bluuebunny/crossref_metadata_2025_split huggingface dataset:
A T lymphocyte subpopulation in multiple sclerosis patients bearing Fc receptors for both IgG and IgM1.
Authors: Merrill J E , Biberfeld G , Kolmodin G , Landin S , Norrby E 
Published: December 2022

Abstract
Abnormally low proportions of total T lymphocytes were found in peripheral blood lymphocytes (PBL) of patients with multiple sclerosis (MS) accompanied by high proportions of T lymphocytes with Fc receptors (FcR) for IgG (T gamma cells). Seventy-five percent of the MS patients had greater than 40% T gamma in the T lymphocyte-enriched population. In 6 out of 16 cases, T mu were also elevated. This elevation, however, did not seem to correlated with disease stage. By mixed rosetting and direct observation with an indirect immunofluorescence test, 30 to 50% of the T gamma cells in MS PBL were also shown to bear FcR for IgM. This population bearing FcR for IgG and IgM, designated T gamma mu, was usually found to be 10% or less of the T gamma population in normal controls. The significance of this T gamma mu population for the MS disease process requires further evaluation.
Defective tumoricidal capacity of macrophages from P/J mice: characterization of the macrophage cytotoxic defect after in vivo and in vitro activation stimuli.
Authors: Boraschi D , Meltzer M S 
Published: December 2022

Abstract
Unlike macrophages from responsive mouse strains, peritoneal cells of P/J mice treated in vivo with viable Mycobacterium bovis, strain BCG, or killed Corynebacterium parvum fail to develop tumoricidal activity. P/J macrophages treated in vitro with lymphokine-rich supernatants, bacterial endotoxic lipopolysaccharides (LPS) or T cell mitogens also fail to develop cytotoxic activity. Experimental manipulation of effector:target cell ratios, doses of activation stimuli, or tumor target cells did not evoke cytotoxic activity. The macrophage defect of P/J mice appeared similar to that of lipid A-insensitive C3H/HeJ mice. The macrophage defect of C3H/HeJ mice is controlled by a gene identical or closely linked to the Lpsd gene. Tumoricidal defects of P/J macrophages, however, appeared independent of the Lpsd gene: responses of P/J spleen cells or macrophages to LPS, which are controlled by the Lps gene, were normal. P/J mice therefore represent a distinct and potentially useful genetic probe for characterization of mechanisms in macrophage activation.
Augmentation of delayed-type hypersensitivity by vesicular stomatitis virus infection in mice.
Authors: Katsura Y , Takaoki M , Kono Y , Minato N 
Published: December 2022

Abstract
Effects of the infection with vesicular stomatitis virus (VSV) on delayed-type hypersensitivity (DTH) to heterologous erythrocytes were investigated in mice. Infection at the time of immunization resulted in production of high levels of DTH that were specific to the antigen used for immunization. The high level of DTH produced in VSV-infected mice could not be attributed to the nonspecific enhancement of the footpad swelling with the infection. Augmentation of DTH was observed in all strains of the mouse (CBA, BALB/c, C3H/He, and C57BL/6) used. The augmenting effect of VSV infection was not as apparent in adult thymectomized mice in which the level of VSV-replicating T cells was reduced. These results strongly suggest that DTH-mediating T cells are resistant to infection by VSV, and also that there are VSV-sensitive cells that may be engaged in the suppression of DTH. It seems improbable, however, that the cells sensitive to VSV infection represent the suppressor cells themselves, since the enhancing effect was not observed in mice in which the suppressor cells were induced by the administration of high doses of the antigen.
Macrophages and T cells control distinct phases of B cell differentiation in the humoral immune response in vitro.
Authors: Hoffmann M K 
Published: December 2022

Abstract
The differentiation of B cells in the in vitro PFC-response to red blood cell antigen proceeds through 2 phases. Antigen-reactive B cells acquire the ability to interact with helper T cells in the first phase. This phase is controlled by macrophages through a mediator that they release (Interleukin 1 ([Il-1]). B cells convert into antibody-secreting cells (PFC) in the second phase, which is controlled by helper T cells or by a mediator that they release (T cell-replacing factors [TRF]). This is demonstrated in experiments in which Il-1 increases the number of B cells capable of responding to T cell help. The majority of antigen-reactive B cells reaches that state of differentiation within 40 hr of incubation with Il-1. After this time, the response of B cells depends no longer on the presence of Il-1 but on the presence of T cells or TRF. The presented data suggest that antigen-primed helper T cells (but not unprimed T cells) induce the release of Il-1 by macrophages, thereby also influencing the early phase of B cell differentiation.
H-2-dependent cell-mediated immunity in vivo: delayed-type hypersensitivity and contact sensitization induced by fluorescein isothiocyanate-conjugated cells.
Authors: Domoto D T , Askenase P W 
Published: December 2022

Abstract
Fluorescein isothiocyanate (FITC) was found to be a suitable hapten to study cell-mediated immunity in vivo in mice. Delayed-type hypersensitivity (DTH) footpad swelling reactions were induced and elicited by injection of FITC-conjugated syngeneic spleen cells, and contact sensitivity (CS) was induced and elicited by skin painting with reactive FITC. Cross-reactive specificity between DTH and CS was demonstrated. Thus, DTH induction with FITC-spleen cells (FITC-SC) also led to the ability to elicit CS; and CS induction by skin painting also led to the ability to elicit DTH with FITC-SC. However, the 2 reactions differed in that the ability to elicit DTH induced by subcutaneous immunization with FITC-SC was evanescent, whereas CS induced by skin painting was long lived. Specificity of these reactions was hapten dependent and additionally required homology at the H-2 locus of the major histocompatibility complex. The H-2 specificity requirement was not evanescent.
"Allergic breakthrough" after antigen sensitization: height of IgE synthesis is temporally related to diurnal variation in endogenous steroid production.
Authors: Bargatze R F , Katz D H 
Published: December 2022

Abstract
Mice of the SJL strain normally display the low IgE responder phenotype. In the course of extensive studies on IgE responses with this strain of mice, it because apparent that the magnitudes of IgE antibody synthesis by SJL mice varied after antigen sensitization either alone or in conjunction with exposure to optimal enhancing doses of whole body irradiation. Analysis of the basis for this variability revealed that SJL respond to antigen sensitization by displaying cyclical IgE response curves determined by the time of day the sensitization is carried out. Moreover, when these low responders are converted to the high responder phenotype by low dose irradiation, the time of irradiation determines the magnitude of the IgE response obtained, whereas the time of antigen challenge determines the potential for generating a good response. The diurnal curve of IgE responses in both unirradiated and irradiation-enhanced low responder mice appears to be determined by normal variations in levels of endogenous corticosteroids, as indicated by the correlation between the normal diurnal curve of endogenous steroid production with the cyclical pattern of IgE responses. This apparent effect of endogenous steroid production on IgE antibody synthesis is supported by experiments demonstrating that the normal IgE pattern in both unirradiated and irradiated mice can be perturbed by administration of cortisone at the proper time of day. These results indicate that IgE antibody synthesis displays unique sensitivity to fluctuations in plasma steroid levels and may have significant implications for the role of steroids in the pathogenesis and management of allergic diseases.
Mouse C3b/C4b inactivator: purification and properties.
Authors: Kai S , Fujita T , Gigli I , Nussenzweig V 
Published: December 2022

Abstract
Mouse C3b/C4b inactivator (C3b/C4bINA) was purified approximately 400 times from mouse serum. It is a beta-globulin and consists of 2 disulfide bonded chains of m.w. 60,000 and 35,000. Under nonreducing conditions, its m.w. is 95,000. It cleaves the alpha'-chain of cell-bound C4b into 3 fragments: alpha 2, alpha 3, alpha 4. The alpha 2 fragments remain bound to the cell surface (C4d), and the rest of the molecule (C4c) is released into the fluid phase. In fluid phase, C3b/C4bINA cleaves the alpha'-chain of C4b in a similar manner but only in the presence of mouse or human C4-binding protein (C4-bp). Mouse C4-bp and human C3b/C4bINA do not cleave human C4b, although mouse C4-bp binds to human C4b. This incompatibility suggests that C4-bp and C3b/C4bINA must interact to cleave fluid phase C4b. Mouse C3b/C4bINA also cleaves the alpha'-chain of human C3b in solution into 2 fragments in the presence of human beta 1H. Therefore, it is likely that mouse and human C3b/C4bINA are homologous proteins. A monospecific antiserum to mouse C3b/C4bINA has been prepared in rabbits. By crossed immunoelectrophoresis, this antiserum detects, in addition to the protein described above, a fast beta-globulin with a m.w. of approximately 200,000 and antigenically identical to C3b/C4bINA but enzymatically inactive. This protein could represent a precursor of C3b/C4bINA.
T11: a new protein marker on activated murine T lymphocytes.
Authors: Gately M K , Martz E 
Published: December 2022

Abstract
Murine lymphocytes were activated in vitro in mixed lymphocyte cultures (MLC) or by the addition of the mitogens concanavalin A (Con A), phytohemagglutinin (PHA), or E. coli lipopolysaccharide (LPS). Activated lymphocytes were internally labeled with 35S-methionine and then disrupted by hypotonic lysis. A plasma membrane-enriched fraction was isolated from each cell population, and the 35S-labeled proteins in this fraction were examined by SDS-polyacrylamide gel electrophoresis (SDS-PAGE). An intensely labeled band, the position of which indicated an apparent m.w. of 11,000, was observed when plasma membrane-enriched fractions from MLC- and Con A-activated cells were subjected to SDS-PAGE. In contrast, plasma membrane-enriched fractions from normal spleen cells, LPS-activated cells, PHA-activated cells, and EL4, RDM4, and P815 tumor cells possessed little or none of this protein, which we have designated T11. T11 was not found in the soluble cytoplasmic protein from MLC-activated cells. Hence the presence of T11 in the plasma membrane-enriched fraction from these cells cannot be attributed to contamination by cytoplasmic protein. Removal of T cells from populations of MLC-activated cells by treatment with monoclonal anti-Thy 1 and complement removed T11. These results suggest that T11 may represent a new protein marker on a subclass of activated T lymphocytes.
Interaction of C-reactive protein with artificial phosphatidylcholine bilayers and complement.
Authors: Volanakis J E , Narkates A J 
Published: December 2022

Abstract
We have examined the interaction of C-reactive protein (CRP) with model membranes and complement. Binding of CRP to multilamellar liposomes or unilamellar vesicles of egg-phosphatidylcholine required the presence of lysophosphatide in the bilayer. The binding was Ca++-dependent, could be inhibited by phosphocholine, and resulted in activation of the classical complement pathway. A weak interaction between CRP and agarose was observed, which was also CA++-dependent and could be inhibited by phosphocholine and galactose. In addition, incorporation of galactocyl cerebroside in phosphatidylcholine:lysophosphatidylcholine liposomes enhanced the binding of CRP. Binding constants of 1.9 X 10(-5) M and 7.1 X 10(-5) M were calculated for liposomes containing and lacking the glycolipid, respectively. Furthermore, CRP bound to galactocyl cerebroside-containing liposomes bound approximately twice as much C1q as the same amount of CRP bound to liposomes lacking the glycolipid. We conclude that: 1) An alteration of the normal organization of phosphatidylcholine bilayers is necessary for binding of CRP. 2) The presence of galactosyl residues on the surface of the bilayer enhances the binding of CRP, perhaps through interaction with a putative secondary binding site on the protein.
A human T lymphocyte differentiation marker defined by monoclonal antibodies that block E-rosette formation.
Authors: Howard F D , Ledbetter J A , Wong J , Bieber C P , Stinson E B , Herzenberg L A 
Published: December 2022

Abstract
A new human T cell surface antigen, Leu-5, has been defined using a set of monoclonal antibodies that block rosette formation between T lymphocytes and sheep erythrocytes (SRBC). Four antibodies obtained from 2 different fusions using 2 immunized mouse strains all reacted with the same antigen. All these antibodies gave identical quantitative immunofluorescence (FACS) profiles, all gave the same staining profiles and intensities when used singly or in combinations, and all precipitated the same molecule. The antigen is a single polypeptide chain, 40,000 to 50,000 Mr, and is found on all thymocytes, peripheral T cells, and some null cells, but not on B cells. Leu-5 is a differentiation antigen that decreases in density as thymocytes mature to peripheral T lymphocytes. Thus, the Leu-5+ subpopulations ranked in order of decreasing Leu-5 density are: a subpopulation of subcapsular thymocytes greater than cortical and medullary thymocytes greater than peripheral T cells (cytotoxic/suppressor subset) greater than peripheral T cells (helper/inducer subset). The density distribution pattern of Leu-5 parallels the relative affinity of thymocytes and peripheral T lymphocytes for SRBC. We suggest that Leu-5 is either identical to or closely associated with the human T lymphocyte receptor for SRBC.
Spontaneous lytic activity against allogeneic tumor cells and depression of specific cytotoxic responses in mice infected with Trypanosoma cruzi.
Authors: Hatcher F M , Kuhn R E 
Published: December 2022

Abstract
The ability of cells from mice infected with Trypanosoma cruzi to generate specific as well as nonspecific cell-mediated cytotoxic responses to allogeneic tumor cells was investigated. The capacity of spleen cells from either C3H/He (C3H) or C57BL/6 (B6) mice to develop cytotoxic responses in vitro against P-815 tumor cells was depressed after the 2nd wk of acute infection initiated with 10(3) parasites. However, spleen cell responses in B6 mice sensitized against P-815 were depressed only in those mice infected for 16 to 22 days and were significantly enhanced in mice infected for shorter or longer periods of time. In subsequent experiments, significant cytotoxic activity against P-815 target cells was observed in cells from infected B6 and, to a lesser degree, C3H mice without prior sensitization with the tumor cells. With the use of both P-815 and YAC tumor cell lines in cytotoxicity assays, two phases of apparently nonspecific T. cruzi-induced lytic activity (TILA) were observed after infection: a 1st phase detected within 2 days against YAC target cells, and a subsequent phase detected against both YAC and P-815 target cells at a time dependent upon the number of parasites injected. Other results demonstrated increased cytotoxic activity against P-815 target cells in 2.5-mo-old C3H mice infected with greater numbers of T. cruzi or when older (4.5 to 6.5 mo) mice were infected with 10(3) parasites. Antibodies cross-reactive to tumor cells were not detected in sera from infected mice, suggesting that TILA is an antibody-independent phenomenon. Possible relationships between the phases of TILA and the modification of specific responses generated in infected mice are discussed.
Monoclonal antibodies against a specific surface determinant on malarial (Plasmodium knowlesi) merozoites block erythrocyte invasion.
Authors: Epstein N , Miller L H , Kaushel D C , Udeinya I J , Rener J , Howard R J , Asofsky R , Aikawa M , Hess R L 
Published: December 2022

Abstract
Twelve hybridoma cell lines secreting monoclonal antibodies against Plasmodium knowlesi merozoites have been produced. Antibodies from 3 of the 12 lines agglutinated merozoites. The 2 monoclonal antibodies (13C11 and 16F8) that markedly agglutinated merozoites blocked merozoite invasion of erythrocytes. Of these 2 lines, the one that induced the most agglutination also blocked invasion most effectively. The third monoclonal antibody (53B3) caused minimal agglutination of merozoites and did not block invasion, nor did the other 9 nonagglutinating antibodies. The 2 blocking monoclonal antibodies bound to antigens around the entire surface of merozoites, as demonstrated by immunoelectron microscopy, and precipitated a single biosynthetically labeled protein of apparent m.w. of 250,000. None of the nonagglutinating lines precipitated this protein. Monoclonal antibodies 13C11 and 16F8 reacted with a common antigenic determinant on a Malaysian and a Philippine strain of P. knowlesi in that they blocked invasion and precipitated a 250,000 m.w. protein from both. Sera from immune monkeys also precipitated this 250,000 m.w. protein.
T lymphocyte characteristics in bone marrow-transplanted patients. II. Analysis with monoclonal antibodies.
Authors: de Bruin H G , Astaldi A , Leupers T , van de Griend R J , Dooren L J , Schellekens P T , Tanke H J , Roos M , Vossen J M 
Published: December 2022

Abstract
The relative distribution of T cell subsets, as defined by the monoclonal antibodies OKT, was analyzed in peripheral blood lymphocytes of 8 children after bone marrow transplantation for aplastic anemia. The percentage of peripheral blood lymphocytes binding OKT3 (directed against a common T cell surface antigen and defining most peripheral T cells) reached normal values shortly after transplantation. In 5 patients, lymphocytes binding OKT8 (directed against an antigen present on the suppressor/cytotoxic T cell subset) were found in high proportion, and lymphocytes binding OKT4 (detecting an antigen present on inducer/helper T cells) in low percentage. This resulted in an inverted ratio OKT4/OKT8 compared with that of lymphocytes from normal individuals. In all patients the lymphocytes bound abnormally high amounts of OKT10 (directed against an antigen present on all thymocytes but not on mature peripheral T cells). In the course of time, a trend towards normalization was observed for all parameters investigated; however, the kinetics of the recovery showed a marked heterogeneity. From the analysis of this phenomenon, it is likely that, among other conditions yet unknown, a minimum of 20% of OKT4-positive lymphocytes is required for a normal proliferative response to T cell mitogens in vitro. No other correlation was found between any lymphocyte phenotype, as defined by the OKT antibodies, and proliferative response in vitro. Furthermore, lymphocytes from the patient with chronic graft-vs-host disease (greater than 50% OKT8 positive) failed to suppress the proliferative response to mitogens and antigens of the lymphocytes of the histo-identical bone marrow donor.
Prevention of tolerance induction by simultaneous administration of anti-Lyb3 antiserum with tolerogen.
Authors: Huber B T , Borel Y 
Published: December 2022

Abstract
Lyb3 serves as a triggering receptor on a mature subset of B lymphocytes. To further investigate the nature of the activating signal received by this receptor, we examined its involvement in hapten-specific B cell tolerance induced in vivo with isologous IgG. We obtained the following results: injection of anti-Lyb3 serum simultaneously with low doses of tolerogen prevented tolerance induction in B cells responsive to TD and TI type-1 antigens but failed to influence B cells responding to a TI type-2 antigen. Furthermore, administration of anti-Lyb3 serum did not change the tolerogenic signal to an immunogenic one, allowing B cell maturation into plaque-forming cells. However, it did make the B cell responsive to a subsequent challenge with antigen. This effect is transient, and dependent on the dose of tolerogen. These results are discussed in terms of our knowledge of the mechanism of B cell tolerance.
Stimulation of immunoglobulin biosynthesis in human B cells by wheat germ agglutinin. I. Evidence that WGA can produce both a positive and negative signal for activation of human lymphocytes.
Authors: Greene W C , Goldman C K , Marshall S T , Fleisher T A , Waldmann T A 
Published: December 2022

Abstract
Wheat germ agglutinin (WGA), previously regarded strictly as a nonmitogenic or anti-mitogenic lectin, can under appropriate conditions markedly stimulate in vitro synthesis and secretion of immunoglobulin (Ig) by human B lymphocytes. Stimulation of Ig production by WGA is 1) confined to a narrow lectin dose range (2 to 10 micrograms/ml; 2) abrogated by the simple sugar N-acetyl-D-glucosamine but not by a variety of other monosaccharides; 3) effective only after early additions of WGA within the initial 72 hr of 12-day cultures; 4) detected in the presence of B and T cells but not B cells alone; and 5) polyisotypic in nature, as indicated by augmented synthetic rates of Ig in each of 3 major classes (IgG, IgA, and IgM). With few exceptions, WGA produces equivalent or greater rates of Ig production as obtained in cultures activated with pokeweed mitogen (PWM), a well-recognized T-dependent polyclonal activator of human B cells. Furthermore, periperal blood lymphocytes from select individuals that respond weakly to PWM are markedly stimulated with WGA. In contrast to these stimulatory effects of WGA on Ig production by lymphocytes exposed to low lectin concentrations, addition of WGA in amounts greater than 15 micrograms/ml to PWM-stimulated human lymphocyte cultures produces marked suppression of the expected level of Ig synthesis. These data indicate that varying doses of WGA can produce contrasting stimulatory and inhibitory effects on human B cell metabolism.
The oxidative metabolism of thioglycollate-elicited mouse peritoneal macrophages: the relationship between oxygen, superoxide and hydrogen peroxide and the effect of monolayer formation.
Authors: Cohen M S , Ryan J L , Root R K 
Published: December 2022

Abstract
The oxygen and glucose metabolism of peritoneal macrophages harvested from untreated mice (resident cells) and mice given an i.p. injection of thioglycollate broth (thioglycollate cells) were examined. Thioglycollate cells consumed approximately 3 times as much O2 at rest and during phagocytosis as resident cells, but oxygen reduction products (superoxide and hydrogen peroxide) could be recovered in only minimal amounts despite triggering by phagocytosis or exposure to PMA. Indirect evidence for the formation of oxygen reduction products such as O2- by thioglycollate cells was obtained by observation of the major pathways for glucose oxidation and NBT dye reduction. When thioglycollate cells were allowed to adhere to a glass surface O2- and H2O2 were easily recovered in the extracellular medium with a 20-fold increase above cells in suspension exposed to PMA. This study suggests that thioglycollate-elicited macrophages have a vigorous oxidative metabolism but that recovery, and perhaps utilization, of O2 reduction products formed will depend on the conditions of incubation. These events may be significant both for the study of parameters of macrophage "activation" in vitro as well as the function of these cells in vivo.