bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunologic consequences of vaccination against abortion in mice.
Authors: Chaouat G , Kolb J P , Kiger N , Stanislawski M , Wegmann T G 
Published: December 2022

Abstract
CBA/J female mice have a high rate of fetal resorption when mated with DBA/2J males. This fetal wastage can be dramatically reduced by immunizing the female with BALB/cJ but not DBA/2J spleen cells. We report here that immunization with BALB/cJ (but not DBA/2J) spleen cells leads to 1) anti-paternal MHC antibody that is predominantly of the IgG1 isotype, and which disappears from the serum during pregnancy; 2) increased active suppression in both the spleen and placenta; and 3) an ability to adoptively transfer the fetal protection and placental suppression with serum from the immunized mice. Congenic absorption studies before adoptive transfer indicate that the active component of the serum is also directed against the paternal MHC haplotype. These results indicate that maternal humoral immunity can lead to increased fetal protection in correlation with local active suppression in the placenta. They also suggest an expansion of the placental immunoabsorbent hypothesis to include the induction of active suppression against maternal cell-mediated immunity.
A role for carbohydrate moieties in the immune response to malaria.
Authors: Ramasamy R , Reese R T 
Published: December 2022

Abstract
Treatment of antigen prepared from asexual blood stages of the human malarial parasite Plasmodium falciparum with a mixture of glycosidases resulted in a reduction in the ability of the antigen to bind antibodies from immune human and monkey sera in an ELISA assay. Some of the epitopes in the parasite material were heat stable, protease resistant, and sensitive to glycosidases. Proteins of Mr 110,000 and 65,000 from parasitized RBC were shown to have reduced antigenicity in Western blots after glycosidase treatment. The carbohydrate side chains of parasite glycoproteins therefore make a contribution to the total antigenicity of the parasite.
Glycopeptides in soluble egg antigen of Schistosoma mansoni: isolation, characterization, and elucidation of their immunochemical and immunopathological relation to the major egg glycoprotein (MEG).
Authors: Lustigman S , Mahmoud A A , Hamburger J 
Published: December 2022

Abstract
The major egg glycoprotein (MEG) of Schistosoma mansoni was purified by ion-exchange chromatography of glycoprotein fraction obtained from soluble egg antigen (SEA) by lectin affinity chromatography. Small carbohydrate-rich fragments (CRF) contained in the glycoprotein fraction of SEA were isolated by ultrafiltration followed by dialysis (10 to 13 kd). Comparison of MEG and CRF yielded the following results: purified MEG (70 kd) contains about 77% carbohydrate, and CRF contains 92.5% carbohydrate. When radioiodinated and run by SDS-PAGE, each yielded a single band with respective Rf values of around 0.33 and 1.0 CRF is capable of inhibiting, in a Farr-type RIA, the binding of 125I-MEG to serum from chronically infected mice. Furthermore, CRF and MEG exhibit a single and continuous line of radioimmunodiffusion. CRF, unlike SEA, SEA glycoproteins, or purified MEG, is incapable of eliciting delayed footpad swelling in egg-sensitized mice or of inducing granulomatous hypersensitivity, when given at amounts equivalent to or higher than MEG by protein or carbohydrate content. Thus, whereas SEA, SEA glycoproteins, or MEG elicited in a representative test net swelling of 0.28 mm, 0.34 mm, and 0.29 mm, respectively, CRF gave net swellings of 0.06 mm, similar to the control value (0.07 mm) in unsensitized mice. Also, mice sensitized to viable eggs, SEA, or purified MEG exhibited, after i.v. challenge with viable eggs, a mean area of granulomas in the lungs of 12,389 micron2, 16,412 micron2, and 12,354 micron2, respectively, as compared with 7940 micron2 in CRF-sensitized mice and 8428 micron2 in unsensitized control mice. Thus, CRF appears to contain fragments of MEG that are serologically active but immunopathologically inactive at the concentrations used.
The immunobiology of T cell responses to Mls-locus-disparate stimulator cells. II. Effects of Mls-locus-disparate stimulator cells on cloned, protein antigen-specific, Ia-restricted T cell lines.
Authors: Katz M E , Janeway C A 
Published: December 2022

Abstract
Cloned, protein antigen-specific, Ia-restricted T cell lines frequently (approximately 20%) also respond strongly to stimulator cells from strains expressing stimulatory alleles at the chromosome 1-encoded Mls-locus. Furthermore, such responses are blocked by monoclonal antibodies specific for Ia antigens expressed by the stimulator rather than the responder cells. However, such responses show no specificity for polymorphic determinants on Ia molecules, although in such responses, as in primary and secondary T cell responses to stimulating Mls-locus alleles, I-E molecules appear to play a central role. These results, combined with the unique immunobiology of the primary T cell proliferative response to Mls-locus-disparate stimulator cells, suggest to us that this response involves the interaction of the receptor on T cells for antigen:self Ia with a relatively nonpolymorphic region of Ia glycoproteins. This hypothesis is supported by the observation that a monoclonal antibody to the T cell receptor will inhibit both responses, although the response to Mls-locus-disparate stimulators appears to be more sensitive to these antibodies. We propose that the interaction of the T cell receptor with Ia is stabilized by a cell interaction molecule encoded or regulated by the Mls-locus gene product permitting the T cell receptor:Ia glycoprotein interaction to lead to T cell activation.
Relationships between terminal transferase expression, stem cell colonization, and thymic maturation in the avian embryo: studies in thymic chimeras resulting from homospecific and heterospecific grafts.
Authors: Penit C , Jotereau F , Gelabert M J 
Published: December 2022

Abstract
Terminal deoxynucleotidyl transferase (TdT) can be detected in 11- to 12-day-old embryonic chick thymuses 5 to 6 days after the first influx of lymphoid stem cells into the thymic rudiment. To identify the main factors of TdT induction, grafting experiments were devised in such a way that the age of the grafted thymus and that of the host were different. Uncolonized embryonic chick thymuses were grafted into chick hosts of different ages. Under these conditions, lymphoid differentiation arose from host lymphoid stem cells (LSC) invading the thymic rudiment. TdT immunofluorescent detection in the first wave of thymocytes showed that the percentages of TdT+ cells were related to the total age of the explant and not to the age of the host (11 to 17 days). Similar results were obtained when the chick thymic rudiment was transplanted into quail embryos, showing that quail LSC have TdT inducibility similar to that of chick LSC while developing in a chick thymic environment. Colonized chick thymuses were also grafted into quail embryos to compare the TdT inducibility of the first lymphoid generation (of chick type) and of the second (of quail origin), taking advantage of the different chromatin structure of quail and chick cells. In these experiments, the majority of chick cells remained TdT negative for as long as 10 days, whereas most lymphocytes of the second generation became TdT+ soon after their arrival in the grafted thymus. Therefore, during embryonic life, most TdT+ cells were derived from the second wave of stem cells, but some early stem cells were also able to acquire the enzyme. In a final series of experiments, early thymic rudiments were cultured in vitro with 14- to 16-day-old bone marrow and then grafted into 3-day-old host embryos. Under these conditions, bone marrow LSC contributed to a variable proportion of the first generation of thymocytes. The percentage of TdT+ cells among the progeny of these bone marrow stem cells was found to be two times higher than that of thymocytes derived from host LSC. These results suggest that, in addition to intrathymic environmental factors, the origin of LSC influences the frequency of TdT expression in their progeny.
Thymic epithelium. I. Lymphoid-free organ cultures grafted in syngeneic intact mice.
Authors: Jordan R K , Bentley A L , Perry G A , Crouse D A 
Published: December 2022

Abstract
Low temperature organ culture of 14 day gestational age mouse thymic lobes leads to the development of a lymphoid-free epithelial matrix. Morphologically, these explants exhibit two distinct epithelial components, which may be indicative of the dual embryologic origin (ectodermal/endodermal) of the thymic epithelium. When such explants are grafted into syngeneic intact recipients, the compound matrix is repopulated by lymphohematopoietic precursors that give rise to an intragraft lymphocyte population. The graft shows additional morphologic development parallel to normal thymus ontogeny. Studies in congenic mice when using the TIa alloantigen as a marker of derivation demonstrate the host origin of these lymphocytes. Cytotoxic assays for the presence of cell surface Thy-1.2, TIa, Lyt-1.2, and Lyt-2.2 reveal that graft lymphocytes express a phenotypic profile and developmental progression that is typical of normal thymocytes. Furthermore, mitogen and mixed leukocyte culture assays show that intragraft lymphopoiesis leads to the generation of a mature population. In addition to the lymphocytes, host-derived Ia+ adherent cells can also be isolated from these thymic epithelial grafts. We conclude that low temperature organ culture-derived thymic epithelium appears to retain those properties of the thymic microenvironment that permit lymphohematopoietic colonization and support thymocyte differentiation.
Immunoregulation in the rat: cellular and molecular requirements for B cell responses to types 1, 2, and T-dependent antigens.
Authors: Eldridge J H , Kimura S , Morisaki I , Michalek S M , Hamaoka T , Hamada S , McGhee J R 
Published: December 2022

Abstract
The requirements for primary in vitro plaque-forming cell (PFC) development in cultures of purified rat splenic B cells have been examined. Rat B cells were directly responsive to the type 1 antigen trinitrophenyl-Brucella abortus (TNP-BA), but both T cells and adherent accessory cells were required for B cell responses to the type 2 antigen TNP-Ficoll and the T cell-dependent (TD) antigen sheep erythrocytes (SRBC). However, the cellfree supernatants from concanavalin A-induced spleen cells of rat or mouse origin replaced the requirement for T cells and macrophages, and resulted in PFC development in response to TNP-Ficoll and SRBC and augmented PFC numbers in response to TNP-BA. Culture supernatants from induced murine T cell and macrophage cell lines were used to partially deduce the molecular requirements for the support of PFC development by rat B cells to these three antigens. Supernatants from the EL-4 (EL-4 sup) and B151 K12 (B15 sup) T cell lines augmented TNP-BA responses, suggesting that B cell growth factor II (BCGF-II) mediated this effect. An admixture of purified interleukin 2 (IL 2) and B15 sup supported PFC development to SRBC; indicating that IL 2, BCGF-II, and the T cell-replacing factor in B15 sup (B15-TRF) were sufficient to support this response. In addition, the IL 2 plus B15 sup-supported anti-SRBC PFC response was increased by the addition of an interleukin 1-containing fraction from the supernatant of the macrophage line P388D1. PFC development in response to TNP-Ficoll had the most stringent requirements and only occurred in the presence of EL-4 sup and B15 sup (IL 2, BCGF-I, BCGF-II, EL-TRF, B15-TRF). These data indicate that different cellular and molecular requirements exist for PFC development in response to types 1, 2, and TD antigens by rat B cells.
Presentation of antigen by B cells: functional dependence on radiation dose, interleukins, cellular activation, and differential glycosylation.
Authors: Frohman M , Cowing C 
Published: December 2022

Abstract
Whether resting B cells can present antigen to T cells is controversial. Several factors can influence the outcome of an assessment of the presenting function of resting B cells: the method of purifying resting B cells and maintaining them in culture without altering their resting state, the sensitivity of resting B cells to gamma-irradiation, the activation state of the T cells used to assess presenting function, and the requirement for exogenous interleukin 1. We have examined all of these variables and find that one adherent antigen-presenting cell is functionally equivalent to four LPS-activated B cells and to 1000 resting B cells. In addition, we have examined the potential functional relevance of the differential glycosylation of Ia molecules on resting B cells compared with adherent antigen-presenting cells. Altering the surface glycosylation of resting B cells by neuraminidase treatment results in a 25-fold increase in B cell antigen presentation without altering their resting state. More important, among antigen-presenting cells the effect of neuraminidase is limited to resting B cells. It also appears to involve a restricting element such as the Ia molecule rather than total cell surface charge, because neuraminidase treatment has no effect on the capacity of resting B cells to serve as accessory cells in the Con A response.
Regulation of the growth of Epstein-Barr virus-infected B cells. I. Growth regression by E rosetting cells from VCA-positive donors is a combined effect of autologous mixed leukocyte reaction and activation of T8+ memory cells.
Authors: Konttinen Y T , Bluestein H G , Zvaifler N J 
Published: December 2022

Abstract
Regression of B cell proliferation in co-cultures of EBV-infected B cells (BEBV) and autologous T cells at 1:4 ratio was studied. 3H-TdR incorporation was used to measure proliferation by the participating lymphocyte populations and a 51Cr release assay was used to document the generation of cells capable of killing autologous EBV-transformed B lymphoblastoid cell lines (LCLEBV). EBV-infected B cells cultured alone transformed to blasts by culture day 10, and continued to proliferate throughout the 22 day observation period. When EBV-infected B cells were co-cultured with E rosetted cells from VCA-positive donors, there was a characteristic proliferative response on day 10 (an augmented autologous mixed lymphocyte reaction; AMLR), followed by the development of T8+ cells capable of killing autologous LCLEBV, as well as over 90% suppression of EBV growth by day 22 as assessed by 3H-TdR incorporation, and confirmed in a visual outgrowth assay. Negative and positive selection techniques were used to define the regulatory components in the T cell population. Depletion of T8+ cells from the blood lymphocytes of VCA-positive donors did not significantly reduce the 10 day proliferative response, but the subsequent development of cytotoxic cells and the regression of BEBV outgrowth was not observed. Thus, the circulating T8+ cells are required for the subsequent appearance of autologous LCLEBV cytotoxicity and BEBV growth regulation. However, when the responder population consisted only of T8+ cells, the augmented AMLR response was absent, cytotoxic cell development was weak or absent, and there was no regression of EBV outgrowth. Therefore, the cells participating in the AMLR, as well as T8+ memory cells from VCA-positive donors, are necessary for the control of the in vitro EBV infection. Growth regression is dependent on the proliferation of the regulatory T cells. Mitomycin C treatment of fresh E rosetting cells or those exposed to BEBV for up to 10 days in culture abrogates growth regression and the subsequent appearance of LCLEBV killer cells. However, E rosetting cells exposed to BEBV for 14 days or more already have developed the ability to kill LCLEBV and no longer need to proliferate to induce growth regression when cultured with newly infected BEBV. These results lend additional support to the view that the control of EBV-induced B cell expansion requires a AMLR-dependent clonal amplification of EBV-specific, T8+ cytotoxic cells.
Interleukin 2-induced lymphocyte proliferation is independent of increases in cytosolic-free calcium concentrations.
Authors: Mills G B , Cheung R K , Grinstein S , Gelfand E W 
Published: December 2022

Abstract
Activation of lymphocytes by mitogenic lectins initiates a sequence of events that culminates in DNA synthesis and cell proliferation. The mitogenic effects of lectins on T lymphocytes leads to the production of a group of lymphokines including the interleukins. The binding of interleukin 2 (IL 2) to its receptor results in activation of the cell leading to DNA synthesis. An increase in cytosolic-free Ca++ ([Ca++]i) is associated with activation of lymphocytes by mitogenic lectins and also appears to be a prerequisite for induction of DNA synthesis and cell proliferation. We have determined whether the proliferative response triggered by IL 2 binding to its receptor is associated with or requires an increase in [Ca++]i. Using human and murine IL 2-sensitive cell lines, we have demonstrated that the IL 2-induced proliferative response, in contrast to that induced by mitogens such as phytohemagglutinin or concanavalin A, is not accompanied by an increase in [Ca++]i as monitored by the fluorescent indicator quin-2. Furthermore, IL 2-dependent triggering of lymphoblasts occurs in the presence of extremely low extracellular calcium concentrations that prevent transmembrane calcium flux. Activation of IL 2 receptor-bearing T cells, therefore, does not appear to be associated with or to require an increase in [Ca++]i as part of the activation and signaling process. The critical step requiring calcium flux in cell signaling by mitogenic lectins must therefore occur elsewhere in the activation cascade.
Suppression of Ag-induced release of EP (IL 1) by spleen cells of specifically desensitized donors: evidence for the role of a suppressor cell.
Authors: Atkins E , Francis L 
Published: December 2022

Abstract
Monocytes or macrophages may be induced to produce IL 1 by activators (e.g., lipopolysaccharide endotoxin) that act directly or by antigens/mitogens (e.g., Con A) that stimulate inducer lymphocytes to release a lymphokine that stimulates macrophages. Using guinea pigs (GP) rendered delayed hypersensitive to ovalbumin (OVA), we investigated the role of spleen cells from normal, sensitized, and specifically desensitized GP in suppressing release of IL 1, measured as endogenous pyrogen (EP), from peritoneal exudates of sensitized GP when incubated with OVA in vitro. Co-cultivation of all three sources of spleen cells with GP peritoneal exudate cells and OVA suppressed EP release as measured in the rabbit fever assay, the effect being most marked with cells from desensitized GP, intermediate with cells from sensitized GP, and least with normal cells. This suppressor activity of spleen cells on in vitro EP release was not explained by nonspecific absorption of EP by the added cells and did not affect EP release by a stimulus that activates macrophages directly (heat-killed staphylococci). It required both lymphocytes and macrophages for its effect, but unlike some other suppressor factors, it was not modified by indomethacin, an inhibitor of prostaglandin release. This appears to be the first reported evidence for cell-mediated suppression of lymphokine-mediated release of IL 1, an important modulator of the immune system through its combined role as a lymphocyte-activating factor and an inducer of fever (EP).
Glycolipid antigens of human polymorphonuclear neutrophils and the inducible HL-60 myeloid leukemia line.
Authors: Symington F W , Hedges D L , Hakomori S 
Published: December 2022

Abstract
Glycolipid and cell surface carbohydrate antigens of human polymorphonuclear neutrophils (PMN) and of HL-60 myeloid leukemia cells were analyzed with a panel of defined, monoclonal anti-carbohydrate antibodies. Antigenicities of intact PMN, HL-60, and retinoic acid-induced HL-60 (r.a.-HL-60) were studied by flow cytofluorometry. These three cell populations displayed quantitative differences, some of which were induction dependent, in their expression of lactosyl, N-acetyllactosaminyl, Y-hapten (Fuc alpha 1----2Gal beta 1----4(Fuc alpha 1----3)GlcNAc beta 1----R), and sialosyl-X-hapten (SA alpha 2----3Gal beta 1----4(Fuc alpha 1----3)GlcNAc beta 1----R) specificities. Structures reactive with antibodies specific for long-chain mono-, and di- or tri- alpha 1----3 fucosylated lacto-series glycolipids were also detected. Glycosphingolipids purified from organic extracts of these cells were analyzed to seek information concerning the chemical basis for these surface antigenic differences, to assess the structural and antigenic diversity of PMN and HL-60 glycolipids, and to quantitate chemically and antigenically prominent glycolipids. Binding of monoclonal antibodies to thin-layer chromatograms demonstrated that each of the specificities on intact cells was carried by one or more distinct glycolipids. The abundance of immunoreactive glycolipids in the extracts paralleled the relative staining intensities of the intact cell populations. Several "cryptic" glycolipid antigens, including alpha 2----6 sialosylated structures enriched five- to 10-fold in PMN extracts, were not detected on intact cells. Lactosylceramide accounted for two-thirds of the approximately 1.5 X 10(9) glycolipid molecules contained in each PMN. The remaining glycolipid antigens appeared to include structurally diverse fucolipids, fucogangliosides, and neutral and sialosylated glycolipids with Gal beta 1----4GlcNAc beta 1----R terminal core structure. The abundance, diversity, and induction-dependent expression of these structures suggest that they may participate in PMN maturation and function.
Demonstration of the interaction of native C1 with monomeric immunoglobulins and C1 inhibitor.
Authors: Ziccardi R J 
Published: December 2022

Abstract
The association of native C1 with physiologically relevant proteins was studied by ultracentrifugation. 125I-C1 was centrifuged through numerous sucrose density gradients, each of which contained a different concentration of monomeric (19S) IgM throughout the gradient. The s-rate of C1 (16S) increased with increasing IgM input to a maximum of 32S. In the absence of C1q, the C1r2s2 subunit did not bind to the Ig. In gradients containing physiologic concentrations of IgM (1.3 mg/ml) at 0.14 M ionic strength, the observed s-rate of C1 was 21S. In the presence of 13 mg/ml IgG, C1 sedimented with an s-rate of 19S. Thus, under physiologic conditions, a significant fraction of native C1 is reversibly bound to monomeric Ig. SDS-PAGE analyses show that this interaction does not lead to C1 activation. The interaction of native C1 with C1 inhibitor (C1-In) was studied by ultracentrifugation at physiologic ionic strength. Purified 125I-C1-In alone sedimented with an s-rate of 4S. However in the presence of excess native C1, one-third of the C1-In co-sedimented with C1 at a 16S position. For these studies, 100 microM nitrophenylguanidinobenzoate (NPGB) was present throughout the sucrose density gradient to prevent C1 activation during centrifugation. As the concentration of NPGB was increased, the percent of 125I-C1-In at 16S decreased, indicating that C1-In was binding (reversibly) to the C1 active site region(s), which is at least partially accessible in uncleaved C1. In controls, when NPGB was omitted or activated C1 was used, the s-rate of 125I-C1-In was only 12S due to the release of C1rC1s(C1-In)2 from activated C1. Thus, under physiologic conditions native C1 is reversibly bound to C1-In.