bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monoclonal antibody SN2 defining a human T cell leukemia-associated cell surface glycoprotein.
Authors: Seon B K , Negoro S , Barcos M P , Tebbi C K , Chervinsky D , Fukukawa T 
Published: December 2022

Abstract
We generated a monoclonal antibody, termed SN2, which defines a human T cell leukemia-associated cell surface glycoprotein, GP37, with an approximate m.w. of 37,000. This antibody was generated by using a human leukemia antigen preparation. The reactivity and specificity of SN2 were characterized by a sensitive radioimmunoassay against a variety of cultured and uncultured human cells. In selected cases, the cell specimens were tested further by indirect immunofluorescence staining. Among the various cultured malignant and nonmalignant human cell lines tested, SN2 reacted only with leukemic T cell lines, with one exception. It reacted with 10 of 11 leukemic T cell lines tested; the 10 reactive cell lines are PEER, JM, MOLT-4, CCRF-CEM, CCRF-H-SB2, RPMI 8402, DND-41, HPB-ALL, SKW-3, and HPB-MLT; the unreactive line was HUT 78. The reactive cell lines were derived from patients either with T cell-type acute lymphoblastic leukemia (the first eight cell lines), with T cell chronic lymphocytic leukemia (SKW-3), or with Japanese adult T cell leukemia-lymphoma (HPB-MLT). The unreactive cell line, HUT 78, was from a patient with Sezary syndrome. Results consistent with the above were obtained from studies in which uncultured malignant cell specimens from different cancer patients were tested against SN2; SN2 reacted only with T leukemia cells. Among various uncultured normal cell specimens tested, SN2 did not react with thymocytes, bone marrow cells, peripheral blood lymphocytes containing B and T cells, purified T cells, monocytes, granulocytes, or erythrocytes. It did, however, react with platelets.
Molecular signals in antigen presentation. II. Activation of cytolytic cells in vitro after ultraviolet radiation or combined gamma and ultraviolet radiation treatment of antigen-presenting cells.
Authors: Granstein R D , Tominaga A , Mizel S B , Parrish J A , Greene M I 
Published: December 2022

Abstract
Murine low-density spleen cells have potent antigen-presenting ability in a hapten-specific cytolytic T lymphocyte (CTL) system using the hapten azobenzenearsonate (ABA). Exposure of these cells to 0.33 KJ/m2 of ultraviolet radiation (UVR) after coupling to hapten results in markedly inhibited antigen-presenting function that can be substantially corrected or bypassed by interleukin 1 (IL 1). These results have been interpreted to reflect an inhibition of Lyt-1+ T cell activation by UVR-treated APC. Treatment of these cells sequentially with 1500 rad of gamma-radiation (GR) prior to hapten coupling, followed by 0.33 KJ/m2 of UVR radiation after coupling, results in an antigen-presenting defect only minimally improved by IL 1. However, partially purified interleukin 2 (IL 2) can completely bypass or correct this defect. Thus, combined GR and UVR induces a different or more profound defect in APC function when compared to UVR alone. However, these cells do provide a signal(s) other than hapten necessary for CTL activation because ABA-coupled high density spleen cells do not activate CTL cells, even with the addition of IL 2. Fluorescence-activated cell sorter analysis demonstrates that exposure of these low density spleen cells to GR or UVR results in decreased I-A antigen expression at 24 hr than either alone. The addition of nonhapten-coupled low-density APC partially reconstitutes the ability of combined GR/UVR-treated LD-APC to present antigen, and this effect is enhanced by the administration of exogenous IL 1. This occurs despite a lack of significant accessory cell activity by the LD-APC for the ABA hapten, and indicates that combined GR/UVR-treatment of APC is not functionally equivalent to completely removing them.
Natural killer cells generated from bone marrow culture.
Authors: Koo G C , Peppard J R , Mark W H 
Published: December 2022

Abstract
By using anti-Nk-1 antiserum, we detected a significant proportion of Nk-1+ cells in bone marrow (BM) with low lytic activity that can be slightly enhanced with interferon (IF). These BM Nk-1+ cells also bind to YAC-1 cells. Because Nk-1 antigen has been found to mark NK cells, BM appears to harbor immature precursors to natural killer (NK) cells. We therefore used concanavalin A (Con A)-conditioned medium to culture BM cells to induce differentiation of the putative NK precursors. After 3 to 4 days in culture, cytotoxic activity to YAC, that peaked at 6 to 7 days, was consistently generated, and the activity still could be detected after 10 to 14 days in culture. In contrast, experiments using spleen cultures, performed in a similar manner, showed peak activity after 4 to 5 days and the activity declined thereafter. The cytotoxic activity of cultured BM cells was also higher than that of cultured spleen cells. Cultures of BM cells from old mice have good cytotoxic activity. The cytotoxic cells generated were Nk-1+ and Qa-5+. Furthermore, these culture conditions did not maintain the proliferation of CFU-C cells.
Effect of pregnancy on augmentation of natural killer cell activity by Corynebacterium parvum and Toxoplasma gondii.
Authors: Luft B J , Remington J S 
Published: December 2022

Abstract
Studies were performed to determine the effect of pregnancy on NK cell activity and the augmentation of NK cell activity which normally follows injection of killed C. parvum or live T. gondii. When compared to cells from virgin mice, peritoneal and splenic cells from unstimulated pregnant mice showed no significant difference in NK activity. In contrast, NK activity of peritoneal cells from pregnant mice that received C. parvum or T. gondii was significantly lower than that found in comparably treated virgin mice. This reduced augmentation of NK activity in the peritoneal cells of pregnant mice could not be altered by the removal of plastic-adherent cells or of T cells by treatment with anti-Thy-1.2 antibody and complement. The number of effector-target conjugates was quantitated with a single cell assay, and was found to be comparable between cells from treated pregnant mice and treated virgin controls. However, the magnitude of lysis of target cells by peritoneal and splenic effector cells from pregnant mice previously injected with C. parvum was markedly and significantly reduced when compared to cells from comparably treated virgin mice. Thus, pregnancy is associated with an impaired ability to augment NK activity. This decrease in NK activity was not due to the depletion or dilution of NK cells, but to a functional impairment of the individual NK cells.
Anti-idiotypic antibodies in a patient with monoclonal rheumatoid factor after pneumococcal bacteremia.
Authors: Abe T , Takeuchi T , Kiyotaki M , Koide J , Hosono O , Homma M , Otake T , Kano S 
Published: December 2022

Abstract
A 51-yr-old Japanese female patient with monoclonal IgM gammopathy with rheumatoid factor activity was admitted because of pneumococcal bacteremia. About 2 wk after admission, her rheumatoid factor activity became undetectable by RAHA test and radioimmunoassay, subsequent to the initial marked elevation. The suppressive capacity of the patient's IgG fraction on the rheumatoid activity of her monoclonal IgM on January 11 was determined. The IgG fraction obtained on February 22 blocked the binding of the rheumatoid factor to rabbit IgG. The suppressive activity in the IgG fraction of February 22 was shown to be localized within the F(ab')2 fragment. Furthermore, the specificity of the suppressive serum factor was shown by the inability to block the binding of SRBC coupled with diazotized phosphorylcholine to anti-pneumococcal antibody. Thus, the marked reduction of rheumatoid factor activity was considered to result from anti-idiotypic antibody transiently appearing in her serum after pneumococcal bacteremia.
Interferon induction in mouse spleen cells by mitogenic and nonmitogenic lectins.
Authors: Ito Y , Tsurudome M , Yamada A , Hishiyama M 
Published: December 2022

Abstract
Twenty-two species of lectin were tested for their ability to induce interferon (IFN) in mouse spleen cells. Twenty-two species of lectins representing four groups, based on competition patterns with monosaccharides, were examined for their ability to induce IFN in cultured mouse spleen cells. The lectins, all belonging to the third group (concanavalin A, succinylated concanavalin A, Lens culinaris lectins type A and B, and poke weed mitogen) induced IFN mainly composed of IFN gamma. They were either T cell or T/B cell mitogens. Five nonmitogenic lectins, Lotus tetragonolobus seed lectin, crude and type II lectins of Ulex europeus, Bandeiraea simplicifolia type II and Salanum tuberosame lectins, and wheat germ agglutinin belonging to either the first or the third group, induced IFN beta. The production of IFN during stimulation IFN beta- and IFN gamma-inducing lectins followed different kinetic curves. WGA induced IFN in circulation when injected i.p. in mice, and a peak titer was found 2 hr after inoculation.
Lymphocyte modulation of fibroblast function in vitro: stimulation and inhibition of collagen production by different effector molecules.
Authors: Postlethwaite A E , Smith G N , Mainardi C L , Seyer J M , Kang A H 
Published: December 2022

Abstract
Increased collagen deposition is a common feature of granulomatous and nongranulomatous inflammation associated with certain types of cell-mediated immune reactions in vivo. In the present study, we found that normal human peripheral blood mononuclear leukocytes cultured in vitro and stimulated by antigens or T cell mitogens release a 100 to 170 K m.w., heat-labile, trypsin-sensitive protein that stimulates dermal fibroblasts to produce increased quantities of type I and III collagens. Our data suggest that this collagen production protein is of T lymphocyte origin and that it preferentially stimulates production of collagen. We also observed that human mononuclear leukocytes release a different effector molecule with an m.w. of 55 K that inhibits fibroblast collagen production. Mononuclear leukocytes in culture are capable of releasing both the stimulator and the inhibitor of collagen production. The relative amounts of each of these factors elaborated by mononuclear leukocytes in culture appear to be influenced by several variables, such as cell density, type of stimulant used, and the duration of the culture period. These observations suggest that collagen production by fibroblasts in close proximity to sites in vivo where cell-mediated immune reactions are occurring might be regulated by both of these effector molecules.
Immunoselection of B cell hybridomas with anti-idiotypic antisera to study the role of heavy and light chains for idiotype expression and antibody activity.
Authors: Ju S T , Pincus S H , Kunar J , Dorf M E 
Published: December 2022

Abstract
Conventional reconstitution experiments with heavy (H) and light (L) offins of hybridoma anti-poly-(Glu60Ala30Tyr10) (anti-GAT) antibodies demonstrated that H and L chains are required for efficient expression of anti-GAT activity and the previously defined common CGAT idiotype. On the basis of this observation, we treated a CGAT+ hybridoma cell line (F9.195.6), which was produced by fusion with an MOPC 21 (gamma 1, K) secretor line, with anti-CGAT idiotypic antibodies plus complement to select CGAT-variants. Such treatment greatly enhanced the frequency of isolating hybridoma variants. Molecules secreted from these variants bear anti-GAT mu-chain and MOPC 21 L chain (as judged by serology and Southern blot studies), lack GAT binding activity and CGAT idiotype, and exhibit a "new" private idiotype (E8). Anti-private idiotypic sera were successfully used to select a series of CGAT+, E8- clones that secrete molecules bearing only the appropriate anti-GAT mu- and K chains. From E8- hybridoma supernatants, CGAT- molecules bearing MOPC 21 H chain and anti-GAT L chain could be obtained. The data indicate that immunoselection of hybridoma clones with anti-idiotypic antibodies is a convenient means of preparing reconstituted antibody molecules. Furthermore, the data demonstrate that CGAT idiotype determinants are expressed on antibody molecules composed of appropriate H and L chains.
Analysis of structural properties and cellular distribution of avian Ia antigen by using monoclonal antibody to monomorphic determinants.
Authors: Ewert D L , Munchus M S , Chen C L , Cooper M D 
Published: December 2022

Abstract
In this report, we describe the analysis of Ia-like antigens in the chicken by using a monoclonal antibody (CIa-1) reactive with monomorphic determinants of the Ia-like (B-L) antigens. This antibody reacts with determinants on B cells in all avian species tested, but does not detect antigens on lymphocytes of representative mammals, reptiles, and amphibians. In addition to B cells, this antibody defines a subpopulation of the monocyte-macrophage series and reacts with mitogen-activated T cells. Immunochemical analysis indicates that the CIa-1 reactive antigen is a 65,000-dalton glycoprotein consisting of an alpha-chain of 32,000 daltons noncovalently bound to a beta-chain of 27,000 daltons. Under nonreducing conditions, the beta-chain migrates with slightly faster mobility. Two-dimensional gel analysis indicates that the beta-chain is the more heterogeneous of the two chains. Thus, the antigen detected by CIa-1 antibody is similar in cell distribution and structure to the murine Ia antigens and human DR antigens. During in ovo development, Ia+Ig- cells were not found in the yolk sac but were detected in the spleen, mesonephros, and bursa of 9-day embryos. Two populations of Ia+Ig- cells were identified in the bursa: 40 to 60% of the bursacytes, mostly larger cells, exhibited brighter immunofluorescence reactivity than the smaller bursacytes.
Functional angiotensin II receptors on macrophages from isolated liver granulomas of murine Schistosoma mansoni.
Authors: Weinstock J V , Kassab J T 
Published: December 2022

Abstract
Isolated liver granulomas from mice infected with Schistosoma mansoni contain components of the renin-angiotensin system. Angiotensin II is a major biologically active component of this system. It was therefore determined whether inflammatory cells within the granuloma possessed receptors for this hormone. Specific binding of angiotensin II to isolated granuloma macrophages was demonstrated by both fluorescence and radioligand assays. The binding of 125I-angiotensin II was saturable, dependent on radioligand concentration, and reversible. Scatchard analysis of binding data suggested a Kd of 0.25 nM with 526 binding sites per cell. The natural analogs of angiotensin II, angiotensin I and III, only weakly competed for angiotensin II binding sites. Exposure of macrophages to appropriate binding concentrations of angiotensin II resulted in a rapid dose-dependent increase in intracellular cAMP. It is therefore concluded that granuloma macrophages possess functional receptors for angiotensin II.
Cell surface antigen phenotypes of MCF-induced thymic lymphomas in AKR mice.
Authors: Yetter R A , Morse H C 
Published: December 2022

Abstract
The hypothesis that the surface antigen phenotypes of MCF-MuLV-induced thymic lymphomas in AKR mice are predictable and characteristic of the inducing virus has been tested. Thymic lymphomas induced by two different MCF-MuLV were assayed by flow microfluorometry for their expression of the surface antigens XenCSA, Thy-1.1, Ly-2, Ly-1, 2C2, H-2K, and Ia. In all cases there was an increase in XenCSA levels. The lymphomas could be divided into three categories on the basis of qualitative difference in Ly-2 expression: Ly-2+ tumors, Ly-2- tumors, and tumors with both Ly-2+ and Ly-2- populations. One lymphoma expressed 2C2, an antigen not normally found on thymocytes. Quantitative differences in expression could be found for all antigens. This variation in surface antigen phenotype was independent of the cloned virus MCF used to induce the lymphoma.
Suppression of Con A mitogen-induced proliferation of normal spleen cells by macrophages from chickens with hereditary muscular dystrophy.
Authors: Kline K , Sanders B G 
Published: December 2022

Abstract
Spleen cells from chickens with hereditary muscular dystrophy (MD) give low blastogenic responses to the T cell mitogen concanavalin A (Con A) while exhibiting normal mitogen stimulated blastogenic responses to the T cell mitogen phytohemagglutinin (PHA). The addition of MD spleen cells to normal spleen cells caused a marked suppression of the Con A response of the normal cells while not affecting the PHA response of the normal cells. The suppressive activity by the MD spleen cells requires viable cells and is contact mediated. The suppressive activity is attributed to the presence in MD spleens of a population of suppressor cells with characteristics typical of macrophages. The suppressor cell activity was not removable by complement-mediated lysis using anti-T or anti-B sera, but it was reversible by treatment with carrageenan or carbonyl iron magnet, by passage through a Sephadex G-10 column, and by adherence to plastic petri dishes or glass beads. MD spleen cells depleted of the suppressor cell population remained unable to respond to Con A.
Immunomodulatory effects of corticosteroids on natural killer and antibody-dependent cellular cytotoxic activities of human lymphocytes.
Authors: Nair M P , Schwartz S A 
Published: December 2022

Abstract
The in vitro effect of prednisolone (PRD) on NK and ADCC activities of human lymphocytes was investigated. PRD at concentrations ranging from 7.5 X 10(-3) to 1 X 10(-5) M significantly inhibited NK activity, while concentrations of 7.5 X 10(-3) to 1 X 10(-4) M inhibited ADCC activities of PBL when added directly to the mixture of effector and target cells. Lymphocytes pre-cultured for 24 hr with PRD at concentrations ranging from 1 X 10(-4) M to 1 X 10(-6) M showed significant suppression of their NK activity. Inhibition was proportional to the concentration of the drug, and was observed at as early as 1 hr of incubation at various effector to target cell ratios with several targets. PRD also inhibited NK and ADCC activities of purified T cells, non-T cells, and NK-enriched effector cells. In target-binding assays, PRD decreased the target-binding capacity of effector lymphocytes in a dose-dependent manner. PRD-induced inhibition could be reversed by incubating lymphocytes for 1 hr with interferon or IL 2. Pretreatment of targets with PRD for 4 hr did not affect cytotoxic activity. Inhibition of cytotoxicity was not due to direct toxicity to effector cells because lymphocytes treated with PRD showed normal spontaneous 51Cr release, and their viability after 24 hr of pre-culture with PRD was comparable to that of untreated control cells. These results demonstrate that PRD has significant immunomodulatory effects on human NK and ADCC activities that may be of clinical relevance.
Beta-endorphin and met-enkephalin stimulate human peripheral blood mononuclear cell chemotaxis.
Authors: van Epps D E , Saland L 
Published: December 2022

Abstract
The neuropeptides beta-endorphin and met-enkephalin are potent analgesics and have a broad spectrum of biologic activities including the recently described alterations of lymphocyte proliferation and antibody production. The current study demonstrates that beta-endorphin and met-enkephalin stimulate human mononuclear cell chemotaxis, as measured by the in vitro leading front assay for migration. The response to both beta-endorphin and met-enkephalin was bimodal, with peak activities occurring at 10(-12) M and 10(-8) M. The distance migrated in response to optimal concentrations of beta-endorphin or met-enkephalin was approximately 80% of that obtained with 10(-8) M formyl-methionyl-leucyl-phenylalanine (f-MLP) and was blocked by prior incubation with 10(-8) M naloxone. Removal of glass adherent cells resulted in a loss of the response to beta-endorphin. Quantitation of the number of cells responding to beta-endorphin showed that only about 50% as many cells responded to beta-endorphin as compared with f-MLP. Human neutrophils showed some migration in response to beta-endorphin and met-enkephalin, although the average optimal migration was less than 30% of that observed with 10(-8) M f-MLP. Studies of the in vivo infusion of beta-endorphin into the cerebral ventricle of the rat resulted in the immigration of macrophage-like cells and are consistent with the in vitro evidence for a chemotactic effect of beta-endorphin.
Inhibition of T suppressor cell expression by histamine type 2 (H2) receptor antagonists.
Authors: Griswold D E , Alessi S , Badger A M , Poste G , Hanna N 
Published: December 2022

Abstract
The effect of histamine type 2 (H2) receptor antagonists, cimetidine and ranitidine, on the induction and expression of hapten-specific suppressor T cells was studied. The activity of DNBSO3 -induced suppressor cells was evaluated after adoptive transfer to naive syngeneic recipients. Treatment with cimetidine or ranitidine markedly inhibited suppressor T cell activity in a dose-related manner and enhanced the contact sensitivity response to DNFB. Both H2 antagonists were effective in inhibiting the expression and, to a lesser extent, the induction of suppressor T cells. In contrast, norburimamide , a non-H2 antagonist structurally related to cimetidine, was inactive. The relevance of these findings to the clinical observation of cimetidine-induced reversal of acquired tolerance to dinitrochlorobenzene in anergic patients is discussed.
Effects of deoxycoformycin in mice. I. Suppression and enhancement of in vivo antibody responses to thymus-dependent and -independent antigens.
Authors: Ratech H , Bell M K , Hirschhorn R , Thorbecke G J 
Published: December 2022

Abstract
The effect of 2'-deoxycoformycin (DCF) on the PFC responses of AKR mice to SE, TNP-Ficoll, and TNP-B. abortus was examined. Subcutaneous injection of DCF 4 days before antigen caused suppression of all three responses by 70 to 78%. In contrast, injection of DCF 1 day after antigen caused enhancement of both the anti-SE and the anti-TNP-Ficoll responses. Although a single high dose of cortisone acetate injected 4 days before antigen caused a similar suppression, the effect of DCF was not mediated via a steroid release, inasmuch as DCF also suppressed the immune response in adrenalectomized mice. The response of BALB/c mice to TNP-Ficoll was also inhibited by DCF pretreatment and enhanced by injection of DCF after antigen. In contrast, in athymic mice DCF caused suppression of the anti-TNP-Ficoll PFC response, whether injected before or after antigen. These results are interpreted as suggesting that DCF causes suppression primarily via an effect on B cells. The enhancement seen in normal but not in athymic mice may possibly be ascribed to an effect on suppressor T cells. Apparently the enhancement of both TD and TI responses caused by DCF injected 1 day after antigen in normal mice is the net result of these two opposing effects. The results imply that helper T cells are resistant to DCF.