bluuebunny/crossref_metadata_2025_split huggingface dataset:
Murine B Cell Leukemia (BCL1): Organ Distribution and Kinetics of Growth as Determined by Fluorescence Analysis with an Anti-Idiotypic Antibody
Authors: Krolick K. A. , Isakson P. C. , Uhr J. W. , Vitetta E. S. 
Published: December 2022

Abstract
The life history of a transplantable B cell leukemia (BCL1) that arose spontaneously in a BALB/c mouse is described. Animals bearing this tumor live from 2 to 4 months in apparently good health despite massive splenomegaly and leukemia. Antibody to the idiotype or λ light chain of the tumor IgM was used in conjunction with the fluorescence-activated cell sorter to identify tumor cells in the BCL1-bearing mice. The results suggest that these cells multiply and differentiate in the spleen and subsequently emigrate to the blood. Tumor cells do not recirculate as evidenced by their failure to enter the thoracic duct or to infiltrate lymph nodes to a significant extent. During tumor growth, a population of T cell blasts appears that may be involved with an immune response against the tumor.
Radiolabeling and Isolation of Thy-1 Active Glycolipids from Murine Brain and Lymphoma Cell Lines
Authors: Kato K. P. , Wang T. J. , Esselman W. J. 
Published: December 2022

Abstract
Murine Thy-1 active glycolipids were isolated and characterized by radiolabeling, thin layer chromatography (TLC), and an immune response-plaque forming cell (PFC) assay. Brain gangliosides were labeled in vivo by intracranial injection of [1-14C]N-acetylmannosamine (ManNAc). Gangliosides were extracted, separated by one and two dimensional TLC, and visualized by autoradiography. The gangliosides isolated from AKR (Thy-1.1) and ICR (Thy-1.2) mice were assayed for Thy-1.1 and 1.2 activity with an anti-Thy-1 PFC assay. One Thy-1.1 active compound was identified out of about 15 AKR gangliosides. None of the AKR gangliosides had Thy-1.2 activity in the PFC assay. Similarly, one Thy-1.2 active ganglioside was identified out of the ICR gangliosides and none of these had Thy-1.1 activity. Thus the brain gangliosides demonstrated allogeneic specificity for Thy-1 antigen.
BW5147 (Thy-1.1) and S49.1 (Thy-1.2) murine lymphoma cell lines that express Thy-1 were also examined for Thy-1 active glycolipids. The cell lines were incubated in vitro with either [1-14C]palmitate or [1-14C]-ManNAc, and the glycolipids were extracted, separated by two dimensional TLC, and visualized by autoradiography. A Thy-1.2 active compound was identified from the S49.1 cells. None of the BW5147 glycolipids had Thy-1.2 activity and none of the S49.1 glycolipids had Thy-1.1 activity. Neuraminidase and mild HC1 treatment of Thy-1 active glycolipids abrogated the subsequent PFC response. The Thy-1 glycolipids bound to DEAE cellulose as expected for gangliosides. We therefore conclude that Thy-1 antigenicity is associated with gangliosides of mouse brain and lymphoma cells.
Inhibition of Growth of ASL-1w Murine Leukemia Cells by Anti-Thymus Leukemia Antigen (TL) Serum in the Absence of Complement
Authors: Wolcott Michael , Pickering Jerry W. , Williams Jackie L. 
Published: December 2022

Abstract
Previous studies have shown that the cell surface expression of thymus leukemia antigen (TL) on ASL-1w leukemia cells varies with the progression of the cells through the growth cycle. Expression of TL is maximal in S phase, and its quantitative expression varies directly with DNA synthesis. In the present study, the effect of anti-TL serum on the growth of ASL-1w cells was examined. The antiserum, tested in the absence of complement, affected the growth of these cells in biphasic manner. When the antiserum concentration was 0.1% or greater, there was a rapid decline in the rate of DNA synthesis, and after 5 to 7 hr, cell death. When the antiserum concentration was 0.067% or less, the decline in the rate of synthesis of DNA did not become apparent until 5 to 6 hr after treatment. Under these conditions, there was approximately a 20% increase in cell number after 24 hr of culture. The hypothesis that treatment of ASL-1w cells with the lesser concentration of anti-TL serum blocks the cells in G2 phase of the cell cycle is discussed.
Lymphocytes Bearing Receptors for IgE
Authors: Yodoi Junji , Ishizaka Kimishige 
Published: December 2022

Abstract
Culture of normal rat lymphocytes with rat IgE at 37°C resulted in an increase in the proportion of FcεR(+) cells. In agreement with this finding, the ability of normal lymphocytes to bind 125I-IgE markedly increased after overnight incubation with IgE. Evidence was obtained that FcεR(+) cells were derived from FcγR(+) cells. FcεR(+) cells were not induced in vitro if FcγR(+) cells were depleted from normal lymphocytes before incubation with IgE. Kinetic studies for the induction of FcεR(+) cells showed that the majority of FcεR(+) cells induced in vitro bore FcγR at the early stage of differentiation. The FcεR-FcγR double-bearing cells converted to FcεR signal-bearing cells after further incubation with IgE. It was also found that induction of FcεR(+) cells by IgE was inhibited by rabbit IgG (RGG) or soluble antigen—IgG antibody complexes that have affinity for FcγR, but FcεR induced in vitro were specific for IgE. The results suggested that the binding of IgE with FcγR provided a signal to form and/or express FcεR.
A high proportion of FcεR(+) cells in the mesenteric lymph nodes from rats infected with Nippostrongylus brasiliensis was maintained if the lymphocytes were cultured in IgE, whereas the proportion markedly diminished if the cells were kept overnight in IgE-free medium. Evidence was obtained that the maintenance in the proportion of FcεR(+) cells does not involve recruitment of FcγR(+) cells to FcεR(+) cells; the proportion of FcεR(+) cells in a FcγR-depleted fraction was maintained by IgE. Neither RGG nor antigen-IgG antibody complexes affected the maintenance of the FcεR(+) cells by IgE. The results collectively suggested that the binding of IgE with either FcγR or FcεR stimulate lymphocytes to form FcεR.
The Kinetics for Binding and Catabolism of Aggregated IgG by Rat Peritoneal Macrophages
Authors: Knutson David W. , Kijlstra Aize , van Es Leendert A. 
Published: December 2022

Abstract
Mononuclear phagocytes in the reticuloendothelial system (RES) bind and catabolize circulating antigen-antibody complexes. These functions were studied with an in vitro model to elucidate the cellular mechanisms and rate-limiting step for catabolism of soluble immune complexes by mononuclear phagocytes. The model consisted of reacting stable heat aggregates of 125I-IgG (A-IgG) (0.01 to 10 µg) at 37°C for 10 min to 24 hr with 1.0 × 106 adhering peritoneal macrophages from normal rats. A-IgG were then separated into cell-associated, acid-precipitable (unreacted) and acid-soluble catabolized fractions. With subsaturating doses of A-IgG, binding and catabolism of A-IgG followed the kinetics for consecutive first-order reactions with binding the ratelimiting step (binding rate constant = ka = 0.7 to 5.5 × 10-3 min-1; catabolism rate constant = kc = 20.0 to 55.0 × 10-3 min-1). At higher doses of A-IgG, the binding step became saturated (and ka fell) while catabolism remained first order (with constant kc). The maximum clearance velocity (Vmax) was a function of A-IgG size in that more micrograms but fewer molecules of A-IgG9 could be cleared per unit time than A-IgG74 (1200 A-IgG9 and 540 A-IgG74 molecules per cell per min). Most cell-associated A-IgG were present on the cell surface where they were accessible to release by trypsin. On the basis of these observations, it was postulated that binding becomes saturated because of limited availability of receptors for the Fc portion of IgG. Assuming that pinocytosis of A-IgG was necessary before A-IgG were catabolized, these data further suggest that pinocytosis of A-IgG is slower than the subsequent catabolic step and that bound A-IgG are pinocytosed at a constant fractional rate. This would seem to require mechanisms to concentrate A-IgG at certain sites on the membrane and then selectively to interiorize the A-IgG bearing portions.
Rabbit B Spleen Lymphocytes and T Helper Cells
Authors: Cavaillon J. M. , Udupa T. N. S. , Chou C-T. , Cinader B. , Haeffner-Cavaillon N. , Dubiski S. 
Published: December 2022

Abstract
The response to anti-allotype (anti-Ab4), Nocardia Water Soluble Mitogen (NWSM), pneumococcal polysaccharide type III (SSS III), and human Fc fragments of various purified and unfractionated rabbit spleen cell populations was determined in terms of 3H-thymidine uptake. B cells were isolated either from untreated suspensions of spleen cells or from suspensions from which adherent and phagocytic cells were removed. The purification factor was greater than the enhancement of 3H-thymidine uptake by anti-Ab4, NWSM, and SSS III as compared with the response of unfractionated spleen cells. It thus appears that a helper cell was involved: the mitogen response of purified B cells was enhanced by the addition of T cells. B subpopulations were separated by sedimentation or by rosetting, which allowed us to separate Fcγ receptor-bearing cells from cells that did not possess this receptor. There were differences between cells responding to B mitogens not only in sedimentation velocity but also in the absolute number of cells. B cells bearing the Fcγ receptor were less responsive to anti-Ab4 and more responsive to SSS III, NWSM, and human Fc than were B cells lacking the Fcγ receptor.
Autologous and Allogeneic Intercellular Interactions: Modulation by Adherent Cells, Irradiation, and in Vitro and in Vivo Corticosteroids
Authors: Katz Paul , Fauci Anthony S. 
Published: December 2022

Abstract
The present study investigated the intrinsic blastogenic reactivity within T and non-T lymphocyte populations as well as between these populations in the autologous and allogeneic mixed lymphocyte reactions (MLR). T cell-depleted lymphocytes exhibited after 6 days in culture, high levels of intrinsic blastogenic activity that were sensitive to irradiation and in vitro hydrocortisone. Depletion of adherent cells shifted the peak T cell-depleted intrinsic blastogenesis from 6 days in culture to 2 to 3 days after initiation of culture. T cellenriched cells displayed low intrinsic blastogenic responses that were relatively unaffected by irradiation and in vitro hydrocortisone. The removal of adherent cells from T cell-depleted suspensions (stimulators) augmented both the autologous and allogeneic MLR, whereas irradiation of cells had no effect on these reactions. In vitro hydrocortisone suppressed the autologous MLR and, to a much lesser extent, the allogeneic MLR. I.V. administration of hydrocortisone to normal volunteers suppressed the autologous MLR at 4 hr after injection. The responsiveness of T cells obtained at 4 hr to autologous and allogeneic non-T cell stimulation was markedly diminished. Non-T cells obtained 4 hr after i.v. hydrocortisone had greater stimulatory capacity for both the autologous and allogeneic MLR than did T cell-depleted cells obtained before hydrocortisone administration. These studies demonstrate that autologous and allogeneic intercellular interactions between lymphoid cells are susceptible to a variety of in vitro and in vivo influences and that such interactions may reflect relevant immunoregulatory events occurring in vivo.
H-2 Unrestricted Cytotoxic T Cell Activity against Antigens Controlled by Genes in the QA/TLA Region
Authors: Forman James 
Published: December 2022

Abstract
The specificity of H-2 unrestricted cytotoxic T cells was analyzed in secondary CML responses. A/J strain effector cells, sensitized against A.Tlab lymphoid cells, lysed target cells from strains with differing H-2 haplotypes but all sharing Qa-1b/Tlab alleles; whereas, target cells from strains with Qa-1a/Tlaa were not. When B6.Tlaa animals were in vivo-primed and challenged in vitro with B6 stimulator cells, no cytotoxic effector cell activity was generated. However, if B6.Tlaa animals were primed in vivo with A.BY cells and then rechallenged in vitro with either A.BY or B6 stimulator cells, cytotoxic effector cells were generated that lysed target cells from strains with Qa-1b/Tlab alleles. This suggests that factors in addition to Qa/Tla may play a role in the generation of anti-Qa/Tla effector cell activity. It was also noted that targets from strains with Qa-1a/Tlaa alleles were killed, although to a much lesser extent than the Qa-1b/Tlab targets. SWR anti-DBA/1 effector cells strongly lysed target cells from strains with Qa-1b/Tlab, lysed Qa-1a/Tlaa targets to a lesser extent, and produced no cytolytic effect on B6.Tlaa target cells. These data suggest that in addition to a CML target antigen associated with Qa-1b/Tlab, there may be an additional specificity recognized by cytotoxic T cells controlled by a gene outside of Qa-1b/Tlab.
Mechanisms of Idiotype Suppression
Authors: Kim Byung S. 
Published: December 2022

Abstract
Specific tolerance of BALB/c spleen cells to phosphorylcholine (PC) was induced in vitro by treatment with antibodies specific for the idiotype of TEPC-15 myeloma protein (anti-T15id) and a PC-containing antigen, R36a. The presence of anti-T15id antibody for at least 2 days was necessary to achieve a full level of suppression (&gt;98%) of anti-PC production in the presence of R36a. The anti-PC response of a nylon wool-separated B cell population was also greatly suppressed (94%) only after a 48-hr treatment with anti-T15id antibody plus antigen. In contrast, either isolated B or unseparated spleen cells treated with anti-T15id alone (without antigen) were fully responsive to PC. Kinetic studies inducated that treatment of cells with anti-T15id antibodies either in the presence or absence of R36a resulted in a gradual suppression of anti-PC responses at a similar rate during an initial 12-hr period. However, further treatment (24 hr) of cells with anti-T15id antibody alone led to recovery of anti-PC response from the suppression, whereas incubation with the anti-idiotype antibody plus R36a induced further suppression. These results indicate that anti-idiotype antibodies can directly inactivate B cells, and this inactivation becomes irreversible only after a continuous exposure to the antibodies in the presence of specific antigen.
Regulation of Cell Mediated Immunity by Antibodies: Possible Role of Anti-Receptor Antibodies in the Regulation of Contact Sensitivity to DNFB in Mice
Authors: Sy Man-Sun , Moorhead John W. , Claman Henry N. 
Published: December 2022

Abstract
The duration of maximal contact sensitivity in the mouse is regulated, at least in part, by specific antibodies. Mice sensitized with optimal doses of 2,4-dinitrofluorobenzene (DNFB) develop maximum delayed hypersensitivity in 4 to 5 days as measured in vivo by ear swelling. The intensity of this reaction declines rapidly, and by 12 days post-sensitization significant immunity is no longer detectable. Serum taken from animals 9 to 15 days post-sensitization will block the ability of DNFB-immune lymph node (LN) cells to passively transfer immunity. The suppressive molecules are immunoglobulins, but they do not have anti-DNP activity and are not associated with DNP as antigen-antibody complexes. The suppressive serum is antigen specific, i.e., it blocks DNFB-immune LN cells but not TNCB- or oxazolone-immune LN cells, and it lacks strain specificity in inhibiting passive transfer. The suppressive serum can be adsorbed by DNFB-immune LN cells (both syngeneic and allogeneic), but not by normal LN cells. Furthermore, the suppressive activity of the serum is adsorbed by and can be recovered from an affinity column conjugated with purified mouse anti-DNP antibodies.
We conclude that blocking antibodies arise during sensitization with DNFB and down-regulate the duration of sensitivity. These antibodies are directed against surface components of immune LN cells. They possess anti-idiotype activity and represent part of the immunoregulatory elements within a complex network of anti-idiotype/idiotype interaction.
Antigenic Determinants of Influenza Virus Hemagglutinin
Authors: Jackson David C. , Brown Lorena E. , White David O. , Dopheide Theo A. A. , Ward Colin W. 
Published: December 2022

Abstract
Polypeptide fragments obtained by cyanogen bromide (CNBr) cleavage of the hemagglutinin (HA) of the A/Memphis/102/72 (H3N2) strain of influenza virus were inoculated into rabbits, and the resulting antisera were examined for the presence of antibodies capable of reacting with intact virus, detergent-solubilized hemagglutinin, hemagglutinin heavy chain (HA1), or CNBr fragments derived from HA. We have shown that it is possible to raise antibodies to individual fragments including those representing regions of the hemagglutinin molecule that are not normally antigenic within the intact virion. The antibodies are specific for the fragment to which they were raised. In those cases where the immunogen contains carbohydrate, a small proportion of the antibody is directed against these side chains, but this can be removed by adsorption with an unrelated influenza virus. Although only antibodies raised against intact HA are capable of neutralization of virus or lysis of infected cells in the presence of complement, some of the antibodies against fragmented HA possess hemagglutination-inhibition activity.
All of the antibody preparations are capable of binding to purified HA1, but only those raised against fragments containing the antigenic polypeptide, HA1CN1, are capable of binding to intact virus. This indicates that within the intact virion the N-terminal CNBr fragment of HA1 carries immunogenic activity.
Antigen-Specific Immunocompetency, B Cell Function, and Regulatory Helper and Suppressor T Cell Activities in Spontaneously Autoimmune Mice
Authors: Creighton W. Dodson , Katz David H. , Dixon Frank J. 
Published: December 2022

Abstract
A comprehensive analysis of the immunocompetency of three murine strains displaying spontaneous autoimmune disease was conducted at various times during the lifespan of these mice. Qualitative and quantitative comparisons have been made for antibody responses to well defined hapten-carrier conjugates between young and old autoimmune as referenced against nonautoimmune inbred mice of the same ages. Responses of intact autoimmune and normal murine strains in two immunoglobulin classes, i.e., IgG and IgE, failed to reveal any general pattern of abnormal immune reactivity that could be ascribed solely to the autoimmune phenotype; grossly deficient antibody-producing capacities that were observed in old mice of the MRL/1 strain do not necessarily relate to the existence of autoreactivity in such animals.
In addition to studies in intact mice, the immunocompetency of isolated B lymphocyte and regulatory T lymphocyte populations of these autoimmune mice were assayed for functional abnormalities by utilizing adoptive transfer systems. No significant differences were observed between young and old autoimmune mice and normal control strains either in the antibody-producing abilities of adoptively primed hapten-specific B lymphocytes or in regulatory functions of antigen-specific helper and suppressor T cells. Even in those circumstances in which intact mice showed marked deficiencies in antibody responses, i.e., old MRL/1, lymphocytes removed from the native environment of such mice displayed normal reactivity patterns in adoptive transfer situations.
Of special note are the results presented herein that clearly demonstrate that antigen-specific regulatory T cell functions of both helper and suppressor types are, in fact, normal in both old as well as young animals of all three autoimmune murine strains. These findings raise serious questions about previous concepts concerning the existence of any single defect or combination of immunoregulatory defects as universal pathogenetic mechanisms in the development of autoimmune diseases.
The Specificity of Human Autoantibodies That React with Both Cell Nuclei and Plasma Membranes: The Nuclear Antigen Is Present on Core Mononucleosomes
Authors: Rekvig Ole P. , Hannestad Kristian 
Published: December 2022

Abstract
We have examined the nature of the nuclear antigen recognized by certain natural human antibodies that react specifically with both cell nuclei and plasma membranes from many species. Partial purification of these antibodies, called X-ANA, is achieved by binding to and rapid elution from the surface of viable human leukocytes. Chicken erythrocyte chromatin was solubilized by digestion with staphylococcal nuclease and fractionated into a 0.15 M NaCl soluble fraction that consisted of core mononucleosomes lacking H1/H5, and a 0.15 M NaCl insoluble fraction composed of polynucleosomes with H1/H5 present. No proteins other than histones were detected. Native and reconstituted mononucleosomes displaced IgG of the leukocyte eluates from nuclei of frozen mouse kidney sections and from the walls of plastic tubes coated with polynucleosomes. The reconstituted core mononucleosomes were 4- 10-fold less efficient inhibitors than native mononucleosomes. Trypsin digested mononucleosomes, free high m.w. DNA, and free histones displayed no or very weak inhibitory activity. The data indicate that X-ANA recognize a complex consisting of the core histones H2A, H2B, H3, H4, and DNA of 140 to 200 base pairs in length.
Plasminogen Activator Production by Human Monocytes
Authors: Greineder Dirk K. , Connorton Kevin J. , David John R. 
Published: December 2022

Abstract
Human monocytes, but not nylon wool column-nonadherent lymphocytes, produce plasminogen activator. The activity is found only in association with intact cells. Exposure of monocytes to activated lymphocytes or to lymphokine-rich supernatants enhances monocyte plasminogen activator production. The assay allows assessment of baseline and activated human monocyte function.