bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional subsets of human monocytes defined by monoclonal antibodies: a distinct subset of monocytes contains the cells capable of inducing the autologous mixed lymphocyte culture.
Authors: Shen H H , Talle M A , Goldstein G , Chess L 
Published: December 2022

Abstract
The induction of most immune responses requires the close cooperation between T cells and antigen-presenting cells (APC), presumably of monocyte/macrophage (M phi) lineage. To characterize human APC further, we used two monoclonal antibodies, OKM1 and OKM5, to isolate and identify M phi subsets. OKM1 has been described and recognizes cell surface antigens on most M phi and granulocytes. OKM5 recognizes cell surface determinants present on the majority of human M phi but does not recognize other hematopoietic cell types. A small subset of peripheral blood M phi is OKM1-OKM5+. Human peripheral blood E- cells were separated into OKM1+ and OKM1- subsets by a rosetting technique utilizing anti-Ig-coated red cells. The capacity to present self antigens in the autologous mixed lymphocyte culture (AMLC) resided predominantly within the E-OKM1- subset, even if surface membrane Ig-positive cells were eliminated. Similar experiments showed that the ability to stimulate in AMLC was contained in the E-OKM5+ population and in fact resided primarily within the E-OKM1-OKM5+ subset. All of these subsets were able to trigger allogeneic T cells to proliferate. The capacity of these APC subsets to present soluble antigens (mumps, tetanus toxoid) was also examined. The data demonstrated that although the majority of these APC are E-OKM1+, E-OKM1-OKM5+ cells can also present foreign antigen. Taken together, these data suggest OKM1 and OKM5 can be used to isolate two functionally distinct human M phi subsets. One subset (E-OKM1+) is capable of presenting soluble antigens but shows minimal ability to trigger AMLC. The other subset (E-OKM1-OKM5+) can also present soluble antigens but is the predominant subset that can trigger AMLC.
Soluble factors for B cell activation: a T cell hybridoma that secretes a specific B cell growth factor.
Authors: Garchon H J , Levi-Strauss M , Carnaud C , Bach J F 
Published: December 2022

Abstract
A murine T cell hybridoma, T91, has been established by fusion of BALB/c Con A-activated spleen cells with BW 5147 HAT-sensitive thymoma cells. T91 constitutively produced a factor that markedly enhanced the proliferative response to LPS of B cells cultured at low cell density. This factor is nonmitogenic by itself. It maintains in the absence of LPS, the proliferation of B cell blasts previously activated with LPS for 3 days. T91 supernatant contains neither IL 1 nor IL 2 nor TRF activity, and mixing experiments indicate the absence of factors suppressing these activities. The data suggest the existence of a specific B cell growth factor compatible with a two-signal model for B lymphocyte activation.
Thymosin peptides and lymphokines do not directly stimulate adrenal corticosteroid production in vitro.
Authors: Vahouny G V , Kyeyune-Nyombi E , McGillis J P , Tare N S , Huang K Y , Tombes R , Goldstein A L , Hall N R 
Published: December 2022

Abstract
There is developing evidence that certain thymosin peptides and lymphokines produce a transient increase in steroid hormones when introduced systemically. Conversely, the repressive effect of adrenocortical steroids on the immune system is well documented. In the present study, the direct effect of certain components of the immune system on steroid output by rat adrenal fasciculata cells was tested. With this system, there was no direct steroidogenic effect of either the partially purified thymosin fraction 5, or any of the purified peptide components tested (thymosin alpha 1, alpha 7, or beta 4). These peptides also did not synergize the cellular response to ACTH, nor did they induce cAMP production by a ACTH- and NaF-responsive adrenal membrane preparation. Supernatants from Con A-stimulated spleen cells, which were demonstrated to contain lymphokine activity, and partially purified mouse interferon were also without a significant direct or synergistic effect on steroidogenesis by adrenocortical cells. These results suggest that the steroidogenic response to these peptides observed in vivo may be mediated by the central nervous system.
Modulation of the biologic activities of IgE-binding factors. I. Identification of glycosylation-inhibiting factor as a fragment of lipomodulin.
Authors: Uede T , Hirata F , Hirashima M , Ishizaka K 
Published: December 2022

Abstract
Splenic T lymphocytes of rats treated with complete Freund's adjuvant (CFA) spontaneously release a lymphokine that inhibits the glycosylation of IgE-binding factors during their biosynthesis and provides the factors with biologic activity: selective suppression of the IgE response. The lymphokine, which is called glycosylation-inhibiting factor, also prevents IgE-induced increases in Fc epsilon R+ cells. The glycosylation inhibiting factor is formed by stimulation of BCG-primed spleen cells with PPD and participates in the selective formation of IgE-suppressive factors. The lymphokine is derived from OX 8+ T cells in both the CFA and BCG systems. The glycosylation-inhibiting factor is a 16,000-dalton peptide, as estimated by gel filtration, and specifically binds to monoclonal antibody against lipomodulin, a phospholipase inhibitory protein. Furthermore, "lipomodulin" was detected by radioimmunoassay in the 16,000-dalton fraction that contained glycosylation inhibiting factor. The fraction did not inhibit phospholipase A2 but after alkaline phosphatase treatment, the fraction did inhibit phospholipase A2. Furthermore, purified lipomodulin obtained from glucocorticoid-treated rabbit neutrophils had the same biologic activities as glycosylation inhibiting factors; i.e., it inhibited both protein glycosylation of IgE-binding factors and IgE-induced expression of Fc epsilon R. The results collectively indicate that glycosylation-inhibiting factor is a fragment of phosphorylated lipomodulin.
An unusually high-titer human anti-Epstein Barr virus (EBV) serum and its use in the study of EBV-specific proteins synthesized in vitro and in vivo.
Authors: Edson C M , Cohen L K , Henle W , Strominger J L 
Published: December 2022

Abstract
Sera from a patient with a chronic Epstein Barr virus (EBV) infection contained unusually high anti-EBV antibody titers (1:2560 to 1:10,240 for EA(D) and 1:5,120 to 1:40,960 for VCA). One of these serum samples was shown by immunoprecipitation to recognize at least 11 EBV-specific proteins from virus producer cells labeled in vivo and 10 EBV-specific proteins from in vitro translations of producer cell mRNA. Six of the in vivo labeled proteins (135,000, 89,000, 50,000 to 55,000 doublet, 46,000, and 34,000 daltons) are "early" by their resistance to phosphonoacetic acid, and five (350,000, 220,000, 160,000, 140,000, and 85,000 daltons) are "late" membrane and capsid proteins. The EBV-specific proteins immunoprecipitated from in vitro translations had molecular masses of 150,000, 140,000, 115,000, 52,000, 50,000, 45,000, 34,000, 29,000, 17,000, and 15,000. Subcellular fractionation studies of cells labeled in vivo revealed that the 135,000-dalton protein and part of the 50,000 to 55,000 dalton protein doublet were found in both the nuclear and the cytoplasmic fractions, and thus are good candidates to be components of the EA(D) diffuse-type immunofluorescence observed with many EA-positive sera.
Maternal-infant transfer of influenza-specific immunity in the mouse.
Authors: Reuman P D , Paganini C M , Ayoub E M , Small P A 
Published: December 2022

Abstract
The effects of maternal-infant transfer of influenza-specific antibody on influenza infection in the infant mouse were studied by following mortality, hemagglutination inhibition antibody, virus shedding from the nose and lung, and pathology of the upper and lower airway. By cross-fostering infants, influenza-specific antibody was shown to be acquired mainly by breast-feeding. Mice acquiring specific antibody survived lethal influenza infection (p less than 0.001) and had no evidence of influenza pneumonitis. There was variable suppression of nasal virus shedding and tracheal desquamation. Infected infants that initially acquired high levels of serum antibody also showed no evidence for serum antibody 10 wk later. Infant mice surviving initial influenza infection were lethally rechallenged 10 wk later. Rechallenged mice had a higher survival rate when compared to control mice (p less than 0.001) in spite of the absence of anti-influenza antibody and the presence of high lung virus titers in both groups 1 day after rechallenge. Rechallenged mice showed evidence for both significantly lower nasal virus titers (p less than 0.001) and a secondary serum antibody response with associated decline in lung virus titer. These results suggest maternal influenza-specific antibody a) is transferred to the infant mouse; b) is transferred mainly by breast-feeding; c) is life saving and lowers lung virus titers in the infant; and d) suppresses the infant's serum antibody production after challenge without affecting local immunity or the ability to mount a secondary antibody response.
Anti-oxazolone hybridomas and the structure of the oxazolone idiotype.
Authors: Kaartinen M , Griffiths G M , Hamlyn P H , Markham A F , Karjalainen K , Pelkonen J L , Mäkelä O , Milstein C 
Published: December 2022

Abstract
Antibodies raised in several mouse and rat strains against the hapten 2-phenyloxazolone (phOx, "oxazolone") regularly contain a fraction recognized by antiidiotypic reagents. We have studied this response in BALB/c and DBA/2 mice by generating over fifty anti-phOx antibody-secreting hybridoma clones. The hybridization was performed either 7 or 14 days after a primary immunization with phOx-protein conjugate. Most of the hybrids secreted IgG1. Whereas over 80% (17/21) of IgG-producing hybrids from day-7 fusions secreted oxazolone-idiotype positive immunoglobulin, all hybridomas originating from day-14 fusions were idiotype negative. The mRNA for heavy (H) and light (L) chains of three idiotype-positive and one idiotype-negative IgG1 hybridomas were sequenced by a modification of Sanger's dideoxynucleotide method of DNA sequencing, using crude mRNA as template, synthetic oligonucleotides as primers, and reverse transcriptase to incorporate both dideoxynucleotides and labeled deoxynucleotides. The sequence of the mRNA coding for the whole variable region of each chain was established using primers complementary to the constant region near the V-C boundary and another two that coded for a framework segment in either VH or VL. This method not only provided more information than protein sequencing but was also faster and simpler. The mRNA preparation did not need fractionation beyond the poly A-containing fraction. The sequences of the H and L chain mRNA of the three idiotype-positive anti-oxazolone antibodies were extremely similar or identical, and from them a tentative oxazolone-idiotype basic sequence was derived. Only three nucleotide differences were detected; these occurred in the D segment of one H chain mRNA, in the V-J boundary of one of the light chain mRNA, and in the first hypervariable region of another. The idiotype-negative antibody had a totally different H chain mRNA and a light chain mRNA that differed by 21 bases, almost all affecting the amino acid sequence.
Native C3 does not bind to the C3b receptor (CR1) of human blood B lymphocytes or alter immunoglobulin synthesis.
Authors: Berger M , Fleisher T A 
Published: December 2022

Abstract
Complement receptors on lymphocytes were first described more than 12 yr ago (1-3) and have come to be used as a common marker for the identification of B cells (4). The function of these receptors on the lymphocyte and their possible role in induction and/or regulation of the immune response remain unclear. In particular, there continues to be controversy as to whether native C3 can bind to the C3b receptor of these cells without cleavage to C3b (5-10). The resolution of this question is critical in order to clarify the expected state of availability of the receptor in vivo, because in plasma, the C3 concentration is relatively high (1.1 to 1.5 mg/ml), whereas there is little or no circulating C3b due to efficient degradation by factor H and the C3-inactivator (11). With the recent development of an improved method for the isolation of C3 from human plasma, it has been possible to obtain biochemically and functionally pure C3 that has not undergone structural or conformational alteration during processing and fully retains the specific hemolytic activity of C3 in fresh serum (12). Berger et al. (13) were able to demonstrate that C3 prepared in this way failed to bind to the C3b receptor of human polymorphonuclear leukocytes or erythrocytes. Similar observations were made by Schreiber et al. (14), also with phagocytic cells and erythrocytes, and by Dixit et al. (15) with an isolated membrane receptor preparation from rabbit macrophages. In the present communication, we extend these observations to human peripheral blood B lymphocytes. Purified C3 in its native state fails to block B lymphocyte-EA (IgM) C4b3b rosettes, whereas C3b causes 50% inhibition at 5 to 6 micrograms/ml. Furthermore, C3 failed to alter polyclonal immunoglobulin (Ig) production by human B cells, whereas C3b inhibited this B cell function. These data suggest that native C3 does not bind to the C3b receptors of B lymphocytes, and thus they are not occupied under normal conditions in vivo.
Use of I region-restricted, antigen-specific T cell hybridomas to produce idiotypically specific anti-receptor antibodies.
Authors: White J , Haskins K M , Marrack P , Kappler J 
Published: December 2022

Abstract
Murine T cell hybridomas bearing receptors for antigen plus I region gene products were used as immunogens in mice in an effort to raise anti-receptor antisera. The antisera were assayed for anti-receptor activity by the ability to inhibit interleukin 2 production by the T cell hybridomas stimulated by antigen and I region expressing antigen-presenting cells. The T cell hybridomas used in these experiments were made by fusing antigen-specific, I region-restricted BALB/c T cell blasts to the AKR thymoma, BW5147. Three groups of mice were immunized with the T cell hybridomas: (BALB/c X AKR)F1 animals, syngeneic to the hybridoma; (BALB.B X aKR)F1 animals, differing from the hybridomas at H2; and (C.B20 X AKR)F1 animals, differing from the hybridomas at Igh. Mice were immunized multiple times and sera from individual animals were assayed for anti-receptor antibodies. In all groups, some mice produced anti-receptor antibodies by the criterion that they were inhibitory in the assay mentioned above. The frequency of mice producing these inhibitory antibodies varied considerably between groups, with the (BALB.B X AKR)F1 animals producing these antibodies most frequently, and the (BALB/c X AKR)F1 animals producing them least often. All inhibitory antisera were idiotypically specific; they inhibited the response of the immunizing T cell hybridomas, but not the responses of closely related hybridomas with different specificities. Moreover, when they could be absorbed, the inhibitory antibodies could only be absorbed by the immunizing hybridoma. It is hoped that these antisera, and B cell hybridomas prepared from the immunized animals, will be useful in the elucidation of the structure of the receptors for antigen plus I region products on T cells.
Macromolecular insoluble cold globulin (MICG): a marker for pluripotential hemopoietic stem cells.
Authors: Batuman O A , Caro J , Schmidt R R , Hauptman S P 
Published: December 2022

Abstract
In embryonic mice pluripotential hemopoietic stem cells (PHSC) originate in the yolk sac and migrate to the fetal liver and from there to the bone marrow. Hemopoietic cells from yolk sac and fetal liver also migrate to the thymic primordium, and within the thymic environment these prothymocytes differentiate into mature T cells. We have recently demonstrated that macromolecular insoluble cold globulin (MICG), a T cell marker, is synthesized and inserted into the plasma membrane of embryonic prothymocytes as soon as these cells appear in the early thymus. In addition, we have shown that MICG+ cells are present within the fetal liver before the thymus has fully formed. In the present study we show that pluripotential hemopoietic stem cells in the fetal liver and bone marrow have MICG on their surface and represent a subpopulation of these MICG+ cells. The implications of these findings in relationship to stem cell differentiation and isolation are discussed.
Inhibition of IgE production in B hybridomas by IgE class-specific suppressor factor from T hybridomas.
Authors: Suemura M , Ishizaka A , Kobatake S , Sugimura K , Maeda K , Nakanishi K , Kishimoto S , Yamamura Y , Kishimoto T 
Published: December 2022

Abstract
The function of IgE class-specific suppressor factor (IgE-TsF) from T hybridomas was studied by employing IgE-producing B hybridomas. IgE-TsF was obtained from IgE class-specific T hybridomas, which had been established by the fusion of a phosphorylcholine-conjugated Mycobacterium-primed T cell population with the T lymphoma cell line BW5147. The absorption experiments showed that IgE-TsF from T hybridomas was composed of the binding site(s) for IgE and I region gene products as observed in conventional IgE-TsF. Incubation of IgE-producing B hybridomas with IgE-TsF for 1 hr at 37 degrees C resulted in the reduction of the number of IgE-secreting cells when assessed by a reverse plaque assay. The proportions of surface IgE-positive cells were concomitantly reduced. After 24 hr incubation with IgE-TsF, the number of cytoplasmic IgE-positive cells was reduced, showing that IgE synthesis was inhibited by IgE-TsF. Antigen-specific TsF from phosphorylcholine-specific T hybridomas did not show any inhibitory effect, and IgE-TsF did not block the antibody production of IgM-producing B hybridomas. Precapping of IgE receptors by anti-epsilon antibody or the simultaneous addition of soluble IgE with IgE-TsF abrogated the suppressive function, suggesting that IgE-TsF acted directly on B epsilon cells through binding with IgE receptors.
Lymphocyte subpopulations in the neonate: identification of an immature subset of OKT8-positive, OKT3-negative cells.
Authors: Maccario R , Nespoli L , Mingrat G , Vitiello A , Ugazio A G , Burgio G R 
Published: December 2022

Abstract
T cell subpopulations of lymphocytes from cord blood (CBL) of 24 newborns and from peripheral blood (a-PBL) of 24 healthy adult volunteers were assessed in T cell-enriched, T cell depleted and unseparated lymphocyte fractions by using OKT3, 4, 6, and 8 monoclonal antibodies. The results show that T cell-enriched CBL include adult numbers of OKT3+, OKT4+, OKT6+ and OKT8+ lymphocytes whereas the T cell-depleted fraction consists of a high percentage of OKT8+, OKT3-, non-E rosette-forming cells bearing a PNA receptor. The presence of the PNA receptor and the lack of the OKT3+ antigen strongly support the hypothesis that the subset of OKT8+ cells in cord blood includes immature T lymphocytes that may represent an intermediate stage between thymocytes and mature peripheral T cells.
TPA, tumor promoter-induced suppression of immunoglobulin secretion in human blood lymphocytes.
Authors: Jagielski P , Gregg S L , Gajl-Peczalska K J 
Published: December 2022

Abstract
12-O-Tetradecanoylphorbol-13-acetate (TPA) modulates DNA synthesis and differentiation of normal and malignant human lymphoid cells. Using the reverse plaque forming assay and radioimmunoassay, we showed that nontoxic concentrations of TPA (5 to 10 ng/ml) inhibited Ig secretion of peripheral blood lymphocytes. This inhibition was dependent on T lymphocytes and not monocytes; TPA treatment of the B cell-enriched fraction slightly enhanced Ig secretion. Suppression was evident when the proportion of TPA-pretreated T lymphocytes exceeded 50%. TPA-induced suppressor cells were present in both OKT8+ (suppressor/cytotoxic) and OKT4+ ("helper/inducer") subpopulations. The suppression was diminished but not abolished by the irradiation of T lymphocytes. In addition, TPA treatment modulated the expression of OKT4 antigen, whereas the expression of OKT8, 9.6 (sheep erythrocyte receptors) and surface Ig remained unchanged. Modulation of OKT4 was energy dependent and was not blocked by a maximal saturation of TPA receptors at 4 degrees C. We postulate that TPA-induced suppression of Ig secretion is T cell dependent and is likely to be associated with proliferation and activation of OKT8+ and OKT4+ lymphocytes and the induction of OKT4+ suppressor cells.
Antigen-specific and polyclonal immunoglobulin production induced by a cloned tetanus toxoid-specific T cell line.
Authors: Friedman S M , Principato M A , Thompson G S , Teichman F 
Published: December 2022

Abstract
This report describes the isolation and the phenotypic and functional characterization of a cloned, IL 2 dependent, TT-specific human helper T cell line (TCL), designated 1A1. 1A1 was derived by limiting dilution culture of a bulk IL 2-dependent TCL that was found to contain both TT and trinitrophenyl (TNP) altered self-reactive T cells. Specifically, 1A1 represents the outgrowth of one well of a microwell cloning plate initially seeded at 1 TCL/well, from which less than 4% (3/96) wells grew. Phenotypic analysis, utilizing a battery of monoclonal antibodies, demonstrates that all 1A1 cells are T cells belonging to a stable and discrete T cell subset: T3+, T4+, T17+, T8-. In proliferative assay, 1A1 responds specifically to TT but not to other soluble antigens against which the donor is sensitized, a panel of allogeneic stimulators, nor to TNP-modified-self. Moreover, 1A1 is HLA-DRw-restricted, proliferating only to TT in association with DRw3+ antigen-presenting cells. Of greater interest is the observation that 1A1 is an antigen-specific helper T cell line. Thus, by utilizing ELISA systems to quantitate class-specific immunoglobulin and antigen-specific antibody, it was determined that co-culture of autologous B cells, 1A1 cells, and a low concentration (1 to 10 ng/ml) of TT results in an IgG response that is predominantly, if not exclusively, antigen-specific antibody. In contrast, the presence of high concentrations of TT (4 micrograms/ml) triggers a polyclonal immunoglobulin response comprised of IgM with a small IgG component that is essentially devoid of anti-TT antibody. These results demonstrate that depending on the mechanism of activation, a cloned antigen-specific helper T cell line can mediate antigen-specific or polyclonal help for autologous B cells.