bluuebunny/crossref_metadata_2025_split huggingface dataset:
Spontaneous Cytotoxicity of Human Peripheral Mononuclear Cells Toward Red Blood Cell Targets in Vitro
Authors: Muchmore Andrew V. , Decker Jean M. , Blaese R. Michael 
Published: December 2022

Abstract
Human peripheral blood mononuclear cells become spontaneously cytotoxic toward a broad range of erythrocyte targets after 6 to 7 days in culture. The presence of high concentrations of fetal calf serum (20%) inhibits the development of spontaneous cytotoxicity, whereas low concentrations (1 to 2%) markedly enhance cytotoxicity. Allogeneic, xenogeneic, and even syngeneic RBC are suitable targets, suggesting little, if any, target cell specificity. The addition of excess unlabeled RBC inhibits 51Cr release from both identical and totally unrelated RBC targets; further arguing that the cytotoxic effector cell is not directed toward one and only one antigenic specificity on the target. Cell separation techniques employed at the beginning of culture demonstrate that cytotoxicity is markedly enhanced by T cell depletion by using a SRBC rosetting technique. Removal of phagocytic cells by incubation with iron particles and a magnet substantially depletes subsequent cytotoxic potential. EA rosette depletion of cells also markedly reduces subsequent cytotoxic potential. Interestingly, EA rosette depletion at the end of 7 days in culture has almost no effect on cytotoxicity, whereas E rosette depletion after 7 days continues to enhance cytotoxicity. Depletion of the cultured effector cell populations over a nylon wool column or with iron and a magnet abolished cytotoxicity. These results suggest that the cell responsible for spontaneous RBC cytotoxicity is a non-T cell which initially expresses an easily detectable Fc receptor and exhibits surface adherence properties. However, after 7 days in culture the cytotoxic cell either no longer expresses an Fc receptor, or its affinity, density, or availability are somehow altered in vitro.
Venom of the Ant Pseudomyrmex Sp.: Further Characterization of Two Factors That Affect Human Complement Proteins
Authors: Schultz Duane R. , Arnold Patricia I. 
Published: December 2022

Abstract
Two factors in the venom of the tropical ant Pseudomyrmex sp. had potent anti-complementary activity. The first (F1) was resistant to boiling and had the properties of a polysaccharide or glycoprotein. It had no effect on purified C4 and C2, but caused activation of C1, resulting in the consumption of C4 and C2 in normal human serum. F1 appeared to activate C1 by forming a complex with a nonimmunoglobulin factor in normal human serum. The serum factor was not C1q. The second venom factor (F2) was heatlabile (56°C, 30 min), and was identified as a tryspin-like enzyme. It hydrolyzed α-N-benzoyl-dl-arginine p-nitroanilide HCl and was inhibited by soybean trypsin inhibitor, but not by EDTA. It caused inactivation of purified complement components, but not components in serum, presumably because of natural serum inhibitors. F1 and F2 were closely associated in native ant venom. After gel filtration of the venom, two complement inactivators were eluted. They had m.w. of 175,000 and 32,500 daltons, but F1 and F2 were associated with both m.w. species. F1 and F2 migrated together after electrophoresis on polyacrylamide gels, and both were identified in the ultrafiltrate of ultrafiltration membranes having an m.w. cut-off of 10,000 daltons.
The results of this report and our previous studies (see Reference 11) show that ant venom is a potent activator/inactivator of components in both the classical and alternative complement pathways.
Synthesis and Release of Thymidine by Macrophages
Authors: Stadecker Miguel J. , Calderon Jesus , Karnovsky Manfred L. , Unanue Emil R. 
Published: December 2022

Abstract
An inhibitor of DNA synthesis and cell proliferation found in macrophage supernatants was subjected to further analysis. The following conclusions were drawn: a. Biochemically, the inhibitor appeared to be thymidine, judging from the migration in three different thin-layer systems and on gel filtration. b. The inhibitor was shown to be synthesized de novo by macrophage monolayers pulsed with a radiolabeled precursor of thymidine such as 14C-formate. c. The amount of inhibitor present in tissue culture fluids proved to be sufficient to block the growth of the EL-4 leukemia cell line in a manner that could be prevented with the addition of 2′-deoxycytidine. The EL-4 line was considerably more sensitive to thymidine blockade than a number of different cells tested.
Soluble Factors in Tolerance and Contact Sensitivity to Dnfb in Mice
Authors: Moorhead John W. 
Published: December 2022

Abstract
Active suppression of contact sensitivity to DNFB in mice is mediated by a·soluble suppressor factor (SSF) which is released in vitro by cultures of LN cells that contain antigen-specific suppressor T cells. For SSF-mediated suppression to occur, identity is required among genes in the H-2 complex between the donor of SSF and the donor of DNFB-immune LN cells. Identity in either the left half or right half of the H-2 complex was found to be both sufficient and required. Additional experiments using congeneic strains with intra-H-2 recombinants showed that the genetic homology which was required mapped to genes contained in the H-2K and/or H-2D regions of the H-2 complex.
Chemical and Biological Properties of a Protein-Rich Fraction of Bacterial Lipopolysaccharides
Authors: Morrison David C. , Lindsay Leroy , Betz Sally J. 
Published: December 2022

Abstract
Lipid A-associated protein (LAP) isolated from preparations of bacterial lipopolysaccharides (LPS, endotoxins) has been demonstrated to initiate the release of amines from rat peritoneal mast cells. The release at low concentrations of LAP requires both cellular energy and calcium, and thus appears to be a true secretory response. At higher concentrations the release is independent of these variables. The time required for maximal response is approximately 10 to 15 min at 37°C. The response appears to be a general property of Escherichia coli LAP preparations since LAP isolated from three serotypes of these organisms all have similar activity. On the basis of heat lability at 100°C, the ability of LAP to initiate mast cell secretion appears to be independent of its ability mitogenically to stimulate murine B lymphocytes.
Complementation Between Genetic Variants Affecting the Response of Chicken Leukocytes to Concanavalin A
Authors: Pink J. Richard , Miggiano Vincenzo C. 
Published: December 2022

Abstract
Birds of the partially inbred G-B1 chicken line can be classified as either high or low responders to Con A, on the basis of the amount of 3H-thymidine incorporated by Con A-containing cultures of their peripheral blood leukocytes. The pattern of inheritance of the high and low responder traits suggests that the variation in response is due to genetic polymorphism at a single autosomal locus. However, the allele responsible for the low responder trait of the G-B1 line is not identical to the allele of the previously described Mr1 locus carried by the inbred low responder CC line, since (CC × G-B1 low responder)F1 birds are uniformly high responders to Con A.
The responses to Con A of mixtures of CC and G-B1 low responder cells are not significantly higher than the responses of either component of the mixture alone. Thus, the gene products responsible for the complementation observed in F1 hybrids cannot complement extracellularly, and are not readily transferable from one cell to another.
Late Acting T Cell Depression of High Avidity IgG Antibody Secretion in the Secondary Response
Authors: Warren Robert W. , Davie Joseph M. 
Published: December 2022

Abstract
Activated T lymphocytes (ATC) suppressed the expression of high avidity plaque-forming cells (PFC) in the secondary immune response when given in vivo 1 day before assay or when mixed in vitro with hyperimmune cells for 90 min before assay. This late acting suppression is a cell dose-dependent, carrier-specific, T cell-mediated phenomenon. The target of this activity is probably the antibody-secreting cell.
Studies on the Cytolytic Activity of Human Lymphocytes
Authors: Ziegler H. Kirk , Geyer Carl , Henney Christopher S. 
Published: December 2022

Abstract
The binding of human K cells to antibody-coated cell monolayers and to immobilized immune complexes was studied under a variety of experimental conditions. Binding could be demonstrated by the depletion of K cell activity in the nonadherent cells as well as the augmentation of lytic activity in the adherent cell fraction. A selective binding of K cells was shown by experiments in which τ90% of K cell-mediated lytic activity was depleted while only 10% of the total lymphocytes were bound.
K cell binding was inhibited by staphylococcal protein A (SPA) indicating a a dependence on interactions between the Fc portion of IgG and homologous Fc receptors. K cell binding was partially inhibited by cytochalasin B and by low temperature (0°C) but was unaffected by the absence of divalent cations or by the presence of cAMP-“active” drugs.
Both SPA and cytochalasin B inhibited the K cell-mediated lysis of target cells coated with low amounts of antibody. This inhibition was reversed, however, by increasing the antibody “coat”. In contrast, inhibition of cytolysis by EDTA and by drugs that raised cAMP levels in human lymphocytes could not be reversed by increasing the amount of target cell-associated antibody.
These findings allow a clear dissection of K cell-mediated cytolysis into two independent events, with distinctive requirements: a binding phase involving K cell-target cell interaction and a lytic phase which follows such accomodation.
The Ontogeny of Thymic Independent Antibody Responses in Vitro in Normal Mice and Mice with an X-Linked B Cell Defect
Authors: Mosier D. E. , Mond J. J. , Goldings E. A. 
Published: December 2022

Abstract
The primary in vitro antibody response of neonatal spleen cells to three thymic independent antigens has been examined. The time of onset of responsiveness to TNP-Brucella abortus and TNP-lipopolysaccharide was significantly earlier than the onset of responsiveness to TNP-Ficoll. This ontologic sequence was not affected by T cell depletion or antigen presentation on adult macrophages. In neonatal mice bearing the X-linked CBA/N defect, the response to TNP-Brucella abortus and TNP-lipopolysaccharide was much delayed and no response to TNP-Ficoll developed. We conclude that different thymic independent antigens address different subpopulations of B cells, one of which appears earlier in ontogeny than the other.
Effect of Lipopolysaccharide on Immunogenicity and Tolerogenicity of HGG in C57BL/6J Nude Mice: Evidence for a Possible B Cell Deficiency
Authors: Parks D. Elliot , Doyle Michael V. , Weigle William O. 
Published: December 2022

Abstract
Studies were performed to define the in vivo and in vitro responsiveness of nude mice to bacterial lipopolysaccharide (LPS). The in vitro responsiveness to LPS of spleen cells from congenitally athymic nude C57BL/6J mice was equivalent to littermate cells when monitored by stimulation of mitogenesis or polyclonal activation. Additionally, although nude spleen cells were incapable of responding to in vitro challenge with the T-dependent antigen, sheep red blood cells (SRBC), the addition of LPS to these cultures promoted specific antibody synthesis indicating classical responsiveness of nude B cells to LPS in vitro. The effects of LPS upon responsiveness to human γ-globulin (HGG) in vivo were also investigated. The injection of deaggregated HGG (tolerogen) into nude mice was demonstrated to induce immune tolerance in the splenic B cells of these mice. This unresponsive state was stable upon transfer into primed, irradiated recipients and persisted in the nude mice for up to 4 months. The induction of this tolerant state established in the absence of detectable T cell activity could be inhibited by the injection of LPS 3 hr after the tolerogen. Although LPS was capable of inhibiting the induction of tolerance in nude mice in vivo, it was incapable of promoting the generation of specific antibody-secreting, plaque-forming cells (PFC) to either HGG or SRBC when injected with these T-dependent antigens. This failure of LPS to replace the requirement for T cells in the production of the PFC response to these antigens did not extend to AT × BM littermate mice. Additionally, LPS itself was recognized as a T-independent antigen by these nude mice. Although the induction of tolerance in the B cells of nude mice demonstrated that T cells are not required for the induction or maintenance of B cell tolerance, the inability of nude B lymphocytes given LPS to respond to T-dependent antigens indicated that the signal received by B cells from the LPS molecule which replaces the requirement for helper T cells may be distinct from other LPS signals. Furthermore, the data from several experimental approaches suggested that nude mice may be deficient in a subpopulation of B cells which is responsive to both antigen and nonspecific B cell activators in normal mice.
Generation of T Helper Cells in Vitro
Authors: McDougal J. Steven , Cort Sheila P. , Gordon David S. 
Published: December 2022

Abstract
Thymocyte-macrophage cultures primed with carrier protein release an alloantigen-related factor that enhances the anti-hapten plaque-forming cell response of hapten-primed spleen cells in vitro. Use of immunoadsorbant columns made with a variety of alloantisera indicates that the relevant antigens in this system are coded for by the H-2 major histocompatibility locus in mice. The data indicate that in H-2d and H-2k strains the important genetic regions are in the I region between the K region and the I-C subregion and suggest, based on current understanding of Ia specificities, that the I-A subregion codes for these antigens.
Experimental Allergic Uveitis. Isolation, Characterization, and Localization of a Soluble Uveitopathogenic Antigen from Bovine Retina
Authors: Wacker Waldon B. , Donoso Larry A. , Kalsow Carolyn M. , Yankeelov John A. , Organisciak Daniel T. 
Published: December 2022

Abstract
The soluble antigen involved in the pathogenesis of EAU was isolated from bovine retinal extract by precipitation with ammonium sulfate followed by molecular sieve and ion exchange chromatography. The purified fraction formed a double precipitin band by immunodiffusion and immunoelectrophoresis, and a doublet by analytical disc electrophoresis. By immunodiffusion one of these components formed a reaction of identity with guinea pig S antigen and the other a reaction of partial identity. Because the two components had the same m.w. and similar electric mobility, they are presumed to be minor structural variants of the same molecule.
The purified antigen had a m.w. of approximately 102,000 by analytical ultracentrifugation, 50,500 by SDS electrophoresis, and 56,000 by gel filtration chromatography. Sedimentation velocity studies with increasing concentrations of antigen indicated self-association. An S20 value of 3.6 was obtained for the monomer, corresponding to an approximate m.w. of 50,000.
The antigen was identified as a protein with a very small amount of lipid. Data are presented on the absorption spectrum, extinction coefficient, and amino acid composition. The molecule was lacking in cysteine and tryptophan, but contained a relatively high proportion of nonpolar amino acids corresponding with a lipophilic protein. It was localized by immunofluorescence to the area surrounding the entire photoreceptor cell in a pattern indicating association with the plasma membrane. The antigen was not rhodopsin, which has been implicated as a probable antigen in the pathogenesis of EAU, but has some properties resembling a recently described photoreceptor cell retinol-binding protein tentatively implicated in the transport of vitamin A from the circulation to the retina.
Assay of the purified fraction for production of EAU in the guinea pig indicated it was highly pathogenic in the microgram range. In agreement with immunofluorescent findings, the photoreceptors were specifically destroyed after cellular infiltration of the uveal tract.
Kinetic Analysis of Target Cell Destruction by Effector T Cells
Authors: Thorn Richard M. , Henney Christopher S. 
Published: December 2022

Abstract
Attempts have been made to test the hypothesis that the affinity of the effector T cell's antigen receptor changes in a predictable manner with respect to the dose of antigen used to elicit effector cells and with time after antigen exposure.
Although we made no direct measurement of the affinity of the antigen receptor we have measured changes in the Kh parameter of cytolytically active lymphocyte populations. We demonstrate that this term, analogous to the Km value of enzymes, is an avidity parameter, reflecting the interaction rate of killer cells with homologous targets. We presume therefore that Kh values of killer T cells reflect the affinity of the cell's antigen receptor site.
Low doses of alloantigen elicited few killer cells of high avidity (low Kh). Killer cell avidity varied inversely with effector cell frequency, reaching minimum avidity when killer cells were present in greatest numbers. There was, however, no constant propertionality between avidity and frequency.
We suggest that these findings imply that T cell antigen receptors are heterogeneous with respect to their affinity for antigen and that clones of cells with receptors of high affinity are selected out when antigen is limiting. This selection is entirely analogous to that previously reported to operate for B cell clones and their product, serum antibody.
Requirements for Inducting Tolerance of Hapten-Specific Delayed Hypersensitivity: Epitope Density
Authors: Moon Michael M. , Redelman Doug , Wolvos T. A. , Bauer D. C. 
Published: December 2022

Abstract
Tolerance to hapten-specific antibody formation and delayed hypersensitivity was examined in adult rabbits. The azobenzenearsonate (ABA) or sulfonate-specific antibody response to hapten-hemocyanin immunogens was suppressed by deaggregated hapten-rabbit IgG conjugates given 21 and 14 days before challenge. High affinity antibody was preferentially suppressed. Delayed hypersensitivity to ABA-tyrosine was suppressed by deaggregated ABA-rabbit IgG conjugates injected 17 and 10 days before challenge. Conjugates with a high hapten density, ABA15–23-rabbit IgG were effective tolerogens. Conjugates with four to six ABA groups per carrier molecule were very poor tolerogens. Increasing the amount of low substituted conjugate injected did not improve tolerogenicity. It appears that a high epitope density is required for effective induction of tolerance to ABA-specific delayed hypersensitivity in the rabbit.
Immune Responses to Vaginal or Systemic Infection of BALB/c Mice with Herpes Simplex Virus Type 2
Authors: Morahan Page S. , Breinig Mary C. , McGeorge Margaret B. 
Published: December 2022

Abstract
The temporal relationships among the humoral and cellular immune responses were defined in BALB/c mice after vaginal or systemic infection with herpes simplex virus type 2 (HSV-2). After vaginal infection, mice showed evidence of clinical vaginitis on days 4 to 6 and HSV-2 replication was detected locally in the vaginal secretions, cervix, vagina, and uterus before the virus subsequently spread to the central nervous system. Death from encephalitis occurred between 7 and 10 days after infection. Vaginal infection was associated with significant delayed type hypersensitivity and splenic proliferative cell-mediated immune responses which appeared during the acute infection and waned by 3 weeks. There was almost no evidence of a systemic neutralizing antibody response at any time after vaginal infection. In contrast to the local vaginal infection, systemic i.v. HSV-2 infection induced a humoral response as well as the two cellular immune responses. Although both cellular immune responses appeared during the acute infection (days 6 to 14) and persisted for approximately 5 weeks, the humoral response appeared in surviving animals and persisted for at least 4 months. Thus, vaginal HSV-2 infection was associated primarily with transient cellular immune responses, whereas i.v. HSV-2 infection induced prolonged systemic humoral and cellular immune responses.
Potentiation of the Immune Response to Influenza Virus Subunit Vaccines
Authors: Webster Robert G. , Glezen W. Paul , Hannoun Claude , Laver William G. 
Published: December 2022

Abstract
Influenza subunit vaccines are poorly immunogenic in unprimed lower animals and man and methods were sought to potentiate the humoral response. Influenza B intact virus vaccines potentiated the antibody response of hamsters to purified vaccines containing influenza A hemagglutinin and neuraminidase subunits. The levels of antibody induced were at least as high as those induced by equivalent doses of whole virus. Similarly, intact heterologous influenza A virus vaccine (A/Victoria/3/75 [H3N2]) potentiated the antibody response of hamsters to A/NJ/76 [Hswl Nl] subunit vaccines but large doses of intact virus were required. Considerably lower doses of homologous intact A/NJ/76 [Hswl Nl] potentiated the antibody response of hamsters and sero-negative people to subunit vaccines. This suggests that future influenza subunit vaccines for use in seronegative people should contain a minimal dose of whole virus vaccine sufficient to potentiate the immune response to the subunits but insufficient to be reactogenic.
A synthetic water soluble adjuvant (N-acetyl-muramyl-L-alanyl-D-isoglutamine) was also shown to potentiate the immune response of hamsters to A/NJ/76 [Hswl Nl] influenza virus subunit vaccines.
A Splenic Requirement for the Generation of Suppressor T Cells
Authors: Sy Man-Sun , Miller Stephen D. , Kowach Helen B. , Claman Henry N. 
Published: December 2022

Abstract
Tolerance to contact sensitization with DNFB may be induced by DNBSO3. This specific unresponsiveness may occur via one or both of two mechanisms — production of suppressor T cells or clone inhibition. We investigated the role of the spleen in this unresponsiveness. Splenectomized mice may be tolerized by i.v. injection of DNBSO3, but they are incapable of serving as donors of lymph node cells for transfer of tolerance to normal recipients. Kinetic studies indicated that the spleen must be present at least three days after tolerization in order to permit development of a significant number of suppressor cells in the peripheral lymph nodes. We interpret these results to indicate that 1) clone inhibition does not require the spleen, 2) the generation of suppressor T cells is dependent on the presence of the spleen, and 3) it is likely that tolerogens in this system induce suppressor cells in the spleen and some of these cells or their products leave the spleen to reach the peripheral lymph nodes.