effect. The IgG-mediated oxidative burst was inhibited by anti-FcγRII Fab and anti-FcγRIII F(ab')2 but not by My43. Conversely, the IgA-mediated oxidative burst was inhibited by My43 but not by anti-FcγRII or anti-FcγRIII. When anti-Fc receptor monoclonal antibodies (mAbs) were used directly as ligands, it was observed that both anti-FcγRII Fab and anti-FcγRII F(ab')2 promoted the oxidative burst when cross-linked. Moreover, My43, when cross-linked with F(ab')2 antimouse IgM, also triggered the oxidative burst, whereas an IgM anti-GDI5 mAb, PM81, did not stimulate function. This demonstrates that IgA receptors on PMNs are function-triggering molecules and that an anti-IgA receptor mAb may be substituted as a ligand.
Recognition of Histoplasma capsulatum yeast-cell antigens by human lymphocytes and human T-cell clones
Authors: Henderson Harold M , Deepe George S 
Published: January 2018

Abstract
We have prepared a detergent extract from the cell wall and cell membrane of Histoplasma capsulatum yeast cells that is recognized by T cells from mice immunized with viable organisms or with the extract. A 62-kd antigen from this extract has been isolated and has been shown to be antigenic and to confer protective immunity in mice. In this study, we examined the in vitro proliferative response by human lymphocytes and human T-cell clones to both the extract from the cell wall and cell membrane and the 62-kd antigen, termed HIS-62. Seven healthy individuals were identified whose peripheral blood mononuclear cells responded to the cell wall and cell membrane extract from H. capsulatum yeast cells. Mononuclear cells from all seven individuals recognized histoplasmin. T-cell clones were generated from peripheral blood mononuclear cells from a single person using the extract from cell wall and cell membrane as the antigenic preparation. Nineteen clones were propagated; all expressed the surface phenotype CD3+, CD4+, T-cell receptor α/β+. The clones were antigen-specific. Of 17 clones studied, none responded to extracts from Blastomyces dermatitidis or Coccidioides immitis or to tetanus toxoid. Sixteen of 19 clones recognized HIS-62 in vitro. Additional analysis revealed that cells from each of the seven individuals who responded to the extract mounted a proliferative response to HIS-62. Thus, the extract from the cell wall and cell membrane and HIS-62 are targets of the human cell-mediated immune response to H. capsulatum. Moreover, HIS-62 appears to be an immunodominant antigen.
Short amino acid sequences derived from C1q receptor (C1q-R) show homology with the alpha chains of fibronectin and vitronectin receptors and collagen type IV
Authors: Ghebrehiwet Berhane , Peerschke Ellinor I B , Hong Yuqun , Munoz Priscilla , Gorevic Peter D 
Published: January 2018

Abstract
The human C1q receptor (C1q-R) is a 65–70-kd, highly acidic, hydrophobic glycoprotein that is expressed on a wide variety of cell surfaces. Although the C1q-R itself appears to bind preferentially to C1q, the region of the ligand to which C1q-R binds is the primary binding site for several other molecules, including fibronectin, laminin, and C1q inhibitor (chondroitin 4-sulfate proteoglycan) as well as the complement C1r2C1s2 tetramer. In order to further characterize the C1q-R molecule with regard to its structure and function, highly purified C1q-R was obtained from Raji cells using DEAE-Sephacel and C1q-Sepharose CL-4B chromatography. Studies performed with 125I-labeled C1q-R demonstrated that whereas the C1q-R molecule binds poorly to a variety of human collagens including types II, III, and V, markedly enhanced binding is observed with type IV collagen and moderately enhanced binding with type I collagen. Amino acid composition studies show that the C1q-R molecule contains approximately 44% hydrophobic and 12.6% hydrophilic residues with a ratio of negatively charged to positively charged residues of about 2:1. Treatment of 125I-labeled C1q-R with endoglycosidase F lowers the apparent molecular size from 70 to 58 kd, whereas endoglycosidase H lowered the size to 64 kd. Treatment with neuraminidase, on the other hand, shifted the size of C1q-R to 60 kd. These results suggest the presence of several highly sialylated complex-type or high mannose–type N-linked oligosaccharide side chains. Because purified C1q-R has a blocked amino terminus, amino acid sequences representing internal fragments of the molecule were generated by electroblotting and in situ enzymatic digestion. When these short sequences were searched against the National Biomedical Research Foundation computer data base, a seven-amino-acid sequence, VSWQGQI, showed significant homology (100% and 80% in a five-amino-acid overlap, respectively) with the α chains of the human fibronectin (α5β1) and vitronectin (αvβ3) receptors, and to a lesser degree with epidermal growth factor receptor and T cell receptor. A second sequence, ISEDNIR, showed homology with mouse collagen type IV (86% in a six-amino-acid overlap), calmodulin (60% in a seven-amino-acid overlap), and a Leishmania major surface antigen, gp63. These observations seem to predict that C1q-R has pockets of conserved sequences that are similar to those not only present in its ligand(s) but also in other cell surface receptors that may, in part, fulfill similar functions.
Superoxide generation by the human polymorphonuclear leukocyte in response to latex beads
Authors: Thomas Michael J , Hedrick Catherine C , Smith Sharon , Pang Jian , Jerome W Gray , Willard Andra S , Shirley Pamela S 
Published: January 2018

Abstract
In this study, superoxide formation was not immediately detected when polymorphonuclear leukocytes were treated with linoleyl alcohol–coated, carboxy-modified latex beads. However, all other measures of neutrophil activation were present. Superoxide was not detected until 30 min after the initial exposure to beads. However, an O−2-producing, NADPH-dependent oxidase is active 15 min after exposure. When polymorphonuclear leukocytes are pretreated with cytochalasin B, superoxide production is detected immediately after exposure to the beads. Superoxide secretion after treatment with linoleyl alcohol–coated latex beads is compared with the response to other latex beads. The results imply that neutrophils form a phagolysosome around linoleyl alcohol–coated latex beads that is tightly sealed and does not allow superoxide to escape into the medium where it could be detected by the reduction of ferricytochrome c.
Development, differentiation, and proliferation of epidermal Langerhans cells in rat ontogeny studied by a novel monoclonal antibody against epidermal Langerhans cells, RED-1
Authors: Mizoguchi Suzuhiko , Takahashi Kiyoshi , Takeya Motohiro , Naito Makoto , Morioka Tohru 
Published: January 2018

Abstract
An antirat monoclonal antibody (mAb) against nonlymphoid dendritic cells, RED-1, was produced using epidermal Langerhans cells (LCs) as the immunogen. This mAb reacted mainly with the LCs and indeterminate dendritic cells (ICs), interdigitating cells in the T cell areas of lymphoid tissues, and monocyte/macrophages in various organs and tissues of adult rats. In the epidermal sheets prepared from adult rats, it specifically recognized the cell surface antigen(s) present on LCs and ICs. In the fetal rat skin, primitive or fetal macrophages migrated into the epidermis and expressed RED-1 at fetal day 17. With advance of gestation, RED-1–positive cells increased, started expressing Ia antigens at fetal day 18, and subsequently differentiated into dendritic cells. Most of them showed Ia expression by fetal day 20 and differentiated into LCs within a few days after birth. The labeling index of 5-bromo-2′-deoxyuridine in RED-1–positive cells was 18% at fetal day 17 and decreased to 5 to 6% in the postnatal period. These results imply that proliferative capacity of RED-1–positive cells is important for the formation and expansion of the IC population in the fetal stage and for the survival of LCs in the postnatal period.
Tumor antigen presentation by epidermal antigen-presenting cells in the mouse: modulation by granulocyte-macrophage colony-stimulating factor, tumor necrosis factor α, and ultraviolet radiation
Authors: Grabbe Stephan , Bruvers Sandra , Lindgren Ann M , Hosoi Junichi , Tan Kong C , Granstein Richard D 
Published: January 2018

Abstract
I-A+ epidermal antigen-presenting cells (APCs, Langerhans cells) have been shown to present tumor-associated antigens (TAAs) and to induce tumor immunity in vivo. This study examined the effects of ultraviolet radiation (UVR) and the cytokines granulocyte-macrophage colony-stimulating factor (GM-CSF) and tumor necrosis factor α (TNF-α) on the ability of epidermal cells (ECs) to induce or to elicit immunity against the murine spindle cell tumor S1509a. Naive syngeneic mice were immunized three times at weekly intervals with ECs that had been cultured in GM-CSF for 18 h and then pulsed with TAA derived from S1509a. This resulted in protective immunity against subsequent tumor challenge, providing a model to study the conditions required for sensitization against TAAs by epidermal APCs. Culture of ECs in GM-CSF was required for induction of significant protective tumor immunity, and UV irradiation or incubation in TNF-α for 2 h after GM-CSF incubation abrogated the immunostimulatory effect of GM-CSF. However, unlike UVR, TNF-α did not significantly inhibit the induction of immunity when ECs were exposed to TNF-α before overnight incubation in GM-CSF, together with GM-CSF, or after pulsing with TAA, and anti-TNF-α antibody treatment did not abrogate the effects of UVR on this system. Furthermore, TNF-α incubation of ECs augmented their ability to elicit delayed-type hypersensitivity (DTH) and also enhanced elicitation of DTH by GM-CSF–cultured ECs, whereas UV-irradiation reduced it in a dose-dependent fashion. Taken together, these results demonstrate that GM-CSF, TNF-α, and UVR are significant regulators of tumor antigen presentation by epidermal APCs and that the effects of the cytokines examined differ with regard to induction or elicitation of immunity.
Differential effects of interleukin-4 on superoxide anion production by human alveolar macrophages stimulated with lipopolysaccharide and interferon-γ
Authors: Bhaskaran Geetha , Nii Akihiko , Sone Saburo , Ogura Takeshi 
Published: January 2018

Abstract
The effect of interleukin-4 (IL-4) on the activation state of human alveolar macrophages (AMs) and blood monocytes induced by lipopolysaccharide (LPS) or recombinant interferon-γ (IFN-γ) was investigated on the basis of their ability to produce superoxide anion (O2-). AMs were obtained from healthy donors by bronchoalveolar lavage, and O2- productions of these cells were assayed by a cytochrome c reduction method after incubation with stimulants for 24 h. AMs produced more O2- than autologous blood monocytes when stimulated with LPS. IL-4 alone had little effect on O2- production by unstimulated AMs but down-regulated O2- production by LPS-stimulated AMs in a dose-dependent manner. IL-4 also suppressed O2- production by AMs induced by the synergistic actions of muramyl dipeptide (norMDP) and IFN-γ. Maximum suppression by IL-4 of O2- production by AMs was observed when IL-4 was added within 1 h after initiation of LPS stimulation. AMs also showed high O2- production when stimulated with IFN-γ alone. In contrast to its suppression of O2- production by LPS-stimulated AMs, IL-4 enhanced O2- production by AMs stimulated with IFN-γ. These data suggest that IL-4 is an important regulator of O2- production by macrophages through different pathways depending on the stimulus.
Constitutive production of PAI-II and increased surface expression of GM1 ganglioside by peripheral blood monocytes from patients with AIDS: evidence of monocyte activation in vivo
Authors: Auci Dominick L , Chice Seto M , Durkin Helen G , Murali Mandakolathur R 
Published: January 2018

Abstract
To characterize the activation state of monocytes during human immunodeficiency virus (HIV) infection, peripheral blood monocytes (PBMs) from patients with acquired immunodeficiency syndrome (n = 10) and from healthy controls (n = 10) were cultured for 4 days. Monocyte culture supernatant (MCS) was collected daily, and levels of urokinase (UK) inhibitor PAI-II, a product of activated monocytes, released into MCS were determined (fibrin plate assay). To examine the activation state of PBMs independently, expression of GM1 ganglioside on PBMs from patients with AIDS (n = 9), patients with AIDS-related complex (ARC) (n = 8), HIV+ asymptomatic patients (n = 6), and HIV” healthy controls (n = 11) was determined (flow cytometry; living cells in suspension). Data are expressed as percent inhibition of UK, or as percent total cells. Patients' MCS collected on days 1–4 of culture contained similar levels of PAI-II because it inhibited UK in similar fashion (70–90%). In contrast, MCS from healthy controls, collected after 2 days, had decreased ability to inhibit UK (15–50%) and thus contained lower levels of PAI-II. Monocyte activation, measured by increased expression of GM1 ganglioside on PBM surfaces, directly correlated with the progression of HIV infection into the development of AIDS, since the order of magnitude of GM1 ganglioside expression on PBMs was AIDS &gt; ARC &gt; HIV+ asymptomatic = healthy controls. Our data indicate that PBMs from patients with AIDS are constitutively activated and suggest that activation directly correlates with disease progression.
Differential induction of prostaglandin E2-dependent and -independent immune suppressor cells by tumor-derived GM-CSF and M-CSF
Authors: Oghiso Yoichi , Yamada Yutaka , Ando Koichi , Ishihara Hiroshi , Shibata Yoshimi 
Published: January 2018

Abstract
Both prostaglandin E2 (PGE2)-dependent (indomethacin-sensitive) and PGE2-independent (indo-methacin-insensitive) suppressor cell activities that inhibited mitogenic T cell blastogenesis appeared in the bone marrow and spleen of mice on days 20 to 30 following transplantation of NFSA fibrosarcoma molecularly expressing mRNA for both macrophage (M) and granulocyte-macrophage (GM) colony-stimulating factors (CSFs). The present study was done to characterize the two different suppressor cells isolated from NFSA tumor-bearing mice and to verify a role of CSFs in the induction of suppressor cells in vitro. Whereas PGE2-releasing suppressor cells were found in bone marrow and spleen cells isolated from tumor-bearing mice, indomethacin-insensitive suppressor cells in both tissues were localized predominantly in adherent cell fractions. An increase in Mac-1+ and Mac-2+ spleen cell populations with two to three times larger cell volumes was observed, and both showed strong PGE2-releasing capacity and indomethacin-sensitive suppressor cell activity. However, after elimination of Mac-1+ or Mac-2+ cells, bone marrow cells still showed higher PGE2-releasing capacity and indomethacin-sensitive suppressor activity. The in vitro cultures of normal bone marrow and spleen cells with NFSA cell conditioned medium (NFSA-CM) induced heterogeneous mixtures of indomethacin-sensitive and -insensitive suppressor cells like those observed in cultures with the combination of M-CSF and GM-CSF. However, cultures with either GM-CSF or M-CSF resulted in the induction of indomethacin-sensitive suppressor cells by GM-CSF and of indomethacin-insensitive suppressor cells by M-CSF. In addition, NFSA-CM pretreated with anti-GM-CSF antibody induced indomethacin-insensitive suppressor cells in in vitro cultures of bone marrow and spleen cells. These results suggest that two distinctly different suppressor cells developed under hemopoiesis of myelomonocytic lineage cells are regulated differentially by the two macrophage growth factors, M-CSF and GM-CSF. J. Leukoc. Biol. 53: 86–92; 1993.
Tumor necrosis factor-α induction by reovirus serotype 3
Authors: Farone Anthony L , O’Brien Patricia CM , Cox Donald C 
Published: January 2018

Abstract
We have reported previously that reovirus, when used in combination with 1,3-bis(chloroethyl)-1- nitrosourea (BCNU) chemotherapy, mediates the rejection of murine ascites tumors. Surviving animals reject a challenge with the same, hut not a different, tumor, which suggests that tumor-specific immunity is induced by the treatment regimen. The present study was designed to characterize the interaction between reovirus and murine peritoneal macrophages, both in vitro and in vivo, to determine whether such a relationship may play a role in immune modulation resulting in tumor rejection. The results demonstrated that reovirus can efficiently infect peritoneal macrophages in vitro and stimulate the secretion of tumor necrosis factor-alpha (TNF-α). In vivo administration of reovirus, however, did not produce high levels of infection in peritoneal exudate cells, even though the cells were stimulated to express detectable levels of membrane TNF-α. These results suggested that infection is not necessary for TNF-α expression and this hypothesis was supported by the observation that this expression was also stimulated in vitro by UV-inactivated reovirus. These findings suggest that one mechanism for immune stimulation by reovirus may be through the induction of TNF-a.—Farone, AX., O’Brien, P.C.M., Cox, D.C. Tumor necrosis factor-α (TNF-a) induction by reovirus serotype 3. J. Leukoc. Biol. 53: 133–137; 1993.
Inhibition of tumor cell mitochondrial respiration by macrophage cytotoxic mediators distinct from interferon-γ
Authors: Tucker Stanley D , Auzenne Edmond J , Sivaramakrishnan Mathoor R 
Published: January 2018

Abstract
Macrophage-mediated inhibition of mitochondrial respiration in EMT-6 murine mammary adenocarcinoma cells can be mimicked in vitro by treatment of the cells with interferon-γ (IFN-γ) in combination with tumor necrosis factor, interleukin-1, or lipopolysaccharide. Conditioned supernatants obtained from activated macrophages appear to contain interferon-γ, suggesting that inhibition of mitochondrial respiration in tumor cells was caused by synergy of IFN-γ with other cytokines. To further characterize monokines that cause inhibition of mitochondrial respiration in tumor cells, EA13.5 macrophage-like cells were isolated and selected for inhibition of mitochondrial respiration in EMT-6 tumor cells. After stimulation with IFN-γ and lipopolysaccharide, the EA13.5 cells released into conditioned supernatants a cytotoxic mediator that induced nitric oxide synthesis and caused lesions in the electron transport chain of EMT-6 cells similar to the lesions caused by activated peritoneal macrophages. Enzyme-linked immunosorbent assay demonstrated that the conditioned supernatants produced by EA13.5 macrophage cells did not contain IFN-γ. Treatment of the EA13.5 cell-conditioned supernatants with neutralizing antibody against IFN-γ did not abrogate the inhibition of mitochondrial respiration in EMT-6 cells caused by these conditioned supernatants. This study demonstrated that unidentified macrophage cytotoxic mediators distinct from IFN-γ are involved in the induction of nitric oxide synthesis and inhibition of mitochondrial respiration in tumor cells. J. Leukoc. Biol. 53: 138–143; 1993.
Relationship between macrophage colony-stimulating factor production by uterine epithelial cells and accumulation and distribution of macrophages in the uterus of pregnant mice
Authors: De Mamata , Sanford Thomas , Wood Gary W 
Published: January 2018

Abstract
Estrogen and progesterone induce production of macrophage colony-stimulating factor (CSF-1) by uterine epithelial cells, and CSF-1 is produced in the uterus during pregnancy in mice. CSF-1 is a lineage-specific stimulator of macrophage proliferation, chemotaxis, and function. High concentrations of macro-phages accumulate in the uterus during pregnancy. Ex-periments were conducted to determine whether a relationship exists between intrauterine CSF-1 production and the number and distribution of uterine macrophages during pregnancy in mice. The study demonstrated that on day 1 of pregnancy CSF-1 bioactivity levels were high. The number of macrophages in the uterus was also high on days 1 and 2, and macrophages were concentrated at epithelial surfaces. The decrease in CSF-1 bioactivity seen between days 1 and 2 was followed by a decrease in the macrophage concentration. An increase in CSF-1 bioac-tivity on day 4 was followed by an increase in the con-centration of intrauterine macrophages. During the im-mediate postimplantation period, macrophages were detected primarily in the myometrium and deep en-dometrium and CSF-1 bioactivity was undetectable. During the second half of pregnancy, when CSF-1 con-centrations were very high, the macrophage concentration was also very high and large numbers of macrophages were detected in association with epithelia. The data confirmed the existence of a direct relationship between intrauterine CSF-1 and macrophage accumulation and suggested that macrophages are attracted to epithelial surfaces by CSF-1. J. Leukoc. Biol. 53: 240–248; 1993.