bluuebunny/crossref_metadata_2025_split huggingface dataset:
Induction and blocking of cytolysis in CD2+, CD3- NK and CD2+, CD3+ cytotoxic T lymphocytes via CD2 50 KD sheep erythrocyte receptor.
Authors: Bolhuis R L , Roozemond R C , van de Griend R J 
Published: December 2022

Abstract
The 50 KD sheep red blood cell antigen receptor CD2 is the earliest T cell differentiation marker and is present on all blood-derived T cells, including natural killer (NK) cells. The CD2 antigen is also known to serve as an important activation site regulating various T cell functions. We report that anti-CD2 monoclonal antibodies (MAb) block MHC-restricted class I- and class II-specific cytolysis by CD2+, CD3+ clones of the relevant target cells, irrespective of whether lysis by these clones is blocked by anti-CD3 or anti-CD8 MAb. Moreover, anti-CD2 MAb (but not anti-CD3 MAb) are able to reduce MHC-nonrestricted, nonspecific cytolysis: a) by CD2+, CD3+ clones of K562 target cells; and b) by CD2+, CD3 NK clones of K562 as well as Daudi cells. Different preparations of anti-CD2 MAb vary in their capacity to inhibit cytolysis. For cloned effector cells, the percent inhibition of lysis by CLB-T11 greater than Lyt-3 MAb, whereas with "fresh" NK cells, the lysis inhibitory ability of Lyt-3 greater than CLB-T11. The antibody-dependent cellular cytotoxicity by "fresh" and cloned NK cells is not inhibited by anti-CD2 MAb. Anti-CD2 MAb also prevent the induction of lysis by cross-linked anti-CD3 MAb, e.g., by CD2+, CD3+ cloned cloned cells against (IgG-FcR+) Daudi cells. Anti-CD2 MAb can also induce cytolysis in some, but not all, CD2+, CD3- NK clones against xenogeneic P815 mouse mastocytoma cells. Anti-CD2 MAb, in combination with lectins (PHA or Con A: pretreatment of effector cells), can also induce cytolytic activity by CD2+, CD3+ clones against Daudi cells. Our data therefore support the concept that the CD2 antigen is an important activation site regulating a wide variety of T cell functions including cytolysis. Whether ligand interaction with the CD2 antigens results in augmentation or inhibition of T cell functions may very well depend on the type of CD2 antigen-ligand interaction, e.g., cross-linked ligand-receptor interaction may, in general, enhance the various T cell functions, whereas noncross-linked ligand-receptor interactions may inhibit such functions, as we and other investigators demonstrated earlier for the CD3/Ti antigen-receptor complex activation site.
Separate ontogeny of two macrophage-like accessory cell populations in the human fetus.
Authors: Janossy G , Bofill M , Poulter L W , Rawlings E , Burford G D , Navarrete C , Ziegler A , Kelemen E 
Published: December 2022

Abstract
Human macrophage-like accessory cells were analyzed as they emerge in the absence of extrinsic antigens during fetal development. Monoclonal antibodies to monocytes/macrophages were used in combination with antibodies to HLA class II molecules. In the yolk sac and mesenchyme sampled at wk 4 to 6 of fertilization age, cells with dendritic morphology formed two populations distinguishable by phenotypic criteria: type i (majority) carried both macrophage-associated (RFD7+) and monocyte-associated markers (UCHM1+) but no detectable HLA-DR antigen, and type ii (minority) constitutively expressed class II (HLA-DR and -DP) but no RFD7 and UCHM1. The emergence of this heterogeneity preceded the formation of both thymus and bone marrow. During additional development, type i and type ii cells seeded to different microenvironments and underwent some additional phenotypic changes. Cells of type i, the RFD7+ population with high lysosomal (acid phosphatase) activity, were seen in the thymic cortex, marginal zone of lymph nodes, splenic red pulp, and in the midst of erythropoietic activity within the bone marrow. These cells were UCHM1- and class II-. Cells of type ii formed the population of HLA-DR+, RFD7- interdigitating cells, early inhabitants of T cell areas in the developing thymic medulla, lymph nodes, spleen, and tonsil. The Type ii cells that had already settled in their nichès expressed not only HLA-DR and -DP but also HLA-DQ, and another class II antigen identified by the antibody RFD1, which shows the restricted tissue distribution of HLA-DQ, but is governed by genes that are outside of and telomeric to the HLA-DQ region (or HLA-DR). Finally, subpopulations of macrophages (RFD7+, acid phosphatase-positive) in the fetal gastrointestinal and hepatic systems were HLA-DR+; the latter appear to include precursors of Kupffer cells in the developing liver.
Cellular mechanisms in the in vitro inhibition of pokeweed mitogen-induced B cell differentiation by immunoglobulin for intravenous use.
Authors: Stohl W 
Published: December 2022

Abstract
Polyspecific monomeric IgG for i.v. use (IgSRK; Sandoglobulin) can inhibit in vitro pokeweed mitogen (PWM)-induced B cell differentiation. This antigen-nonspecific inhibition is an early event, because removal of the IgSRK from cultures of PWM-stimulated peripheral blood mononuclear cells (PBMC) after as short a period as 24 hr could not reverse the inhibitory effects. Furthermore, replacement of the IgSRK-exposed T cells after 48 hr of culture with fresh autologous T cells could not abrogate the inhibition. In addition, IgSRK exerted an inhibitory effect on non-T cells even before their activation by PWM. Neither augmentation of T suppressor activity nor inhibition of T helper activity could be demonstrated as a consequence of interaction with IgSRK. Irradiation of the T cells before culture, supplementing the culture medium with exogenous interleukin 2, monocyte depletion, or depletion of the Leu-11+ population had no effect on the IgSRK-mediated inhibition. Tonsil cells were as susceptible to the inhibitory effects of IgSRK as were unseparated PBMC. Taken together, these experiments point to a direct inhibitory effect of IgSRK on the B cell in this antigen-nonspecific system. However, minor roles for monocytes, T cells, and/or Leu-11+ cells cannot be excluded. This inhibitory capacity of IgSRK might be efficacious clinically in the treatment of autoimmune disorders in which pathogenic autoantibodies play a role. However, such treatment might also inhibit desired antibody responses to vaccinations and/or infectious agents.
Activated terminal complement in cerebrospinal fluid in Guillain-Barré syndrome and multiple sclerosis.
Authors: Sanders M E , Koski C L , Robbins D , Shin M L , Frank M M , Joiner K A 
Published: December 2022

Abstract
A quantitative enzyme-linked immunosorbent assay was used to measure the concentration of fluid-phase complement C5b-9 complexes (SC5b-9) in the cerebrospinal fluid (CSF) of 14 patients with acute monophasic Guillain-Barré Syndrome (GBS), 21 patients with multiple sclerosis (MS), and 11 patients with noninflammatory central nervous system (CNS) diseases. SC5b-9 complexes were detected in the CSF of 13 of 14 patients with acute GBS (mean, 3.08 micrograms/ml; range, 0 to 7.1 micrograms/ml) and 16 of 21 patients with MS (mean, 1.83 micrograms/ml; range, 0 to 7.5 micrograms/ml). In the control group of patients with noninflammatory CNS diseases, SC5b-9 was not detected in eight of 11 and was present in low concentrations in the remaining three patients (mean, 0.28 micrograms/ml; range, 0 to 1.7 micrograms/ml). The finding of SC5b-9 complexes in the CSF of patients with GBS and MS suggests that terminal complement components may participate in the tissue-damaging processes in these diseases.
Evidence that Leishmania donovani utilizes a mannose receptor on human mononuclear phagocytes to establish intracellular parasitism.
Authors: Wilson M E , Pearson R D 
Published: December 2022

Abstract
The pathogenic protozoan Leishmania donovani must gain entrance into mononuclear phagocytes to successfully parasitize man. The parasite's extra-cellular promastigote stage is ingested by human peripheral blood monocytes or monocyte-derived macrophages in the absence of serum, in a manner characteristic of receptor-mediated endocytosis. We have found remarkable similarities between the macrophage receptor(s) for promastigotes and a previously characterized eucaryotic receptor system, the mannose/fucose receptor (MFR), that mediates the binding of zymosan particles and mannose- or fucose-terminal glycoconjugates to macrophages. Ingestion of promastigotes by monocyte-derived macrophages was inhibited by several MFR ligands. Mannan (2.5 mg/ml) decreased ingestion by 63.7% (p less than 0.001), and the neoglycoproteins mannose-BSA and fucose-BSA (20 micrograms/ml) inhibited parasite ingestion by 46.5% and 39.6%, respectively (p less than 0.04). In contrast, promastigote ingestion by monocytes was unaffected by MFR ligands. These results are consistent with reports that MFR activity is present in monocyte-derived macrophages but not in monocytes. Furthermore, attachment of promastigotes to macrophages, assessed by using cytochalasin D to prevent phagocytosis, was reduced 49.8% by mannan. Reorientation of the MFR to the ventral surface of the cell was achieved by plating macrophages onto mannan-coated coverslips, reducing MFR activity on the exposed cell surface by 94% as assessed by binding of 125I-mannose-BSA. Under these conditions, ingestion of promastigotes was inhibited by 71.4% (p less than 0.006). Internalization of the MFR by exposure of macrophages to zymosan before infection with promastigotes resulted in a 62.3% decrease in parasite ingestion (p less than 0.006). Additionally NH4Cl, a weak lysosomotropic base that impairs MFR recycling, decreased macrophage ingestion of promastigotes by 38.2% (p less than 0.03, 30 mM NH4Cl). Subinhibitory concentrations of NH4Cl (10 mM) and of mannan (0.25 mg/ml) together inhibited parasite ingestion by 76.4% (p less than 0.002). These studies suggest that L. donovani promastigotes may utilize a receptor system on human monocyte-derived macrophages, the MFR, to efficiently parasitize the human host.
Synergistic defense system by cooperative natural effectors against metastasis of B16 melanoma cells in H-2-associated control: different behavior of H-2+ and H-2- cells in metastatic processes.
Authors: Kawano Y , Taniguchi K , Toshitani A , Nomoto K 
Published: December 2022

Abstract
H-2+ and H-2- cells of B16 melanoma were established by repeated fluorescence-activated cell sorting. The H-2- line formed no metastasis in untreated C57BL/6 mice, whereas the H-2+ cells showed evidence of metastatic development. This difference was ascribed mainly to the increased susceptibility of H-2- cells to attack by natural effector mechanisms, particularly asialo GM1+ NK cells. After treatment with both anti-asialo GM1 serum and whole body irradiation (400 rad), numerous colonies of H-2- cells formed in the lung, whereas the metastasis was only marginally enhanced by irradiation and moderately by treatment with anti-asialo GM1 serum. With the H-2+ cells, treatment with each modality significantly increased the number of metastatic colonies. Therefore collaboration of asialo GM1+ NK cells and radiosensitive natural effectors seems to be the main mechanism involved in the synergistic effects on defense against H-2- cell metastasis, and to a lesser extent against H-2+ cell metastasis. Irradiation (1000 rad) to the right lung to abrogate the organ-associated defense increased the colonies, particularly in the H-2+ cells. On the other hand, treatment with anti-asialo GM1 serum increased colonization in the early phase of metastasis with H-2- cells and may have abolished asialo GM1+ NK cells capable of recognizing the reduced expression of H-2 antigens and eliminating H-2- cells in the blood-born phase. Natural defense mechanisms probably exert suppressive effects on the metastasis of H-2+ cells, mainly in the organ-associated phase after extravasation.
Regulation of granulomatous inflammation in murine schistosomiasis. III. Recruitment of antigen-specific I-J+ T suppressor cells of the granulomatous response by I-J+ soluble suppressor factor.
Authors: Mathew R C , Boros D L 
Published: December 2022

Abstract
Down-modulation of the schistosome egg-induced granulomatous response involves various interacting subsets of T suppressor (TS) lymphocytes. In the present study the inductive phase of the process of modulation was analyzed. A soluble, I-J+ granuloma TS cell recruiting factor (Gr-TSRF) derived from spleen cells of chronically infected mice is described. This factor eluted from immunoabsorbent columns coupled with anti-I-Jk alloantisera induced the recruitment and expansion of antigen-specific I-J+ TS cells from a TS precursor cell population in the spleens of acutely infected mice. The recruited TS cells suppressed the granulomatous response of normal recipients in a 2-day adoptive transfer model. The antigenic specificity of the recruited TS cells was demonstrated by their inability to suppress KLH-induced artificial granulomatous response. This mechanism of recruitment described in the current study and illustrated by adoptive transfer experiments is likely to be active in vivo in initiating the process of spontaneous modulation. The I-J+ Gr-TSRF and the I-J+ TS cell described in this paper, together with the previously described H-2 restricted I-C+ factor and the subsets of TS cells (THs, TSe, TSpr), indicate the existence of an intricate, regulatory pathway(s) that operates during the modulation of the granulomatous response.
Paul-Bunnell antigen in murine T cell differentiation: abnormal expression in MRL/Mp-lpr/lpr mice.
Authors: Katagiri T , Tomiyama H , Kano K 
Published: December 2022

Abstract
Expression of Paul-Bunnell (P-B) antigen was studied on lymphoid cells of normal mice, autoimmune MRL/Mp-lpr/lpr (lpr), and congenic MRL/Mp-+/+(+/+) mice. Evidence was presented that the P-B antigen is a differentiation-associated antigen of murine T cells: Cells with high P-B pattern and density on normal T cells increased as their differentiation proceeded in the peripheral lymphoid tissues. In thymus, P-B antigen was predominantly expressed on hydrocortisone resistant and PNA nonagglutinable cells. The degree of P-B expression on T cells of peripheral lymphoid tissues correlated well with that of Lyt-1 and Lyt-2 antigens (r greater than 0.7). Similar studies on lymphocytes obtained from lpr and +/+ mice at different ages revealed that P-B antigen on the peripheral T cells of lpr mice began to decrease at 6 to 8 wk of age and that the majority of the cells became low P-B cells by 10 wk, accompanied by decrease in expression of Lyt-1 antigen. In contrast, its expression on lpr thymocytes did not differ from that of +/+ or normal mice. The lymph node cell population of lpr mice at the height of the lymphadenopathy was composed of 80% of low P-B and dull Lyt-1 cells and less than 15% of "normal" P-B and Lyt-1 positive cells. These results indicate distorted differentiation of the lpr peripheral lymphocytes that are responsible for the massive lymphadenopathy and the morbid processes.
Thymic hormone-containing cells. VII. Adrenals and gonads control the in vivo secretion of thymulin and its plasmatic inhibitor.
Authors: Dardenne M , Savino W , Duval D , Kaiserlian D , Hassid J , Bach J F 
Published: December 2022

Abstract
The influence of adrenals and gonads on the intrathymic production and the circulating level of thymulin was evaluated in young adult mice. Adrenalectomy (Adx) and gonadectomy (Cx) induce a temporary decrease of thymulin serum level. One simultaneously notes, as a compensatory phenomenon, an increase in the thymic content of the hormone-producing cells. The decrease of serum thymulin levels after Adx and Cx is at least partially due to the appearance of low m.w. thymulin-inhibitory molecules. The fact that thymectomy prevents the appearance of these inhibitors suggests that the effects of Adx and Cx could be explained by a negative control by sex hormones of the synthesis or activity of thymulin inhibitors produced or controlled by the thymus. Specific hormone replacement therapy of castrated/adrenalectomized animals normalized thymulin serum level and thymic content. Such correction was also spontaneously observed after 4 mo, suggesting that other mechanisms (e.g., an influence of the hypothalamus-hypophysis axis) might be involved in the endocrine control of thymic hormone secretion.
Identification and characterization of a human T cell line-derived lymphokine with MAF-like activity distinct from interferon-gamma.
Authors: Lee J C , Rebar L , Young P , Ruscetti F W , Hanna N , Poste G 
Published: December 2022

Abstract
Culture supernatants of several human T cell leukemia cell lines were screened for macrophage-activating activity (MAF) as defined by induction of tumoricidal activity against human melanoma cells in a 72-hr assay. Two cell lines, MT-2 and C10/MJ2, were found to produce high levels of MAF activity constitutively, but the MT-2 cell line, unlike C10/MJ2, produced little IFN-gamma. This observation was confirmed by Northern blot analysis performed with specific IFN-gamma cDNA probe. The MT-2 cell line thus provides a useful system to evaluate the existence of lymphokines with MAF activity that are distinct from IFN-gamma. The MAF activity produced by MT-2 cells was distinguished from IFN-gamma by the following criteria. MAF activity was not removed by immunoaffinity chromatography with the use of immobilized specific polyclonal antibodies to IFN-gamma and was not neutralized by a monoclonal antibody to IFN-gamma. Heat or acid treatments of IFN-gamma resulted in loss of its antiviral activity, but these treatments had no effect on MAF activity. MAF activity was not abolished by polymyxin B sulfate, suggesting that this activity is not mediated by or dependent on LPS. Initial characterization studies performed by using membrane filtration, gel filtration chromatography, and isoelectric focusing indicate that the non-IFN-gamma MAF activity produced by MT-2 cells has an apparent m.w. of 55,000 and an isoelectric point of 5.5. Collectively, these data suggest that the MT-2 human T cell line constitutively produces high levels of MAF and low levels of IFN-gamma and offers a useful source for the further purification of a unique human lymphokine with macrophage-activating activity that is distinct from IFN-gamma.
Frequent T4-positive cells with cytolytic activity in spleens of patients with Hodgkin's disease (a clonal analysis).
Authors: Maggi E , Parronchi P , Del Prete G , Ricci M , Bosi A , Moretta L , Romagnani S 
Published: December 2022

Abstract
Purified T lymphocytes isolated from spleens of untreated patients with Hodgkin's disease (HD) were cloned by using a microculture system previously shown to allow clonal expansion of virtually all peripheral blood T lymphocytes. Cells were plated under limiting conditions with irradiated feeder cells and PHA. Interleukin 2 (IL 2)-containing supernatants were added 48 hr later. The phenotypic and functional characteristics of a total number of 221 clones derived from six different HD spleens were investigated and compared with those of 133 clones obtained from three spleens of otherwise healthy individuals who underwent posttraumatic splenectomy. The majority of T cell clones derived from HD spleens expressed the T4+ (helper/inducer) phenotype. However, further functional characterization showed that as much as 50% of these T4+ clones displayed cytolytic activity in a lectin-dependent lytic assay allowing detection of cytolytic cells of any specificity. In contrast, less than 10% T4+ clones derived from control spleens were cytolytic, as assessed by the same lectin-dependent lytic assay. The cytolytic potential of T4+ and T8+ clones established from spleens of patients with HD did not reflect the induction of lymphokine-activated killer cells, because only a minority of them displayed natural killer (NK) activity against NK-sensitive K562 and MOLT-4 cell lines. These findings indicate that T lymphocytes found in the spleens of patients with HD may represent, at least in part, the expansion of a subset present in small percentages among normal peripheral blood or spleen T lymphocytes, which is involved in a cytotoxic reaction.
Interferon-gamma enhances expression of cellular receptors for tumor necrosis factor.
Authors: Tsujimoto M , Yip Y K , Vilcek J 
Published: December 2022

Abstract
Incubation of several human tumor cell lines with human interferon-gamma (IFN-gamma) increased the specific binding of subsequently added 125I-labeled recombinant human tumor necrosis factor (TNF). A similar increase in TNF binding was seen in murine L929 cells after incubation with murine IFN-gamma, but not after incubation with human IFN-gamma. Increased TNF binding to cells incubated with IFN-gamma was due to an increase in the number of TNF receptors, with no demonstrable change in binding affinity. In one out of two human cell lines tested, IFN-alpha and IFN-beta also produced increased TNF binding, albeit with a lower efficacy than IFN-gamma. A maximal increase in TNF binding was seen after about 6 to 12 hr of incubation with IFN. Increased TNF binding due to enhanced TNF receptor expression may contribute to the enhancement of TNF cytotoxicity seen in some tumor cell lines after INF treatment. Modulation of TNF receptor expression by IFN may also influence other biological activities of TNF.
Induction of the synthesis of tumor necrosis factor receptors by interferon-gamma.
Authors: Ruggiero V , Tavernier J , Fiers W , Baglioni C 
Published: December 2022

Abstract
Human HT-29 colon carcinoma and HeLa D98/AH2 and SK-MEL-109 melanoma cells were sensitive to synergistic growth inhibition by concentrations of recombinant human tumor necrosis factor (rTNF) and interferon-gamma (rIFN-gamma) which individually were only slightly inhibitory. We investigated whether this synergism could be explained by the presence of an increased number of TNF receptors in cells treated with rIFN-gamma. These receptors were measured by incubating cells resuspended from monolayers with 125I-rTNF. HT-29 cells treated for a few hours with rIFN-gamma could bind more 125I-rTNF than control untreated cells, but this binding returned to the level of control cells after 24 hr. The treatment with rIFN-gamma did not change the binding affinity of TNF receptors, but increased their number to 1800 per cell from a basal level of about 800 per cell. Inhibitors of RNA synthesis prevented this increase. HT-29 cells were significantly more growth-inhibited when treated first for 6 to 12 hr with rIFN-gamma and then with rTNF, than when treated first with rTNF and then with rIFN-gamma. Untreated HeLa D98/AH2 and SK-MEL-109 cells had 2400 and 9000 receptors per cell, with a KD similar to that of HT-29 cells (approximately 2 X 10(-10)M). A significant increase in TNF receptors after treatment with rIFN-gamma was observed in HeLa D98/AH2, but not in SK-MEL-109 cells. No increase in TNF receptors was detected in cells treated with rIFN-alpha 2. These results indicate that the synergism between rTNF and rIFN-gamma may be due, at least in part, to a transient induction of the synthesis of TNF receptors by rIFN-gamma in cells with a relatively low number of these receptors.
Amino acid residues 56 to 69 of HLA-A2 specify an antigenic determinant shared by HLA-A2 and HLA-B17.
Authors: Ways J P , Rothbard J B , Parham P 
Published: December 2022

Abstract
The mouse monoclonal antibody MA2.1 was previously used to define an epitope shared by native HLA-A2 and HLA-B17 molecules and amino acid sequence comparison of nine HLA-A,B,C molecules identified residues 62 to 65 as the region most likely to form this epitope. An unabsorbed rabbit antiserum raised against a peptide corresponding to residues 56 to 69 of HLA-A2 gives highly specific reactions with HLA-A2 and HLA-B17 heavy chains in Western blots. No interactions with native HLA-A2 and B17 molecules were detected in a variety of assays. Although the topographic relationship between the epitopes recognized by the rabbit antiserum and the monoclonal antibody could not be determined, the results show that residues 56 to 69 of HLA-A2 can form epitopes with specificity for HLA-A2 and HLA-B17.