bluuebunny/crossref_metadata_2025_split huggingface dataset:
Correlation between differentiation, expression of monocyte-specific antigens, and cytotoxic functions in human promyelocytic cell lines treated with leukocyte-conditioned medium.
Authors: Dayton E T , Perussia B , Trinchieri G 
Published: December 2022

Abstract
Human promyelocytic cells lines treated with conditioned medium from PHA-stimulated leukocytes acquire several phenotypic and functional markers of differentiated monocytes. In this paper, we demonstrate that promyelocytic cells treated with conditioned medium express, among other markers, monocyte-specific and HLA-DR antigens absent from the parental cells and become potent effectors of antibody-dependent cell-mediated cytotoxicity against erythrocytes and tumor cells. In cultures of promyelocytic cell lines maintained in the presence of conditioned medium, an equilibrium between proliferation and differentiation is established, and two cell populations can be separated on the basis of expression of differentiation surface markers. One population has a differentiated morphology, expresses nonspecific esterase activity, Fc receptors, C receptors, monocyte-specific and HLA-DR antigens, is able to mediate antibody-dependent cytotoxicity, and has a limited ability to proliferate. A second population retains the phenotype of undifferentiated promyelocytes and continues to proliferate. The differentiated monocyte-like cells originate from a proportion of the proliferating promyelocytes that respond to the differentiation inducers contained in the conditioned medium.
Estimation of polymeric IgA in human serum: an assay based on binding of radiolabeled human secretory component with applications in the study of IgA nephropathy, IgA monoclonal gammopathy, and liver disease.
Authors: Newkirk M M , Klein M H , Katz A , Fisher M M , Underdown B J 
Published: December 2022

Abstract
Binding of 125I-human secretory component (SC) to human polymeric immunoglobulin A (pIgA) was employed to measure quantitatively the pIgA present in human sera. Interference by IgM in some sera was prevented by removal of IgM with glutaraldehyde polymerized anti-IgM antibodies. 125I-SC complexed to pIgA was measured by precipitation with anti-IgA antibodies and the quantity of pIgA in human serum was estimated by comparing the quantity of 125I-SC bound by several dilutions of human serum to that bound by standard quantities of human monoclonal pIgA proteins. The assay was specific for pIgA because heat-aggregated monomeric IgA or hypogammaglobulinemic serum did not bind 125I-SC greater than a precipitate formed with human monoclonal IgG and anti-IgG. Moreover, analysis of a series of IgA myeloma sera indicated no correlation between the IgA content of the serum and the quantity of pIgA measured. The quantity of pIgA found in 30 normal human sera was 0.13 +/- 0.08 mg/ml (1S.D.), which consisted of 11.3 +/- 5.3% (1 SD) of the total IgA. Patients with IgA monoclonal gammopathy were most often found to have predominantly monomeric IgA. Patients with IgA nephropathy also showed an elevation of pIgA, but this appeared to be a consequence of an overt IgA elevation. IgA nephropathy patients with elevated serum IgA in fact showed a significant elevation of monomeric IgA. Selective elevation of pIgA was observed in patients with primary biliary cirrhosis and alcoholic liver disease. A comparison of this assay with other assays to measure pIgA is discussed.
Immune islet killing mechanisms associated with insulin-dependent diabetes: in vitro expression of cellular and antibody-mediated islet cell cytotoxicity in humans.
Authors: Charles M A , Suzuki M , Waldeck N , Dodson L E , Slater L , Ong K , Kershnar A , Buckingham B , Golden M 
Published: December 2022

Abstract
Because immune mechanisms are associated with insulin-dependent diabetes, multiple organ specific and xenogeneic cytotoxicity assays were developed. Human cellular and antibody effector systems were incubated with 51Cr-labeled dispersed normal rat islet target cells. In eight of 11 diabetic patients, nonenriched mononuclear cells incubated with islet target cells were more cytotoxic than cells from age- and sex-matched controls (p less than 0.01). When non-T cell-enriched mononuclear cells were used at diabetes onset, seven of 11 patients' cells showed excessive islet cytotoxicity (p less than 0.05). In four patients showing elevated cytotoxicity at diabetes onset, cytotoxicity decreased to control levels during diabetes remission. Islet specificity was suggested in that mononuclear cells derived from diabetic subjects did not mediate cytotoxicity against rat spleen or macrophage target cells. Three cytotoxic antibody mechanisms were also evaluated. C-dependent antibody-mediated cytotoxicity with the use of patient serum-coated islet target cells was elevated above control levels in four of 14 patients. Antibody-dependent cellular cytotoxicity exceeded control values in only two of 16 patients, although four assay systems were evaluated. C-augmented antibody-dependent cellular cytotoxicity was elevated in three of 14 patients. No differences were observed for antibody-mediated mechanisms in four patients evaluated at both diabetes onset and remission. Cytotoxic antibody was present in only about one-half of the patients showing increased cellular cytotoxicity, whereas most patients expressing increased cytotoxic antibody had cellular cytotoxicity. Islet cell cytotoxicity assays with the use of effector systems from patients with recent onset insulin-dependent diabetes suggest that direct cellular cytotoxicity is more active than antibody-mediated cytotoxic mechanisms, and that cellular cytotoxicity can correlate with disease activity.
Detection of autoimmune cells proliferating to myelin basic protein and selection of T cell lines that mediate experimental autoimmune encephalomyelitis (EAE) in mice.
Authors: Ben-Nun A , Lando Z 
Published: December 2022

Abstract
A procedure is described for the detection of an in vitro proliferative response to the autologous mouse myelin basic protein in mice injected with mouse spinal cord homogenate (MSCH) or with myelin basic proteins (BP) of mouse (MBP) or rat (RBP) origin. The administration of MSCH, but not of MBP or RBP, in a suitable adjuvant could produce a reproducible clinical disease. Nevertheless, a proliferative response to the autologous MBP could not be detected after either inoculation. Only the removal of the adherent cell fraction from the immunized cell population and its replacement with fresh naive accessory cells could reveal a proliferative response to the autologous MBP and to the heterologous RBP. A heteroclitic cross-reactivity between MBP and RBP is demonstrated. The possibility of detecting an in vitro proliferative response to BP allowed the selection and propagation in vitro of cells specific to BP. T cell lines were established that specifically proliferated in response to BP and mediated EAE in normal mice. Intravenous inoculation of as few as 10(6) line cells was capable of producing clinical signs of EAE in normal recipients within 5 to 6 days. Thus, although an inoculation of MSCH was required for active induction of the disease, T cells specifically reactive against BP are sufficient for mediation of EAE in mice.
Interferon-induced enhancement of macrophage Fc receptor expression: beta-interferon treatment of C3H/HeJ macrophages results in increased numbers and density of Fc receptors.
Authors: Vogel S N , Finbloom D S , English K E , Rosenstreich D L , Langreth S G 
Published: December 2022

Abstract
Previous studies demonstrated that the augmentation of Fc receptor-(FcR) mediated phagocytosis and binding of opsonized sheep erythrocytes is cytokine mediated. Specifically, beta-interferon- (beta-IFN) and gamma-IFN-rich preparations were shown to increase binding and phagocytosis of opsonized erythrocytes by C3H/HeJ macrophages. In this report we extend these studies by examination of the mechanisms by which highly purified beta-IFN increases FcR capacity in C3H/HeJ macrophages. Our findings indicate that beta-IFN augments FcR function for both IgG2a and IgG2b receptor subclasses. Moreover, this increased ability to bind and phagocytose opsonized erythrocytes is associated with a concomitant increase in both the number and surface membrane density of FcR.
Potentiation of the cytolytic activity of peripheral blood monocytes by lymphokines and interferon.
Authors: Fischer D G , Golightly M G , Koren H S 
Published: December 2022

Abstract
Human peripheral blood monocytes obtained by EDTA-reversible adherence to plastic surfaces precoated with autologous serum can rapidly lyse a variety of tumor cells. That the effector cells in this system are indeed monocytes has been demonstrated (1). Using a short-term (3 to 4 hr) 51Cr-release assay and the single cell conjugate cytotoxic assay, we studied the effects of lymphokine-rich supernatants containing gamma-interferon and partially purified fibroblast interferon on the monocyte cytolytic activity. Overnight incubation of the monocytes in fetal bovine serum-containing medium resulted in a relatively small decrease in cytotoxic activity compared to the one obtained with monocytes incubated in autologous serum. The addition of lymphokines or interferon under both incubation conditions resulted in augmented activity as measured in the 51Cr-release assay. However, the proportions of binding and cytotoxic monocytes, determined in the single cell conjugate assay, did not increase. These results suggest that augmented activity is not due to recruitment of inactive cells. Kinetics studies of tumor cell lysis indicate the increase in killing efficiency is probably due to both an increase in the rate of killing and in the recycling ability of the cytotoxic cells. Using the conjugate/agarose technique, we also demonstrated that excess tumor cells could impair the lytic machinery of freshly isolated monocytes, whereas monocytes treated with lymphokines or interferon partially lost their sensitivity to this inhibitory effect. The ability of tumor cells to impair the lytic machinery of monocytes could be one of the mechanisms by which tumors escape immunosurveillance.
Characterization of human B cell growth factor (BCGF) from cloned T cells or mitogen-stimulated T cells.
Authors: Yoshizaki K , Nakagawa T , Fukunaga K , Kaieda T , Maruyama S , Kishimoto S , Yamamura Y , Kishimoto T 
Published: December 2022

Abstract
An assay system for the measurement of human BCGF was established by employing anti-id-stimulated B-CLL cells, anti-mu-stimulated normal B cells, or a transformed B cell line. PHA-Sup from PHA-stimulated T cells induced proliferation of anti-lg-stimulated B cells or augmented proliferation of a B cell line, and the activity was dose-dependent. BCGF, IL 2, and BCDF activities in PHA-Sup were eluted in a 17K fraction by gel filtration in 0.5 M NaCl. BCDF activity (pl 5.8) was isolated by chromatofocusing, but BCGF and IL 2 activities (pl 6.5 and 6.9) were not separated. Absorption with an IL 2-dependent T cell line or anti-id-stimulated B-CLL cells showed BCGF and IL 2 were distinct molecules. An IL 2-dependent helper T cell clone, d4, secreted BCGF with the m.w. of 50K. The 50K-BCGF fraction had no IL 2 activity and was eluted in a 19K fraction by gel filtration in 4 M urea and 1 M NaCl. PMA stimulation of normal T cells induced 50K-BCGF, the m.w. of which was reduced to 19K in 4 M urea and 1 M NaCl. 50K-BCGF from d4 cells and 17K-BCGF from PHA-Sup showed a synergistic effect on the proliferation of anti-lg-stimulated B cells. The results show the existence of two distinct kinds of BCGF and the presence of the synergism between them.
Anaphylatoxin-mediated regulation of the immune response. II. C5a-mediated enhancement of human humoral and T cell-mediated immune responses.
Authors: Morgan E L , Thoman M L , Weigle W O , Hugli T E 
Published: December 2022

Abstract
C5a derived from the fifth component of human complement was found to potentiate both specific and non-specific human in vitro humoral immune responses. In addition, C5a is capable of potentiating antigen- and alloantigen-induced T cell proliferative responses. In contrast to these results, C5a was unable to modulate mitogen-induced B and T cell proliferative responses. The carboxyterminal arginine of C5a is not essential in order for C5a to enhance immune responses. C5ades Arg was found to augment the immune response to the level of C5a-mediated enhancement. The serum carboxypeptidase inhibitor, 2-mercaptomethyl-5-quanodinopentanoic acid, which prevents cleavage of the terminal arginine, allowed us to assay the effects of C5a on in vitro immune responses in the presence of serum. Helper T cells are involved in C5a-mediated immuno-potentiation. Substitution of T cells by soluble T cell-replacing factors, (Fc)TRF, rendered lymphocyte cultures refractory to the enhancing properties of C5a.
Presence of an intrastrain cross-reactive idiotype on A/J antibodies of the IgE class specific for the p-azophenylarsonate group.
Authors: Hirano T , Kojima S , Hirayama N , Nelles M J , Inada T , Nisonoff A , Ovary Z 
Published: December 2022

Abstract
An intrastrain cross-reactive idiotype, CRIA, is associated with a large proportion of the anti-p-azophenylarsonate (anti-Ar) antibodies of A/J mice. The present experiments, in which the methods of direct and reverse passive cutaneous anaphylaxis (RPCA) were used, indicate that IgE anti-Ar antibodies are produced in A/J mice upon stimulation with a protein-Ar conjugate and that a large proportion of these antibodies express CRIA. The use of monoclonal anti-CRIA for RPCA eliminated the strong nonspecific reactions previously observed. The results provide a basis for studying factors that regulate the switch to IgE biosynthesis during an immune response.
Studies of the Epstein-Barr virus receptor found on Raji cells. I. Extraction of receptor and preparation of anti-receptor antibody.
Authors: Simmons J G , Hutt-Fletcher L M , Fowler E , Feighny R J 
Published: December 2022

Abstract
Raji, a human lymphoblastoid cell line, expresses a membrane receptor (EBVR) specific for Epstein Barr virus (EBV). A component that binds EBV was extracted from this cell line by treatment of the cells for 3 hr on ice with Tris buffer containing 10% glycerol. The treatment reduced the capacity of the cells to bind virus, and after concentration the receptor extract (RE) inhibited both EBV binding and superinfection of fresh Raji cells. Similarly prepared extracts of EBVR- cells lacked such activity. An antibody was made to the extract (anti-RE), which after absorption with EBVR- cells, bound to the same percentages of EBVR+ lymphoblastoid cell lines, EBVR+ human/mouse somatic cell hybrids, and fresh peripheral B cells as the virus did. In reciprocal assays, preincubation of EBVR+ cells with anti-RE inhibited virus binding. Doubly stained patches were observed on membranes of EBVR+ cells that had been incubated simultaneously with virus and anti-RE and stained respectively with rhodaminated and fluoresceinated reagents. The major polypeptide immunoprecipitated by anti-RE from radiolabeled Raji cells had an approximate calculated m.w. of 150,000.
Schistosoma mansoni adult microsomal antigens, a serologic reagent. II. Specificity of antibody responses to the S. mansoni microsomal antigen (MAMA).
Authors: Tsang V C , Hancock K , Kelly M A , Wilson B C , Maddison S E 
Published: December 2022

Abstract
The purified Schistosoma mansoni adult microsomal antigen, MAMA, was used in the quantitative single-tube kinetic dependent enzyme-linked immunosorbent assay (k-ELISA) to measure antibody levels of various human patient sera. The 511 serum specimens tested were from patients with both homologous and heterologous infections. Sera from U.S., Egyptian, Brazilian, and Puerto Rican patients infected with S. mansoni reacted strongly with MAMA. Chinese patients infected with S. japonicum, and Nigerians or Egyptians infected with S. haematobium produced much lower responses to this antigen than those infected with S. mansoni. Sera from patients with echinococcosis, filariasis, paragonimiasis, clonorchiasis, trichinosis, amebiasis, and hepatitis and from healthy uninfected control individuals generally contained no detectable antibodies against this antigen. The S. mansoni adult microsomal antigen, MAMA, therefore, appears to be a highly potent and specific reagent for the serodiagnosis of S. mansoni infections.
Anti-Lyt-1 monoclonal antibody inhibits induction of anti-self-TNP but not of alloreactive cytotoxic T lymphocytes.
Authors: Guimezanes A , Schmitt-Verhulst A M 
Published: December 2022

Abstract
The role of Lyt-1+ T cells in the induction of anti-self + TNP and anti-allogeneic CTL was investigated by the use of monoclonal antibodies directed against these molecules. When present during the 5 days of in vitro induction of CTL, anti-Lyt-1.1 mAb partially inhibited the induction of anti-self + TNP CTL but did not affect the induction of alloreactive CTL. The inhibitory effect was dose-dependent, Lyt-1 allotype-specific, and directed at the responding cells. The inhibition could be abolished by the addition of interleukin 2-containing supernatants. These results suggest that under some experimental conditions, Lyt-1-specific mAb can be shown to affect a T cell function, probably a helper function. Possible differences in the induction mechanisms of anti-self + TNP and alloreactive CTL are discussed.
Cytolytic T lymphocyte clones that proliferate autonomously to specific alloantigenic stimulation. II. Relationship of the Lyt-2 molecular complex to cytolytic activity, proliferation, and lymphokine secretion.
Authors: Glasebrook A L , Kelso A , MacDonald H R 
Published: December 2022

Abstract
Previous analyses of the inhibitory effects of anti-Lyt-2 monoclonal antibodies (mAb) on cytolytic activity suggested that Lyt-2/3 antigens expressed on the surface of murine cytolytic T lymphocytes (CTL) are involved in antigen recognition. In the present study, we investigated the effects of anti-Lyt-2 mAb (in the absence of complement) on the functional activities of H-2K/D-specific Lyt-2+ CTL clones that proliferate to antigenic stimulation in the absence of helper T cells or added interleukin 2 (IL 2) and secrete lymphokines. For those clones that were inhibited in cytolysis by anti-Lyt-2 mAb, a parallel inhibition of antigen-dependent proliferation and lymphokine secretion (interferon, macrophage-activating factor) was observed. Inhibition of proliferation or lymphokine secretion could be overcome by the addition of IL 2 or lectin, respectively. Collectively, these results would strongly suggest that anti-Lyt-2 mAb were inhibiting CTL antigen recognition. Not all CTL clones, however, were inhibited in cytolysis by anti-Lyt-2 mAb, in which case proliferation and lymphokine secretion were similarly unaffected. This heterogeneity of Lyt-2+ CTL clones in their susceptibility to inhibition of cytolytic activity, proliferation, and lymphokine secretion by anti-Lyt-2 mAb is discussed in the context of a model proposing that Lyt-2/3 molecules function to stabilize the interaction between CTL receptors and the corresponding target/stimulating cell antigens. Such a stabilization may be required by CTL possessing few and/or low affinity receptors.
Analysis of murine T lymphocyte markers during the early phases of GvH-associated suppression of cytotoxic T lymphocyte responses.
Authors: Hurtenbach U , Shearer G M 
Published: December 2022

Abstract
Graft-vs-host- (GvH) associated immune-suppression was generated by injecting nonirradiated (B6 X C3H)F1 hybrid mice with 40 to 60 X 10(6) B6 or C3H parental spleen cells. Susceptibility to suppression as well as the potential of parental donor lymphocytes to generate suppressor activity was investigated in allogeneic cytotoxic T cell responses by mixing spleen cells from the inoculated F1 recipients with syngeneic responder cells from untreated mice. The susceptibility to suppression in F1 recipients, as well as the potential of parental lymphocytes to induce suppression in F1 mice, varied with the age of the mice. Cellular analysis revealed that GvH-suppression was mediated by 500 R radiosensitive parental T cells during the period tested (from day 5 until day 8 after injection of B6 parental spleen cells). In contrast, selected F1 lymphocytes from recipients injected with parental spleen cells failed to exhibit suppressor cell activity. The sensitivity of parental GvH suppressor cells to anti-Lyt reagents was time dependent. Thus, suppressor cells were sensitive to monoclonal anti-Lyt-1 or anti-Lyt-2 and C (usually until day 7 after injection of parental spleen cells); subsequently, suppression became insensitive to anti-Lyt-1, but remained sensitive to anti-Lyt-2 and C treatment.
Suppression of lymphocyte proliferative responses: characterization of the suppressor and kinetics of suppression.
Authors: Stout R D , Fisher M 
Published: December 2022

Abstract
Culturing spleen cells for 2 or more days in the absence of mitogenic stimulation results in the generation of suppressor cells that can effectively inhibit the proliferative responses of freshly prepared spleen cells to mitogen or alloantigen stimulation. Suppression does not appear to be mediated by prostaglandins nor other soluble factors produced during the preculture period. The suppressor cell is described as a plastic-adherent Thy-1.2-, IgM-, FcR+ macrophage-like cell. Significant suppression of Con A responses can be detected at suppressor to target ratios as low as 1:100. The plastic-adherent suppressor is capable of terminating Con A-induced proliferation of spleen cells whether added at the onset of the Con A response or added as late as 48 hr after mitogenic stimulation. The suppressed spleen cell population displays an absence of large blast cells and a decrease in surface density of Thy-1.2 determinants.
Presence of circulating anti-idiotype-bearing cells after booster immunization with tetanus toxoid (TT) and inhibition of anti-TT antibody synthesis by auto-anti-idiotypic antibody.
Authors: Geha R S 
Published: December 2022

Abstract
We have previously documented the appearance of auto-anti-idiotypic (anti-Id) antibody in the serum of normal subjects after booster immunization with tetanus toxoid (TT) antigen. In the present study circulating auto-anti-Id-bearing cells and the regulatory role of auto-anti-Id antibody on anti-TT antibody synthesis were examined. Two adult volunteers were boosted with TT antigen, and IgG (Fab')2 anti-TT was prepared from plasma obtained 7 and 10 days after boosting. Auto-anti-Id antibody directed against autologous IgG (Fab')2 anti-TT became detectable in the serum starting 2 wk and up to 4 mo after booster immunization with TT. Circulating cells capable of specifically binding fluorescein-conjugated autologous IgG (Fab')2 anti-TT were identified starting 3 wk after immunization and throughout the 3- to 4-mo study period. Auto-anti-Id-bearing cells were predominantly B cells and secreted auto-anti-Id antibody after stimulation with pokeweed mitogen (PWM) in vitro. When added to cultures of peripheral blood lymphocytes (PBL) obtained 10 days after immunization, serum auto-anti-Id antibody inhibited the PWM-induced synthesis of IgG anti-TT. This inhibition was idiotype specific and affected predominantly the synthesis of anti-TT idiotypes recognized by the auto-anti-Id antibody. Auto-anti-Id antibody did not affect the synthesis of IgG anti-TT by PBL that co-circulated with the auto-anti-Id antibody. These results suggest that auto-anti-Id antibodies play a role in the regulation of the normal human immune response.