bluuebunny/crossref_metadata_2025_split huggingface dataset:
Adjuvant effects of nonionic block polymer surfactants on liposome-induced humoral immune response.
Authors: Zigterman G J , Snippe H , Jansze M , Willers J M 
Published: December 2022

Abstract
The ability of several surface-active agents to stimulate the humoral immune response in mice against haptenated liposomes was tested. The surfactants were block copolymers of hydrophilic polyoxyethylene (POE) and hydrophobic polyoxypropylene (POP) that differed in m.w., percentage of POE, and mode of linkage of POP to POE. The liposomes were haptenated with tripeptide-enlarged dinitrophenyl coupled to phosphatidylethanolamine, which was incorporated into the liposomal membrane. Additional injection of mice with surfactant stimulated serum hemagglutination titers and splenic plaque-forming cell (PFC) numbers to varying extents. Block polymers with POP chains flanking a POE center, as well as polymers with POE chains flanking a POP center, displayed high adjuvant activity. These block polymers stimulated the antibody response in a dose-dependent manner. They stimulated the antibody response with both high and low antigen doses. Furthermore, the addition of one of these adjuvants (25R1) reduced the amount of carrier lipid required in the liposome in order to obtain an optimal antibody response. The surfactants, which displayed high adjuvant activity, did not interfere with liposome stability as measured with a liposome lysis assay. Moreover, in vitro preincubation of liposomes with a block polymer did not affect their immunogenicity. Optimal adjuvant activity was observed when both adjuvant and liposomes were administered by the same route. Simultaneous injection of both components, however, is not a prerequisite. Conclusively, it can be stated that nonionic block polymer surfactants are potent adjuvants for stimulation of the antibody response against haptenated liposomes.
Retention of T cell reactivity to mitogens and alloantigens by Peyer's patch cells of aged mice.
Authors: Ernst D N , Weigle W O , Thoman M L 
Published: December 2022

Abstract
Immune function generally declines with advancing age. However, recent evidence suggests that this decline may differentially affect the lymphoid compartments comprising the immune system. The effect of age on the T cell-mediated competency of cells from two different lymphoid compartments, Peyer's patch (PP) and spleen, was studied. PP cells of aged C57BL/6 mice retained a greater capacity to proliferate in response to concanavalin A, phytohemagglutinin, and alloantigen and to generate alloimmune cytotoxic cells than did splenocytes of aged mice when compared with their young counterparts. These results could not be explained by significant shifts in the response kinetics or in the proportions of T cells in individual tissues. These results support the concept that lymphoid compartments are not equally sensitive to the deleterious effects of the aging process.
The kinetics of emergence and loss of mediator T lymphocytes acquired in response to infection with Mycobacterium tuberculosis.
Authors: Orme I M 
Published: December 2022

Abstract
Mice infected i.v. with the virulent Erdman strain of Mycobacterium tuberculosis exhibited three distinct phases of infection within the spleen. These consisted of a primary phase, characterized by the progressive growth of the organism; a secondary phase, in which the viable organism was progressively eliminated; and a tertiary phase, characterized by a chronic or slowly recrudescing disease state. Passive transfer experiments, in which T cell-enriched spleen cells from immune donors were infused into T cell-deficient recipients and were measured for their capacity to adoptively protect these mice from challenge with M. tuberculosis, provided evidence that at least three separate populations of protective T cells were acquired in response to the infection within the time frame of the experiments. These populations of T cells could be distinguished in that they differed in their expression of the L3T4 and Lyt-2 cell surface molecules, in terms of their kinetic profiles of emergence and loss, and (c) in terms of their susceptibility to cyclophosphamide. The results may suggest that different populations of protective T cells can be generated at different times during the infection as various classes of antigens (for example, metabolic or structural antigens) become available for presentation by host macrophages. It is hypothesized, furthermore, that the kinetics of emergence and loss of these various populations may reflect switching in the mode of immunity being expressed, particularly during the chronic phase of the infection, from that of a state of active immunity to one of immunologic memory.
Human T clones reactive to the sexual stages of Plasmodium falciparum malaria. High frequency of gamete-reactive T cells in peripheral blood from nonexposed donors.
Authors: Good M F , Quakyi I A , Saul A , Berzofsky J A , Carter R , Miller L H 
Published: December 2022

Abstract
Malarial gametocytes, which are taken up by mosquitoes during a blood meal, develop in the gut of the mosquito into gametes. Gametes and gametocytes contain the target antigens of transmission-blocking immunity. Here, we show that the peripheral blood of nonexposed donors contains Plasmodium falciparum gamete-reactive T cells at frequencies ranging from 1/300 to 1/4000. Studies on long-term clones demonstrated that these cells often recognized antigens shared between gametes and asexual stage parasites or even between heterologous gametes, although it has been possible to derive a P. falciparum gamete-specific T clone. The T clones examined were T3+, T4+, T8-, and either HLA-DR- or HLA-DQ-restricted. They responded to gametes by both proliferation and the secretion of gamma-interferon. The gamete-specific clone and other asexual cross-reactive clones examined could be stimulated in vitro by a preparation of mature gametocytes within RBC, but not by RBC alone, suggesting that gametocytes are immunogenic or can become immunogenic for T cells in vivo. The significance of these observations to mosquito transmission of malaria and development and application of a gamete vaccine are discussed.
Protective immunity to progressive tumors can be induced by antigen presented on regressor tumors.
Authors: Flood P M , Schreiber H , Ron Y 
Published: December 2022

Abstract
Immunization of animals with 1591-RE tumor cells, a highly immunogenic UV-induced epithelia cell tumor from C3H/HeN mice, that were haptenated with trinitrophenol (TNP) leads to protective immunity against a challenge of TNP-haptenated 3152-PRO tumor cells, a progressive highly malignant. MCA-induced fibrosarcoma from syngeneic mice. Animals that rejected TNP-1591-RE and subsequently TNP-3152-PRO tumor cells showed increased tumor-specific resistance to another challenge of 3152-PRO tumor cells, even when these fibrosarcoma cells had not been haptenated with TNP. Induction of protection required the presence of TNP-hapten groups on both 1591-RE and 3152-PRO during the initial immunization, and could be induced by immunization with other haptenated syngeneic highly immunogenic regressor tumor lines. In addition, TNP-haptenated progressor variants of the 1591-RE were ineffective in generating protection, suggesting that the immunogenicity of the haptenated tumor used for the initial immunization was a determining factor in whether or not protective immunity against the highly malignant tumor was later generated. Protection required at least two T cell types: a Lyt-1-2+ T cells, and a Lyt-1+2- T cell that also expressed I-J determinants and was Vicia villosa lectin adherent, suggesting it was not a classical helper T cell. These results suggest that presentation of a hapten by highly immunogenic tumor cells can lead to enhanced protective immunity to poorly immunogenic noncross-reactive tumors that co-express the same hapten, and rejection of these haptenated poorly immunogenic tumors leads to enhanced protection against a subsequent challenge of the same, but not noncross-reactive progressor tumors.
Defective lymphopoiesis in the bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mutant mice. II. Description of a microenvironmental defect for the generation of terminal deoxynucleotidyltransferase-positive bone marrow cells in vitro.
Authors: Medlock E S , Goldschneider I , Greiner D L , Shultz L 
Published: December 2022

Abstract
We have presented evidence in a previous paper that the development of prothymocytes, pre-B cells, and TdT+ lymphoid precursor cells in the bone marrow of motheaten (me/me) and viable motheaten (mev/mev) mice is defective. In the present study, we have used a selective culture system that supports the generation of rat- and mouse-origin TdT+ bone marrow lymphoid cells in vitro to further investigate the early stages of lymphopoiesis in me/me and mev/mev mice. The results demonstrate that bone marrow stromal cell feeder layers derived from me/me and mev/mev mice do not support the growth of rat TdT+ cells in vitro, whereas stromal cell feeder layers from heterozygous (+/-) littermates and wild type (+/+) control mice do. Moreover, composite feeder layers formed by mixing as few as one part me/me and mev/mev bone marrow cells with 7 to 9 parts +/- littermate bone marrow cells also fail to effectively support the generation of TdT+ cells in vitro. In contrast to me/me and mev/mev mice, other mutant mouse models of autoimmune (NZB, NZB/W), immunodeficient (nu/nu), and hemopoietic (W/Wv, Sl/Sld) disorders form feeder layers that support normal to elevated levels of TdT+ cell growth in vitro. Thus, to date, only the me/me and mev/mev mutant mice have been found to lack the appropriate microenvironment for the generation of TdT+ bone marrow cells. Histologic analysis of the stromal cell feeder layers that are formed in our culture system shows that multilayered cellular patches, which normally are the most active sites of TdT+ cell development in vitro, are absent in feeder layers of me/me and mev/mev cells. Moreover, feeder layers from mev/mev mice contain a population of MAC 1+, basophilic, nonvacuolated, macrophage-like cells; whereas feeder layers from control mice contain MAC 1+, eosinophilic, vacuolated macrophage-like cells. Stromal cell feeder layers formed by mixtures of me/me or mev/mev and control mouse bone marrow cells contain numerous multilayered cellular patches and vacuolated mononuclear cells, but also contain large numbers of basophilic mononuclear cells. These composite feeder layers have a disproportionately reduced capacity to support the generation of TdT+ cells in vitro. Although the stromal microenvironment of me/me and mev/mev bone marrow does not support the growth of TdT+ cells in vivo or in vitro, the bone marrow from these mutant mice contains detectable numbers of pre-TdT+ cells. Thus, when cultured on normal mouse feeder layers, mutant mouse bone marrow rapidly generates TdT+ cells in vitro, albeit at significantly reduced levels as compared to +/- littermate controls.(ABSTRACT TRUNCATED AT 400 WORDS)
Precursor phenotype of lymphokine-activated killer cells in the mouse.
Authors: Salup R R , Mathieson B J , Wiltrout R H 
Published: December 2022

Abstract
Lymphokine-activated killer (LAK) activity has been proposed to functionally differ from natural killer (NK) activity largely on the basis of a broader target cell spectrum and different kinetics of response to interleukin 2 (IL 2). Similarly, it has been proposed that the precursor cells for LAK activity are phenotypically distinct from NK cells. In most precursor studies, phenotype comparisons have been made between fresh NK cells and LAK cells which have been generated by 3 to 5 days of culture in IL 2. In the present study, we utilized positive selection with monoclonal antibodies to characterize the surface phenotype of precursor cells which give rise to rIL 2-augmented NK activity within 24 hr and to classically generated LAK activity which appears after 3 to 5 days of culture in rIL 2. The results demonstrated that highly purified (93 to 95%) Lyt-2+ or L3T4+ T lymphocytes were unable to generate appreciable amounts of either augmented NK activity or LAK activity when cultured with rIL 2, whereas the highly purified (98%) Lyt-2-, L3T4-, asialo GM1+ lymphocyte subset gave rise to both augmented NK and LAK activities. These findings demonstrate that both augmented NK and LAK activities can arise from precursors expressing the same phenotype. Overall, the results suggest that NK cells in mouse spleen constitute a major precursor component for the generation of LAK activity from that organ.
Requirements for triggering of lysis by cytolytic T lymphocyte clones.
Authors: Lancki D W , Weiss A , Fitch F W 
Published: December 2022

Abstract
Cloned murine cytolytic T lymphocytes (CTL) having defined specificity were triggered by the phorbol ester together with a calcium ionophore (either A23187 or Ionomycin) to lyse syngeneic or third party target cells efficiently. Neither phorbol 12-myristate 13-acetate (PMA) nor calcium ionophore alone induced efficient lysis. The characteristics of the lytic process induced by these signals are similar to those of antigen-specific or lectin-facilitated lysis by CTL. Lysis is calcium and temperature dependent and shows kinetics which are not grossly different from lysis mediated via the antigen receptor. Two helper T lymphocyte clones were not induced to lyse efficiently EL-4 target cells by concanavalin A or PMA + ionophore. Triggering of lysis induced with PMA plus ionophore by the CTL clone L3 differed from antigen-mediated lysis in specificity and in the susceptibility to inhibition by cytochalasin B. Properties of the target cell determine which cell surface associative recognition structures are important in the efficient lysis of these cells. Anti-LFA-1 monoclonal antibodies inhibited efficiently both antigen-mediated and PMA + ionophore-induced lysis of P-815 or EL-4 target cells which are of hematopoietic origin. However, anti-LFA-1 antibodies do not inhibit antigen-mediated, lectin-facilitated, or PMA + Ionomycin-induced CTL cytolysis of target cells derived from the L cell fibroblast line. We conclude that two intracellular signals, which can be provided by the combination of PMA + ionophore, are required for efficient lysis by antigen-specific murine CTL clones. When the T cell receptor for antigen is bypassed using PMA + ionophore to trigger lysis, we show that Lyt-2 and LFA-1 molecules may be required for efficient lysis. These associative recognition structures appear to play an important role in postactivation steps leading to efficient delivery of the lethal hit to the target cell.
Immunoregulation by antigen/antibody complexes. I. Specific immunosuppression induced in vivo with immune complexes formed in antibody excess.
Authors: Caulfield M J , Shaffer D 
Published: December 2022

Abstract
Specific immune complexes, prepared at different ratios of antibody to antigen, were examined for their effects on the antibody response of BALB/c mice to the cell wall polysaccharide antigen (PnC) extracted from Streptococcus pneumonia R36a. Mice immunized with complexes formed in antigen excess developed a PnC-specific antibody response that was equivalent to that in mice injected with free antigen. On the other hand, mice injected with complexes formed in antibody excess developed very little PnC-specific antibody. Furthermore, administration of immune complexes (formed in antibody excess) resulted in suppression of the response to an immunogenic dose of PnC given concurrently or 1 day after injection of immune complexes but not when the antigen was given 1 day before injection of the immune complexes. Injections of free antibody (TEPC-15) also resulted in suppression of the response to antigenic challenge; however, suppression was greatest when the antibody was injected concurrently with the antigen, suggesting that the suppression was mediated through the formation of immune complexes in vivo. The suppression appears to be specific for the antigen (PnC), since in mice injected with TEPC-15/PnC complexes (formed in antibody excess) and challenged with PnC coupled to sheep RBC, only the response to PnC was suppressed.
Immune complexes bind to cultured rat glomerular mesangial cells to stimulate superoxide release. Evidence for an Fc receptor.
Authors: Sedor J R , Carey S W , Emancipator S N 
Published: December 2022

Abstract
Contractile mesangial cells (MC) possess a number of macrophage-like characteristics, including oxygen radical generation. We suggest that under certain conditions MC may serve as immune effector cells in glomerulonephritis. Immune complex (IC) deposits are a hallmark of glomerulonephritis. Because IC elicit oxygen radicals from other cell types and because oxygen radicals can induce glomerular injury, we measured release of O2- by cultured rat MC in response to IC and, in separate experiments, the binding of IC to MC. Soluble and insoluble IC markedly stimulated dose- and time-dependent, saturable O2- release. Specific antibody (Ab) alone or mixtures of nonimmune Ab and antigen had no significant effect. IC-induced O2- release was not affected by cytochalasin B, an inhibitor of phagocytosis. Binding studies with radioiodinated IC demonstrated specific binding with an affinity of 1.56 X 10(6) M-1 and 1.02 X 10(5) receptors per cell. Both binding and O2- release required the Fc region of Ab. IC formed with F(ab')2 fragments did not bind specifically to or stimulate O2- release by MC. Cultured cells from rats depleted of bone marrow-derived phagocytes by irradiation produced amounts of O2- similar to cells from normal rats. These results provide evidence that IC affect the biology of the contractile glomerular MC in a manner that is dependent on the Fc region of Ab and suggest that MC structure and function may be altered at sites of injury.
Lymphokine activation of T4+ T lymphocytes and monocytes.
Authors: Cruikshank W W , Berman J S , Theodore A C , Bernardo J , Center D M 
Published: December 2022

Abstract
The function of the T4 antigen, a marker for a differentiated T cell subset, is not well understood. Our previous observation that a chemoattractant human lymphokine, lymphocyte chemoattractant factor (LCF), which selectively induces motile responses in unactivated T4+ lymphocytes, led us to investigate whether LCF could also induce T4+ cell activation. Because LCF acts selectively on T4+ cells, we next determined whether the T4 antigen has a function in this LCF-induced cellular activation. A T4+ lymphocyte migratory response is induced by divalent anti-T4 antibody, but not by corresponding Fab fragments of the same antibody. Fab fragments of anti-T4 antibody, but not Fab fragments of anti-T3 antibody, block the migratory effect of both LCF and divalent anti-T4. Furthermore, LCF but not divalent anti-T4, evokes the expression of interleukin 2 (IL 2) receptors and HLA-DR antigen on T4+ lymphocytes in 24 hr. These effects are quantitatively similar to those observed by anti-T3 antibody activation. LCF-induced IL 2 receptor expression is blocked by co-incubation with anti-T4 antibody and anti-T4 Fab fragments, whereas anti-T3 activation is not inhibitable by anti-T4 Fab fragments. Because cultured monocytes express the T4 antigen, we investigated the action of LCF on cultured monocyte migration and HLA-DR expression. Induction of monocyte migration by LCF and anti-T4 antibody increases proportionally as T4 antigen expression increases in vitro. This enhanced migration is inhibitable by anti-T4 Fab fragments. Monocyte activation, as measured by augmented HLA-DR expression 24 hr after incubation with LCF, but not anti-T4 antibody, is quantitatively similar to the effects of interferon-gamma. Augmented HLA-DR expression is blocked by anti-T4 Fab fragments but not by antibody to interferon-gamma. These studies indicate that LCF interacts with T4+ lymphocytes and monocytes to induce migration and cellular activation.
Cytokine-dependent granulocytic differentiation. Regulation of proliferative and differentiative responses in a murine progenitor cell line.
Authors: Valtieri M , Tweardy D J , Caracciolo D , Johnson K , Mavilio F , Altmann S , Santoli D , Rovera G 
Published: December 2022

Abstract
Human granulocyte colony stimulating factor (G-CSF) can support the survival and short term proliferation of the interleukin 3 (IL 3)-dependent diploid murine hemopoietic progenitor cell line 32D C13. After 8 days in the presence of 30 U/ml of G-CSF and in the absence of IL 3, the great majority of 32D C13 cells becomes positive for myeloperoxidase (a marker that appears at the promyelocytic stage of the granulocytic lineage) and progressively differentiates into lactoferrin-containing neutrophilic granulocytes. Myeloperoxidase mRNA rapidly increases after 24 to 48 hr of treatment with G-CSF, peaks at day 6 and is no longer detectable at day 9 and 12, paralleling the appearance of myeloperoxidase-positive promyelocytes and myelocytes in the culture. After 12 days, 100% of the cells terminally differentiate, and clonogenic assays in IL 3-containing semisolid media indicate that the whole population has irreversibly lost proliferative capability. By using varying concentrations of both murine IL 3 and recombinant human G-CSF, the cultures develop an heterogeneous population of cells representing all the differentiation stages of the myeloid lineage, and the relative ratios of immature proliferating precursors and terminally differentiated cells present in the cultures can be modulated by modifying the concentrations of IL 3 or recombinant human G-CSF. Isobolic curves indicate that IL 3 and G-CSF have an antagonistic effect on the proliferation of 32D C13 cells. Thus, these cells represent a simplified in vitro model of normal granulocytic differentiation whose extent may be modulated completely in the presence of serum by two well-defined growth and differentiation factors: IL 3 and G-CSF.
A polymorphism of the complement regulatory protein MCP (membrane cofactor protein or gp45-70).
Authors: Ballard L , Seya T , Teckman J , Lublin D M , Atkinson J P 
Published: December 2022

Abstract
Membrane cofactor protein (MCP or gp45-70) is a recently described regulatory glycoprotein of the complement system which binds iC3 or C3b and is present on human platelets, T cells, B cells, monocytes, and mononuclear-derived cell lines. On sodium dodecyl sulfate-polyacrylamide gel electrophoresis, MCP migrates as a doublet with an Mr of the upper band of 63,000 and the lower band of 58,000. The same pattern was found on all cell populations in a given individual and was stable over time. In order to further characterize the two band pattern on sodium dodecyl sulfate-polyacrylamide gel electrophoresis, MCP was isolated by affinity chromatography or immunoprecipitation from 72 healthy unrelated donors. All individuals expressed both bands and, based on the densitometric scanning of gels, three patterns were noted: upper band predominant in 65%, approximately equal distribution of upper and lower bands in 29%, and lower band predominant in 6%. These observed phenotypic frequencies fit with expectations based on Hardy-Weinberg equilibrium for a two-allele system. Family studies also support this model as none of the 26 offspring had a phenotype that deviated from the expected, assuming an autosomal codominant model of inheritance. These results are consistent with a simple two-allele system that controls the expression of the two bands of MCP.