bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of a cloned ultraviolet radiation (UV)-induced suppressor T cell line that is capable of inhibiting anti-UV tumor-immune responses.
Authors: Roberts L K 
Published: December 2022

Abstract
Ultraviolet radiation (UV) is a potent carcinogen for the induction of skin tumors. In this regard, UV represents a unique carcinogenic agent, in that depending on the dosage and conditions of administration it can function as either a complete carcinogen, a carcinogenic promoting agent, or an immunologic modulator of anti-tumor rejection responses. The immunologic modulatory activity of UV has been demonstrated in numerous studies. These studies have shown that subcarcinogenic doses of UV induce a population of suppressor T lymphocytes (Ts cells) that allow for the emergence and progression of UV-induced tumors. Although the phenotypic and functional properties of these cells have been established, it was unclear as to whether the UV-induced Ts cell population consisted of multiple Ts cell clones able to recognize a range of unique tumor antigens or a limited number of Ts cell clones with functional specificity directed toward a common tumor-associated antigen (TAA). To address this question, an interleukin 2-dependent, UV-induced cloned Ts cell line was derived, by limiting dilution without exogenous antigen stimulation, from the splenic T cell population of a C3H mouse that had been exposed to a subcarcinogenic dose of UV. This Ts cell line, designated UV2.10, was selected for its ability to suppress the in vitro differentiation of cytotoxic T cells from the draining lymph nodes of UV-induced tumor-immune mice. When transferred into non-UV-irradiated syngeneic mice, which normally reject a UV-induced tumor implant, the UV2.10 cells rendered their hosts susceptible to the growth of a battery of UV-induced tumors. Although capable of suppressing in vitro and in vivo UV-induced tumor-immune responses, UV2.10 cells did not inhibit the elicitation of contact hypersensitivity responses, the rejection of allogeneic skin grafts, responses, the rejection of allogeneic skin grafts, or the rejection of allogeneic UV-induced tumors. These data suggest that the cloned UV2.10 Ts cell line possesses functional antigenic specificity that may be limited to the regulation of immune responses that are directed toward the TAA expressed by syngeneic UV-induced tumors. Employing monoclonal antibodies and FACS analysis, the cell surface phenotype of the UV2.10 cell line was determined to be: Thy-1.2+, Lyt-1-, Lyt-2+/- (dim), L3T4a-, I-A/E-, and I-J+. This cell surface phenotype is indicative of a suppressor T cell. These data lend further support to the hypothesis that the UV-induced Ts cell population is clonal in nature and functions through its ability to recognize a common TAA(s) that appears to be expressed by virtually all UV-induced tumors.
Membrane defects of the tolerant B cell. IV. Failure to accelerate antigen receptor loss.
Authors: Meucci V , Ashman R F 
Published: December 2022

Abstract
Mechanisms of immunologic tolerance affecting antibody responses include conditions extrinsic to the B cell such as dominant suppression by T cells (1), regulation by anti-idiotype (2), and tolerance in T helper cell populations (3). But tolerance can also result from changes in the antigen-reactive B cells such as their deletion (4), or that mysterious process by which they become "intrinsically tolerant", i.e., refractory to stimulation (5). One approach to learning more about the mechanism of intrinsic tolerance at the level of cell physiology is to determine which of the activation events that normally follow antigen contact occur or fail to occur in such cells. An established model of intrinsic B cell tolerance previously exploited in such studies in the trinitrophenyl (TNP)-self-induced tolerance model of Fidler and Golub (6). Having established that BDF1 mice injected with 2,4,6-trinitrobenzene sulfonic acid (TNBS) become tolerant to TNP, they showed by appropriate transfer experiments that the tolerance could be not induce antibody to TNP in such mice (8). cells (7). They also showed that lipopolysaccharide could not induce antibody to TNP in such mice (8). Together, these data indicated that in this example, tolerance is intrinsic to the B cells. B cells with receptors for TNP remain in these mice (9), providing an opportunity to study activation events in intrinsically tolerant B cells. This paper is part of an ongoing series of studies of activation events in TNP-antibody-binding cells (ABC)2 using this tolerance model (9-11). It shows that a TNP-antigen that normally induces rapid loss of antigen receptors on TNP-ABC cannot do so in mice rendered tolerant to TNP.
Production and characterization of a monoclonal antibody (A1-3) that binds selectively to activated monocytes and inhibits monocyte procoagulant activity.
Authors: Ewan V A , Cieplinski W , Hancock W W , Goldschneider I , Boyd A W , Rickles F R 
Published: December 2022

Abstract
We describe the generation and characterization of a new monoclonal antibody, A1-3, which possesses two unique properties. First, A1-3 binds selectively to stimulated human monocytes. Secondly, A1-3 inhibits the procoagulant activity expressed by stimulated monocytes and by human brain tissue factor. Unstimulated human peripheral blood cells (granulocytes, lymphocytes, monocytes, red blood cells, and platelets), prepared in the absence of detectable endotoxin, express no procoagulant activity and fail to bind A1-3. Stimulation of peripheral blood monocytes. alveolar macrophages, or the monocyte-like cell line U937, however, results in the expression of procoagulant activity and the binding of A1-3. The surface antigen recognized by A1-3 was recovered from endotoxin-stimulated human monocyte vesicles by immune precipitation and demonstrated an apparent m.w. of approximately 52,000. It is proposed that the monoclonal antibody A1-3 detects a differentiation antigen on human monocytes that is expressed in response to stimuli for monocyte activation.
Immunohistological studies with A1-3, a monoclonal antibody to activated human monocytes and macrophages.
Authors: Hancock W W , Rickles F R , Ewan V A , Atkins R C 
Published: December 2022

Abstract
A wide variety of monoclonal antibodies (mAb) have now been produced which recognize cell surface antigens on human peripheral blood monocytes. However, few of these mAb demonstrate specificity for monocytes, and fewer still recognize antigens exclusively on monocytes activated by one or more stimuli and/or block specific monocyte functions. The mAb A1-3 binds to lipopolysaccharide (LPS)-stimulated monocytes but not to resting blood monocytes, and inhibits the procoagulant activity of these LPS-activated cells. By using this mAb, we examined the reactivity of monocytes/macrophages (MO) in a broad range of normal and inflammatory tissues by means of a sensitive, four-layer immunoperoxidase technique. Cells of the MO system, in addition to lymphocytes and dendritic cells resident in lymphoid tissues, liver, lung, and other organs, were nonreactive with the A1-3 mAb. In contrast, intense staining of inflammatory MO was found in biopsies from patients with renal allograft rejection, acute glomerulonephritis, or granulomatous diseases. This apparent restriction of A1-3 binding to inflammatory, "activated" MO suggests that A1-3 mAb will be useful for the analysis of MO "activation" in many pathologic processes.
Autoimmune effector cells. VIII. Cellular requirements for the induction of autoreactive T cells of experimental allergic encephalomyelitis in nonimmune rats.
Authors: Silberg D G , Swanborg R H 
Published: December 2022

Abstract
We utilized a system of sequential in vitro cell culture and adoptive transfer to investigate the sequence of events which lead to the activation of effector cells responsible for the induction of experimental autoimmune encephalomyelitis (EAE) in Lewis rats. This procedure involves only naive (nonimmune) rats, and eliminates the requirement for adjuvants. Spleen cells (SpC) from naive donors were sensitized in vitro to myelin basic protein (BP), then transferred to intermediate (primary) hosts. Although these recipients did not develop EAE, they were primed for disease because they exhibited accelerated onset of active EAE when challenged with BP in adjuvant. Moreover, SpC from nonchallenged primary recipients transferred EAE to secondary recipients subsequent to in vitro exposure to antigen. The cells from the naive cultures which primed the intermediate recipients were radioresistant (1500 R); other studies have indicated that these are macrophages. In contrast, the cells which transferred EAE to the secondary recipients were radiation-sensitive T lymphoblasts. The finding that these cells also elicit disease in lethally irradiated (850 R) secondary recipients suggests that the transferred cells either are the actual effector cells of EAE or induce disease in collaboration only with radioresistant host cells.
Interleukin 1 is a radioprotector.
Authors: Neta R , Douches S , Oppenheim J J 
Published: December 2022

Abstract
Pretreatment with recombinant interleukin 1 (IL 1) protects mice in a dose-dependent manner from lethal effects of ionizing radiation. Two thousand units of IL 1, given i.p. 20 hr before irradiation, protect 88% of C57B1/6 mice from an LD100/17 radiation dose (dose of radiation that kills 100% mice in 17 days), and 1000 U of IL 1 protect 100% of DBA/1 mice from an LD50/30 dose. This finding provides the first evidence that a cytokine, IL 1, which acts as a differentiation- and maturation-inducing agent for a variety of cells, also can serve as a signal that initiates radioprotective events in vivo. Because many of the exogenous immunomodulators that have been shown to be radioprotective also induce endogenous IL 1 production, our observation suggests that IL 1 may mediate their radioprotective effects.
Recombinant human interleukin 1 alpha: purification and biological characterization.
Authors: Gubler U , Chua A O , Stern A S , Hellmann C P , Vitek M P , DeChiara T M , Benjamin W R , Collier K J , Dukovich M , Familletti P C 
Published: December 2022

Abstract
Interleukin 1 (IL 1) is a polypeptide hormone produced by activated macrophages that affects many different cell types involved in immune and inflammatory responses. The cloning and expression of a murine IL 1 cDNA in Escherichia coli encoding a polypeptide precursor of 270 amino acids has been reported, and expression of the carboxy-terminal 156 amino acids of this precursor in E. coli yields biologically active IL 1. By using the murine IL 1 cDNA as a probe, we have isolated its human homolog from cDNA generated to lipopolysaccharide-stimulated human leukocyte mRNA. Nucleotide sequence analysis of this cDNA predicts a protein of analysis of this cDNA predicts a protein of 271 amino acids (termed IL 1 alpha) which shows congruent to 61% homology to its murine counterpart but only 27% homology to a recently characterized human IL 1 precursor (IL 1 beta). We have expressed the carboxy-terminal 154 amino acids of IL 1 alpha in E. coli, purified this protein to homogeneity, and have compared it with pure recombinant murine IL 1 in several different IL 1 assays based on murine and human cells. Recombinant IL 1 is capable of stimulating T cell and fibroblast proliferation and inducing fibroblast collagenase and prostaglandin production, thus proving that a single molecule has many of the activities previously ascribed to only partially purified IL 1 preparations. Our results indicate that there exists a family of at least two human IL 1 genes (alpha and beta) whose dissimilar protein products have similar biological activities.
Molecular mapping of a histocompatibility-restricted immunodominant T cell epitope with synthetic and natural peptides: implications for T cell antigenic structure.
Authors: Berkower I , Buckenmeyer G K , Berzofsky J A 
Published: December 2022

Abstract
We have prepared synthetic and natural peptides that have allowed delineation of a major antigenic site of myoglobin recognized by histocompatibility (I-Ed)-restricted T cell clones. The smallest peptide capable of stimulating T cell proliferation consisted of residues 136-146. Residues Glu 136, Lys 140, and Lys 145 were essential for antigenicity, whereas Lys 133 and Tyr 146 added potency but were not required for antigenicity. The periodicity of these residues suggests that folding the peptide into its native alpha-helical structure may be essential for antigenicity either by forming a hydrophilic binding site for the T cell receptor or by participating in antigen presentation. The same folding could also produce a hydrophobic site on the opposite side of the alpha-helix that could participate in hydrophobic interactions. The extrapolation of these findings to other known peptide antigens suggests that this tendency to form an amphipathic alpha-helix may be a general property of antigenic sites recognized by T cells, perhaps due to a different functional role of each type of site in eliciting T cell responses.
Molecular mapping of idiotopes of anti-arsonate antibodies.
Authors: Jeske D , Milner E C , Leo O , Moser M , Marvel J , Urbain J , Capra J D 
Published: December 2022

Abstract
As part of understanding molecular function in structural terms, we have been attempting to map the idiotypic topography of specific anti-arsonate (Ars) antibodies. A panel of anti-Ars hybridomas of which the complete primary sequences are known were used. These molecules show a varied reactivity profile with a panel of monoclonal anti-idiotypic antibodies. By judicious chain recombination experiments and chemical modifications that altered this reactivity profile, we were able to identify particular amino acid residues or discreet regions of anti-Ars antibodies as having crucial roles in the expression of idiotypic determinants. Idiotopes were mapped to the heavy chain second hypervariable region and D segment, and to the light chain first and third hypervariable regions.
Human lung macrophage-derived histamine-releasing activity is due to IgE-dependent factors.
Authors: Liu M C , Proud D , Lichtenstein L M , MacGlashan D W , Schleimer R P , Adkinson N F , Kagey-Sobotka A , Schulman E S , Plaut M 
Published: December 2022

Abstract
Human lung macrophages obtained from surgical specimens spontaneously secreted a factor(s) (which we term macrophage factor) during 24-hr culture that induced calcium-dependent histamine release from human basophils and lung mast cells. Macrophage factor induced noncytotoxic histamine release from purified (85%) basophils. The kinetics of release were relatively slow and similar to that of anti-IgE. We performed a series of experiments to test the IgE dependence of macrophage factor-induced release. Preincubation of basophils with anti-IgE in calcium-free medium resulted in complete desensitization to macrophage factor-induced histamine release (i.e., when calcium and macrophage factor were added to the basophils, no histamine release occurred), and preincubation with macrophage factor in calcium-free medium resulted in partial desensitization to anti-IgE-induced histamine release. Pretreatment of basophils with pH 3.9 lactic acid buffer, which dissociates basophil IgE from its receptors, markedly reduced the capacity of basophils to release histamine in response to macrophage factor. Basophils that were incubated with IgE myeloma (but not with IgG) after lactic acid treatment partially or completely regained their capacity to release histamine in response to macrophage factor. Fluid-phase IgE myeloma (15 micrograms/ml) (but not IgG) inhibited basophil histamine release induced by two macrophage-derived supernatants, whereas IgE myeloma (200 micrograms/ml) did not inhibit release due to other supernatants. IgE-affinity columns removed the histamine-releasing activity of five macrophage-derived supernatants, and IgG-affinity columns had similar effects. However, neither affinity column removed the histamine-releasing activity of three other macrophage-derived supernatants. On Sephadex G-75 chromatography, nearly all of the histamine-releasing activity migrated as single peak with an apparent m.w. of 18,000. These results suggest that, although macrophage factor are heterogeneous, they are related, as they are a IgE-dependent factors that induce histamine release by interacting with cell surface IgE. These macrophage factors may be responsible for stimulation of basophil/mast cell mediator release in chronic allergic reactions.
Secretory IgA specific for Toxoplasma gondii.
Authors: McLeod R , Mack D G 
Published: December 2022

Abstract
Secretory IgA specific for Toxoplasma gondii was identified in intestinal secretions of mice infected perorally with bradyzoites (encysted in brain) of the Me49 strain of T. gondii by using immunofluorescence microscopy and an ELISA. This activity was absorbed with tachyzoites of T. gondii but not mouse brain. To determine whether increased total amount of intestinal IgA might cause a nonspecific reaction in the ELISA for T. gondii-specific IgA, mice were immunized perorally with cholera toxin. This immunization produced intestinal IgA antibody to cholera toxin and increased the total amount of intestinal IgA, but there was no reactivity of intestinal secretions in the ELISA for T. gondii-specific IgA. Experiments in which ELISA were performed with monoclonal IgA, IgG, or IgM and antisera to IgA, IgG, or IgM demonstrated that the ELISA was specific for each Ig class. In addition, monoclonal IgA competed with the anti-Toxoplasma IgA activity of intestinal secretions obtained from mice infected with T. gondii.
L3T4+, B2A2+ thymocytes from infant mice produce IL 2 after interaction with accessory cells expressing self class II antigens.
Authors: Lattime E C , Stutman O 
Published: December 2022

Abstract
The presence of a thymocyte population in infant (3 to 10 day old), but not adult mice, that produces IL 2 after self class II MHC antigen stimulation is described. The responding thymocyte expresses the antigenic phenotype: Thy-1+, Ly-1+, Ly-2-, L3T4+, B2A2+. Cell-cell mixing experiments and limiting dilution analysis were consistent with a loss of the self-Ia-reactive IL 2-producing thymocyte in the adult, with no evidence for active suppression found. Although thymocytes from adult animals failed to generate IL 2 after self class II stimulation, a similar frequency of IL 2-producing cells was demonstrated in both infant and adult after allo stimulation. These findings, taken with the recent demonstration of IL 2 receptors on neonatal thymocyte subpopulations, demonstrate a mechanism for IL 2 production in the thymus that may play a role in intrathymic differentiation of T cells.
Inhibition of DNA repair by deoxyadenosine in resting human lymphocytes.
Authors: Seto S , Carrera C J , Wasson D B , Carson D A 
Published: December 2022

Abstract
Profound lymphopenia is characteristic of immunodeficient children who lack adenosine deaminase (ADA). When ADA is inactive, deoxyadenosine (dAdo) is phosphorylated by immature T lymphoblasts and inhibits cell division. However, dAdo also causes the slow accumulation of DNA strand breaks in nondividing, mature human peripheral blood lymphocytes. To explore the basis for this phenomenon, we have assessed the effects of dAdo and other deoxynucleosides on the repair of gamma-radiation induced DNA strand breaks in resting normal lymphocyte cultures. As measured by a sensitive DNA unwinding assay, most DNA strand breaks were rejoined within 2 hr after exposure of lymphocytes to 500 rad. In medium supplemented with deoxycoformycin, a tight binding ADA inhibitor, dAdo retarded DNA rejoining in a dose and time dependent manner. The inhibition required dAdo phosphorylation. Over an 8-hr period, 10 microM dAdo gradually rendered peripheral blood lymphocytes incompetent for DNA repair. Among several other compounds tested, 2-chlorodeoxyadenosine, an ADA resistant dAdo congener with anti-leukemic and immunosuppressive activity, was the most powerful inhibitor of DNA repair, exerting significant activity at concentrations as low as 100 nM. Both dAdo and 2-chlorodeoxyadenosine blocked unscheduled DNA synthesis in irradiated resting lymphocytes, as measured by [3H]thymidine uptake. On the basis of this and other data, we suggest that quiescent peripheral blood lymphocytes break and rejoin DNA at a slow and balanced rate. The accumulation of dATP progressively retards the DNA repair process and thereby fosters the time-dependent accretion of DNA strand breaks. By inhibiting DNA repair, dAdo, 2-chlorodeoxyadenosine and related compounds may substantially potentiate the toxicity of DNA damaging agents to normal and malignant lymphocytes.
Suppression of natural killer cell activity by human seminal plasma in vitro: identification of 19-OH-PGE as the suppressor factor.
Authors: Tarter T H , Cunningham-Rundles S , Koide S S 
Published: December 2022

Abstract
Human seminal plasma (SP) was found to contain a potent suppressor of human natural killer (NK) cell cytotoxic activity against the K562 erythroleukemia target in vitro. Pooled and filter-sterilized SP reduced the NK cell activity of normal blood donors in a concentration-dependent manner; strong reduction of target cell lysis was observed at a final dilution of 1/400. Possible toxic effects of SP on NK cells were ruled out, because donor leukocytes incubated in a final SP dilution of 1/100 remained greater than 99 percent viable as determined by trypan blue exclusion. SP did not affect the lysability of the tumor targets, but suppressed the cytotoxic activity of the effector leukocytes, an effect that was reversed after washing the leukocytes free of the SP. The suppressive action of SP was retained after heating to 95 degrees C for 10 min, but was removed after adsorption with activated charcoal (Norit-A). Lipids extracted from SP were tested for suppression of NK cell cytotoxic activity, and the active principle was identified with the acidic lipid fraction. Components of the acidic lipid fraction of a single freshly obtained SP sample were separated by high pressure liquid chromatography, and suppression of NK cell cytotoxic activity was found to be associated with the predominant prostaglandins (PG) in this fraction, 19-OH-PGE1 and 19-OH-PGE2. Suppression of cellular immune functions by SP has been described; however, the identity of the suppressor factor (or factors) is unknown. The 19-OH-PGE are present in high concentration in primate semen, and may minimize immunologic sensitization to sperm in females after insemination. In addition, these compounds may suppress NK cell antitumor and antiviral activities in the vagina, as well as in their tissues of origin.