bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation by PGE2 of the production of oxygen intermediates by LPS-activated macrophages.
Authors: Metzger Z , Hoffeld J T , Oppenheim J J 
Published: December 2022

Abstract
The regulation by prostaglandin E2 (PGE2) of production of oxygen radicals by bacterial lipopolysaccharide-(LPS) activated macrophages was studied in vitro. A 48-hr incubation of murine thioglycollate-elicited macrophages with LPS (0.1 micrograms/ml) resulted in an enhanced ability of these cells to produce oxygen radicals when challenged with phorbol myristate acetate (PMA). Macrophages incubated for 48 hr without LPS did not produce measurable amounts of oxygen radicals when exposed to this triggering stimulus. Thus, PMA-triggered production of oxygen radicals was the result of macrophage activation by LPS. The PMA-triggered production of oxygen radicals by the LPS-activated macrophages was inhibited when PGE2 (10(-5) to 10(-9) M) was present during the incubation with LPS. Inhibition by PGE2 occurred during the early stages of macrophage activation, since the addition of PGE2 24 hr after LPS no longer inhibited the production of oxygen radicals by the macrophages. This inhibitory effect of PGE2 on the LPS-induced activation of macrophages could be reproduced by cyclic-adenosine-monophosphate (cAMP) agonists, such as isoproterenol and cholera toxin as well as by the cAMP analog dibutyryl-cAMP, suggesting a cAMP-mediated mechanism for the inhibitory effect of PGE2 on macrophage activation by LPS. Previous reports have implicated prostaglandins as mediators of destructive processes associated with chronic inflammation. Our findings suggest that PGE2 may, on the other hand, reduce tissue damage in a chronic inflammatory site by inhibiting the production of oxygen radicals by macrophages activated in the sera.
Adherent spleen cells from mice acutely infected with cytomegalovirus suppress the primary antibody response in vitro.
Authors: Bixler G S , Booss J 
Published: December 2022

Abstract
In the present study, we have demonstrated that the hemolytic plaque response of spleen cells from mice acutely infected with murine cytomegalovirus (MCMV) is suppressed in vitro. Mishell-Dutton cultures established with spleen cells from C57BL/6 mice infected 4 days earlier with 4.2 X 10(3) plaque-forming units of MCMV were found to produce significantly fewer direct plaques upon stimulation with sheep red blood cells than corresponding control cultures. Suppression could not be attributed to a generalized lytic destruction of spleen cells, nor was it produced by addition of virus directly to uninfected spleen cell cultures. However, in cultures containing various mixtures of cells from control and infected mice, the direct plaque response was markedly below the predicted response, suggesting that the uninfected cells were actively suppressed by cells from infected mice. Suppression was dependent on the presence of intact spleen cells, since it was not found in the presence of lysed cells. The capacity of spleen cells from infected mice to mediate suppression was demonstrated in the plastic-adherent subpopulation. Treatment of these cells with anti-thymocyte serum (ATS) and complement did not abolish the capacity to suppress the immune response. Thus, adherent ATS-resistant cells from the spleens of mice acutely infected with MCMV, rather than virus alone, have the capacity to actively suppress the hemolytic plaque response in vitro.
IgE responses in human filariasis. I. Quantitation of filaria-specific IgE.
Authors: Hussain R , Hamilton R G , Kumaraswami V , Adkinson N F , Ottesen E A 
Published: December 2022

Abstract
We have developed a noncompetitive solid phase radioimmunoassay to quantitate human IgE antibodies against soluble adult antigens of Brugia malayi (B.m.), a filarial parasite, in sera of patients with various forms of clinical filariasis in Madras, India. A single reference serum was shown to contain 23 micrograms/ml of B.m.-specific IgE by depletion analysis and was used as a standard serum throughout the study. The levels of specific IgE ranged in the patients sera from 2 to 23,000 ng/ml. When these individuals were divided into clinical groups, the individuals with tropical pulmonary eosinophilia had the highest levels (mean = 8630 ng/ml) and were significantly higher than all the other groups (p less than 0.001). The lowest levels were seen in patients with circulating microfilariae (mean = 30.5 ng/ml). Patients exhibiting lymphatic obstruction (i.e., chronic pathology group) had levels slightly higher than microfilaremics (mean = 68 ng/ml) but were not significantly different (p less than 0.1). Surprisingly, individuals living in endemic areas but who had no clinical signs of filariasis also showed appreciable levels of B.m.-specific IgE (mean = 55 ng/ml). The B.m.-specific IgE represented 0.1 to 48% of the total IgE. High percentages of specific IgE may be responsible for evoking allergic symptomatology in patients with tropical pulmonary eosinophilia.
A mitogenic lactose-binding lectin from the sponge Geodia cydonium.
Authors: Bretting H , Phillips S G , Klumpart H J , Kabat E A 
Published: December 2022

Abstract
Two lectins with affinity for hog A + H blood group substance were extracted from the Mediterranean sponge Geodia cydonium. One, termed Geodia lectin I, was purified to near homogeneity by lactose elution from a column of hog A + H coupled to Sepharose 4B. Geodia lectin I was a glycoprotein (carbohydrate content about 14%) with m.w. of about 60,000 and an isoelectric point of pH 4.4. Subunits of about 15,000 daltons were linked by disulfide bonds. The lectin precipitated with various snail galactans composed entirely of DGal and LGal, to a slight degree with guaran, which has DGal alpha 1 leads to 6 in a terminal nonreducing position, and with blood group substances. Of 42 sugars tested, only lactose, dGal beta 1 leads to 4 DGlcNAc, DGal beta 1 leads to 3DGlcNAc, DGalNAc, inhibited precipitation. In view of the relatively high concentration of those disaccharides that inhibited relative to other lectins, the specificity of interaction is thought to be via beta-linked DGal residues that are part of a more complex combining site. Geodia lectin I was mitogenic for human peripheral blood lymphocytes with an optimal concentration of about 5.6 micrograms/ml if serum was omitted for the first 24 hr of culture to allow "triggering." Fetal calf serum apparently contained a high concentration of substances that inhibited mitogenicity and hemagglutination by Geodia lectin I, presumably by specifically interacting with the binding site.
Identification of a macrophage antigen-processing event required for I-region-restricted antigen presentation to T lymphocytes.
Authors: Ziegler K , Unanue E R 
Published: December 2022

Abstract
The mechanism of macrophage-antigen handling was studied using a system that involves the quantitation of the antigen-specific binding of Listeria monocytogenes-immune T cells to macrophages. Specific T cells did not bind to native antigen. Because the specific binding of T cells to macrophages could be measured during a short (5- to 15-min) interaction, it was possible to follow the temporal development of a T cell-binding substrate with increasing time of antigen-macrophage interaction. In contrast to the rapid (5-min) uptake of Listeria by macrophages, the development of T cell-binding ability required a 30- and 60-min period of antigen-macrophage interaction. During this processing period, Listeria organisms bound to the macrophage surface were ingested and partially catabolized. Unlike antigen uptake, antigen processing was a temperature-dependent and energy-requiring event. Although macrophages treated with paraformaldehyde before antigen processing did not develop T cell-binding activity, macrophages treated with paraformaldehyde after a 60-min antigen-processing period retained T cell-binding ability. The kinetics of antigen catabolism correlated with antigen processing, and inhibition of antigen catabolism was associated with a corresponding inhibition of antigen processing for T cell binding. Anti-Ia antibodies had no effect on Listeria uptake of catabolism. These results supply direct evidence for a macrophage-antigen processing event relevant to T cell recognition of antigen.
Immunosuppression in murine malaria: a soluble immunosuppressive factor derived from Plasmodium berghei-infected blood.
Authors: Khansari N , Segre M , Segre D 
Published: December 2022

Abstract
Mice infected with Plasmodium berghei have a depressed immune response to a variety of antigens. We report the extraction, purification, and characterization of a soluble immunosuppressive substance derived from P. berghei-infected mouse blood. A crude extract, prepared by solubilization of infected erythrocytes in a Parr cell disruption bomb, reduced the anti-DNP PFC response of mice injected with the extract 1 day before immunization. Purification of the immunosuppressant was accomplished by precipitation with 50% saturated ammonium sulfate followed by chromatography on Sephadex G-150 in the presence of 6 M guanidine hydrochloride. The immunosuppressive activity was recovered in the last fraction eluted from the Sephadex G-150 column that contained low m.w. components. The activity was abrogated by trypsin digestion, but not by periodate oxidation. Volume for volume, the purified immunosuppressant had a 100-fold greater activity than the crude extract from which it was derived. It suppressed the response to the T-dependent antigens DNP-KLH and SRBC, but not to the T-independent antigen DNP-Ficoll.
The human autologous mixed lymphocyte reaction. I. Suppression by macrophages and T cells.
Authors: Smolen J S , Sharrow S O , Reeves J P , Boegel W A , Steinberg A D 
Published: December 2022

Abstract
The autologous mixed lymphocyte reaction (AMLR) is a proliferative response of T cells to signals from autologous non-T cells. The AMLR has been an enigma to immunologists because spontaneous proliferation of cells removed from the body is usually substantially less than that observed with a strong AMLR. However, the AMLR is thought to represent an important in vitro function, since it has the attributes of other immune responses, and it is abnormal in a variety of disease states thought to have an immune basis. We reasoned that if the AMLR represented a fundamental immune phenomenon, it should be subject to regulation. In the present study, we present evidence for suppression of the AMLR by macrophages and by T cells. Macrophages inhibited the T cell proliferation to (B + null) cells in a dose-dependent fashion and throughout the time course of the AMLR. Elimination of suppressor T cells by a specific antiserum led to an increase in the AMLR, which was again suppressed in a dose-dependent way by addition of the suppressive T cells. It may be concluded that the AMLR itself is subject to immune regulation and that the suppressive influences observed probably strongly inhibit the AMLR in vivo. Removal of the suppressive principles allows the maximal expression of the AMLR in vitro. We believe that our demonstration of regulation of the AMLR should remove the enigma associated with it and lead to a better understanding of normal cell-cell interactions as well as the basis for abnormalities in a variety of immune-mediated diseases.
Cross-induction of predominant NPb idiotypic antibodies with derivatives of (4-hydroxy-3-nitrophenyl) acetyl.
Authors: Ju S T , Dorf M E 
Published: December 2022

Abstract
Immunization of C57BL/6 mice with bovine gamma-globulin (BGG) conjugated with (4-hydroxy-3-nitrophenyl) acetyl (NP) induced a population of anti-NP antibodies that bear predominantly lambda light chain, exhibit heteroclitic affinity for heterologous NP derivatives, and share NPb idiotype. The present study analyzes the idiotypes of antibodies induced with BGG conjugated with the iodo-, bromo-, or nitro-NP derivatives (NIP, NBrP, and NNP). NIP-BGG, NBrP-BGG, and NNP-BGG, induce specific antibodies bearing NPb idiotype in C57BL/6 or C57BL/10 congenic mice, but not in many other inbred strains. Furthermore, the quantity of NPb idiotype in immune sera from various mouse strains immunized with NIP-BGG, NBrP-BGG, and NNP-BGG was similar to that in sera from mice immunized with NP-BGG. Anti-idiotypic antisera against C57BL anti-NP, anti-NIP, or anti-NBrP antibodies exhibit extensive idiotype binding of specifically purified B6 anti-NP, -NIP, -NBrP, and -NNP antibodies. These purified antibodies contain a high percentage (greater than 70%) of lambda-chain-bearing molecules. The data indicate that an extensively shared repertoire composed of predominantly lambda-bearing NPb-positive idiotypic antibodies is used in response to NP and its derivatives in C57BL mice.
Positive correlation between degree of parasitemia, interferon titers, and natural killer cell activity in Plasmodium falciparum-infected children.
Authors: Ojo-Amaize E A , Salimonu L S , Williams A I , Akinwolere O A , Shabo R , Alm G V , Wigzell H 
Published: December 2022

Abstract
Natural killer (NK) cell activity and interferon levels have been measured in the peripheral blood of children acutely ill with Plasmodium falciparum infection. The NK cell levels were found to be raised in the malaria-infected children, with a positive correlation between the degree of parasitemia and lytic activity. Comparatively high titers of antiviral activity was discovered in sera from the majority of P. falciparum-infected children, again positively correlating with the degree of parasitemia and NK levels. The characteristics of the antiviral factor indicated alpha-type interferon to be the dominating agent involved. Addition of exogenous interferon in vitro potentiated the NK levels of PBL from normal children while having no significant impact on cells from malaria-infected children.
Generation of alloreactive cytotoxic T lymphocytes: production of T cell and macrophage helper factors in addition to IL 1 and IL 2 by peritoneal cells from mice immunized to Listeria monocytogenes.
Authors: Finke J H , Sharma S D , Scott J W 
Published: December 2022

Abstract
We investigate the production and biological activity of soluble helper factors produced by peritoneal T cells and macrophage derived from mice primed in vivo with Listeria monocytogenes. Supernatant fluids from co-cultures of these immune T cells and activated macrophages contained Interleukin 1 (IL 1) and Interleukin 2 (IL 2), and had the ability to assist the generation of cytotoxic T lymphocytes (CTL) from a population of nylon wool nonadherent spleen cells sensitized to allogeneic heat-treated thymocytes. The ability to assist CTL development involved T cell and macrophage factors in addition to IL 1 and IL 2. Immune T cells cultured alone produced a factor, devoid of significant IL 2 activity, that assisted CTL development only if adherent cells were present in the responding population. Activated macrophage produced a 38,000 dalton component, distinct from IL 1 on the basis of m.w., that assisted the development of CTL from nylon wool nonadherent splenic cells. Supernatants fluids from co-cultures of immune T cells and allogeneic, nonactivated macrophage contained a CTL helper factor but did not contain IL 1 or IL 2 activities. In contrast, supernatant fluids from co-cultures of immune T cells and syngeneic, nonactivated macrophage contained all 3 activities. This suggests a genetic restriction for the production of IL 1 and IL 2 that does not restrict the production of a CTL helper factor. These results demonstrate that T cell- and macrophage-derived helper factors distinct from IL 1 and IL 2 participate in the development of CTL.
Antigen-specific human T lymphocyte clones: induction, antigen specificity, and MHC restriction of influenza virus-immune clones.
Authors: Lamb J R , Eckels D D , Lake P , Johnson A H , Hartzman R J , Woody J N 
Published: December 2022

Abstract
Human peripheral blood lymphocytes from an HLA-Dw1,3 individual were primed in vitro with influenza A virus (A/Texas/1-77/x-49) and subsequently cloned by limiting dilution in TCGF. Of the 96 TLCs originally obtained, nine were characterized in detail. TLCs were antigen specific, responding to influenza A virus, not to influenza B, TGAL, GAT, tetanus toxoid, or KLH, and only when antigen was presented by cells unable to form rosettes with AET-treated SRBC. Presentation of antigen by unseparated PBL often resulted in significant "back stimulation," probably via production of growth factors. The MHC requirements for the induction of TLC proliferation were analyzed. Of four representative clones analyzed, three required Dw1;DR1 compatibility for successful presentation of viral antigens by a panel of antigen-presenting cells. In contrast, one TLC showed an unusual pattern of response that could not be correlated to a particular HLA haplotype. Monoclonal anti-T cell antibody analysis of the surface phenotype of two TLCs maintained in continuous culture for 5 mo indicated that they were OKT3+, 4+, and 8-, consistent with an inducer/helper phenotype. To confirm the clonal nature of TLCs, data on the functional properties of TLC subclones are also presented.
Cellular origin and interactions involved in gamma-interferon production induced by OKt3 monoclonal antibody.
Authors: Chang T W , Testa D , Kung P C , Perry L , Dreskin H J , Goldstein G 
Published: December 2022

Abstract
OKT3 monoclonal antibody, a human T cell mitogen, induced interferon production by cultured mononuclear cells at 10(-11) M concentrations. Interferon was secreted only under conditions wherein OKT3 was mitogenic, and production was correlated with cell proliferation. Thus, like mitogenesis, interferon secretion reached a peak 3 days after OKT3 stimulation, was inhibited by a factor(s) in human serum, and required 1000 times higher concentrations of Fab and F(ab')2 fragments of OKT3 for induction. The interferon was most likely of "gamma" (immune) type, because pH 2 and 56 degrees C treatments denatured it, whereas anti-alpha or -beta interferon antibodies did not. Mononuclear cells were fractionated into subpopulations that contained OKT4+ cells (helper/inducer T cells), OKT8+ cells (cytotoxic/suppressor T cells), and OKM1+ cells (monocytes) by combining sheep red blood cell rosetting and complement-mediated lysis using monoclonal antibodies against specific cell types. Both OKT4+ and OKT8+ cells proliferated upon OKT3 stimulation with the absolute requirement of OKM1+ cells. However, OKT4+ cells plus OKM1+ cells were necessary for the secretion of interferon. Studies with selective pretreatments with mitomycin C suggested that gamma-interferon was secreted by the OKT4+ cells and that the OKM1+ population subserved an accessory function.
Activation of rat B lymphocytes. II. Functional and structural changes in "aged" rat B lymphocytes.
Authors: Rosenberg J S , Gilman S C , Feldman J D 
Published: December 2022

Abstract
Anti-mu, anti-gamma, and anti-delta antibodies induce proliferation of splenic B lymphocytes from young Lewis rats, measured by 3H-TdR uptake. In contrast, splenic B cells of aged Lewis rats respond poorly or not at all to these reagents. T lymphocytes or interleukin 2 (IL-2) of young or aged rats augment the uptake of 3H-TdR in cultures of "young" B cells responding to anti-Ig reagents or LPS and DxS, but have no significant effect on the responses of "old" B cells. Analysis of spleen cells of young and aged rats in a fluorescence-activated cell sorter indicates the density of mu, gamma, and delta isotypes is reduced in "old" B cells, and that B cells of aged rats are significantly larger than those of young rats. These results delineate anatomic and structural changes in B lymphocytes of aged rats.
B lymphoblast antigen (BB-1) expressed on Epstein-Barr virus-activated B cell blasts, B lymphoblastoid cell lines, and Burkitt's lymphomas.
Authors: Yokochi T , Holly R D , Clark E A 
Published: December 2022

Abstract
Two new cell surface antigens expressed on B lymphoblastoid cell lines (B-LCL) were defined with cytotoxic mouse monoclonal antibodies. One marker, BB-1 (for B lymphoblast antigen-1), was detected on human and nonhuman primate B-LCL, Epstein-Barr virus (EBV)-activated B cell blasts, most Burkitt's lymphomas, and Ia+ B lymphoblast-like myelomas. Polyclonal B cell activators such as pokeweed mitogen (PWM) and lipopolysaccharide (LPS) also induced the expression of BB-1 on immunoglobulin (Ig)-positive cells. In contrast, BB-1 could not be detected on normal lymphoid tissues by complement-dependent cytotoxicity and immunofluorescence (IF) assays or by analysis with a fluorescence-activated cell sorter (FACS). T cell blasts, T cell leukemias, and pre-B cell or erythroblastic leukemia cell lines were also BB-1 negative. Of particular interest was the finding that BB-1 was expressed on the Jijoye lymphoma but only marginally on a subline of Jijoye, P3HR-1, that lacks receptors for EBV and produces a defective virus incapable of transforming lymphocytes. A second lymphoblast antigen (LB-1) unlike BB-1, was present on both T and B cell blasts and virus-transformed T- and B-LCL but not on normal lymphoid tissues.
Suppression of transferred BXSB male SLE disease by female spleen cells.
Authors: Hang L , Izui S , Theofilopoulos A N , Dixon F J 
Published: December 2022

Abstract
The severe autoimmune disease from which BXSB males die at an early age (young) can be transferred into lethally irradiated female recipients by inoculating them with male spleen or bone marrow cells; similar recipients of female spleen or bone marrow cells develop the late-life disease typical of BXSB females. Using this syngeneic cell transfer model, we investigated the possible ability of female splenic and bone marrow cells to modulate the transferred male disease. We found that female spleen cells or the T-enriched subpopulation of such cells successfully retarded the transferred male disease, as observed by the decreased and delayed glomerulonephritis-associated mortality and lowered levels of serum IgG, autoantibodies, and immune complexes. Transfers of female bone marrow or thymus or female splenic T-depleted subpopulations were incapable of suppressing the accelerated male disease. These results indicate that abnormalities of the male spleen or bone marrow inocula responsible for the transferred early autoimmune disease can be modified by female spleen cells, in particular the female T cell component.
Genetic and regulatory contributions of the major histocompatibility complex to the developing cytolytic T lymphocyte repertoire.
Authors: Sherman L A 
Published: December 2022

Abstract
The specificity repertoire of H-2Kb-specific CTL derived from 10- to 14-day-old neonates was examined. Analogous to the adult repertoire, the neonatal repertoire is composed of a large number of receptor specificities, each of which is represented at a low frequency, as well as a small number of highly recurrent specificities, which thereby serve as repertoire markers. The expression of most specificities appears to be independently regulated during development, resulting in the expression of a different set of recurrent specificities for neonates and adults within the same strain. The neonatal and adult repertoires were also compared with respect to the influence of the MHC on repertoire. Unlike adults, neonates of MHC different congenic strains (B10.D2 and B10.BR) have in common approximately half their recurrent specificities. Additionally, most parental specificities are expressed codominantly in neonatal F1 hybrids. These results may be interpreted as indicating either that 1) some, but not all, receptor genes demonstrate MHC-linked polymorphism and both parental alleles are expressed in F1 neonates, or 2) T receptor genes are nonpolymorphic in MHC congenic strains and the observed MHC-related repertoire differences are attributable to a positive selection mechanism. Since adults of these same strains do not display significant repertoire similarity, it is suggested that this increased repertoire divergence may be the result of encounters with environmental antigens in association with self-MHC antigens.