bluuebunny/crossref_metadata_2025_split huggingface dataset:
Human helper T cell factor(s). III. Characterization of B cell differentiation factor I (BCDF I).
Authors: Hirano T , Teranishi T , Onoue K 
Published: December 2022

Abstract
Staphylococcus aureus Cowan I (SAC) induced proliferation of human B cells but did not lead the cells to differentiate to immunoglobulin (Ig)-producing cells. The differentiation of SAC-stimulated B cells to IgG-producing cells was totally dependent on T cells or T cell factor, designated B cell differentiation factor I (BCDF I). BCDF I exerted its effect on B cells between 48 and 72 hr after the initiation of the culture, at which time the 3H-TdR uptake of SAC-stimulated B cells had already reached a maximal level. Highly purified human IL 2 did not induce the differentiation of SAC-stimulated B cells for IgG-producing cells. Therefore the differentiation-inducing ability of BCDF I was not due to the residual T cells in a purified B cell preparation, which might have been activated by a possible contamination of IL 2 in the BCDF I preparation. The apparent m.w. of BCDF I was estimated to be 20,000 by gel filtration. Isoelectric focusing analysis showed that its activity was distributed in three fractions corresponding to pI 6.5, 7.0, and 8.0. In contrast, BCDF II, which induced IgG production in an Epstein Barr virus-transformed B lymphoblastoid cell line, was focused in the fractions with pI range of 4.8 to 5.5. Thus there are at least two different kinds of BCDF for human B cells, designated here as BCDF I and BCDF II.
Lymphokine regulation of activated (G1) lymphocytes. II. Glucocorticoid and anti-Tac-induced inhibition of human T lymphocyte proliferation.
Authors: Bettens F , Kristensen F , Walker C , Schwuléra U , Bonnard G D , de Weck A L 
Published: December 2022

Abstract
The regulation of the first cell cycle of human, activated (G1) PBL was analyzed by flow cytometry and [3H]thymidine incorporation. Endogenous IL 2 production was blocked in situ by pharmacologic concentration of DEX (100 to 1000 nM), resulting in an 80 to 90% reduction of thymidine uptake. Although T lymphocyte activation (G0-G1a transition) by PHA was unaltered, cells remained in the G1a phase of the cell cycle due to insufficient RNA synthesis for proliferation. The addition of IL 2-containing supernatants reversed this inhibitory effect of DEX by allowing the cells to synthesize more RNA (G1a-G1b transition). Such cells could enter the S phase and proliferate. Similar studies were performed on cells treated with a monoclonal antibody (anti-Tac) against the IL 2 receptor. In these studies, IL 2-induced RNA synthesis, and subsequent proliferation of DEX-treated and PHA-stimulated cells was inhibited by anti-Tac. Anti-Tac did not, however, inhibit the effect of endogenous IL 2 (PHA-stimulated PBL without DEX treatment), although it did bind equally well to such cells. Thus, IL 2 directly or indirectly regulates human T cell proliferation at the level of RNA synthesis. Furthermore, anti-Tac can inhibit the mitogenic signal given by endogenous IL 2, but not by in situ produced IL 2, an observation of importance to further investigations of the mechanisms by which IL 2 interacts with specific receptors to elicit proliferation.
Serologically detectable polymorphism of the HLA-DC alpha-subunit.
Authors: Tosi R , Tanigaki N , Sorrentino R , Centis D , Ferrara G B 
Published: December 2022

Abstract
Two 8th Workshop alloantisera, 8W1062 and 8W614, which were classified respectively as anti-DR5 and anti-DR3, were found to react with an Ia preparation from LG38 cells (DR5,5) that was depleted of DR and BR molecules and enriched in DC molecules by pretreatment with a monoclonal antibody and an antiserum against alpha-subunits of DR and BR molecules. The reaction of both alloantisera was inhibited by DR3-positive, DR5-positive, and DRW13-positive individuals. This pattern does not correspond to any of the hitherto reported supertypic specificities. Both antisera were shown to bind to the alpha-subunit isolated from the DC-enriched preparation but not to the beta-subunit. The specificity has been named DC alpha 3. Family studies show the segregation according to the HLA haplotype patterns. This demonstrates by formal genetics criteria the HLA linkage of the locus controlling the DC alpha-subunit.
Glucocorticoid activation of a calcium-dependent endonuclease in thymocyte nuclei leads to cell death.
Authors: Cohen J J , Duke R C 
Published: December 2022

Abstract
Dexamethasone and corticosterone kill mouse thymocytes, as measured by eosin uptake, after several hours of in vitro incubation. This killing requires RNA and protein synthesis, because it is inhibited by cycloheximide, emetine, or actinomycin D. An earlier event than cell death is the extensive fragmentation of nuclear DNA into oligonucleosomal subunits; this fragmentation also requires RNA and protein synthesis. The DNA cleavage results from the action of an endonuclease that preferentially cleaves DNA in the linker regions between nucleosomes. This endonuclease is found constitutively in the nuclei of thymocytes and some other cells, and requires calcium and magnesium ions for its activation; if isolated fresh thymocyte nuclei are incubated with these ions, as much as 77% of their DNA is cleaved within 90 min. Thus, the protein for which synthesis is necessary for glucocorticoid-induced thymocyte death is not the endonuclease itself, but is in some way involved in its activation; we suggest that it may be part of a system for transporting calcium into the nucleus. The endonuclease is inhibited by zinc, which also prevents thymocyte death. It appears that glucocorticoids cause thymocyte death by activating an enzyme that rapidly and extensively degrades DNA. This "death from within" is biochemically and morphologically different from toxic or accidental cell death, such as that induced by azide, heat, or antibody and complement treatment. Although mature T cells also contain the endogenous endonuclease, they lack the glucocorticoid-inducible mechanism for activating it, and are thus glucocorticoid-resistant.
Oxidative killing of the intraerythrocytic malaria parasite Plasmodium yoelii by activated macrophages.
Authors: Ockenhouse C F , Shear H L 
Published: December 2022

Abstract
The capacity of macrophages activated in vivo and in vitro to kill Plasmodium yoelii was investigated. Macrophages activated by BCG-, Con A-, or malaria-induced lymphokines (LK) were cultured with P. yoelii-parasitized erythrocytes (PE). In some experiments, effector and target cells were separated by a 0.45-micron filter. Parasite viability was assessed a) in vivo by injection of mice and quantitative detection of parasites by RIA or b) in vitro by the incorporation of 3H amino acids into parasite proteins. Activated macrophages killed target PE in a dose-dependent manner by elaborating a membrane-permeable soluble factor(s). The addition of small amounts of immune serum augmented the killing of the parasites. LK-activated macrophages underwent an oxidative burst upon the phagocytosis of PE as evidenced by the accumulation of reduced formazan in the NBT assay. The magnitude of the oxidative response corresponded to the number of parasites that were ingested. The phagocytosis-induced oxidative burst was necessary for subsequent killing of Plasmodium. Parasites incubated in microchambers separated from macrophages by a 0.45-micron filter were susceptible to H2O2 released by LK-activated macrophages incubated with PMA, opsonized zymosan, or P. yoelii antigen. Inhibition of protein synthesis by parasites exposed to products of activated macrophages was abrogated by preincubating macrophages with catalase but not with SOD, mannitol, or histidine. These results suggest that phagocytosis-associated oxidative mechanisms mediate the destruction of the malaria parasite. Hence, cell-mediated as well as antibody-dependent mechanisms cooperate in the immune response against malaria.
Monoclonal antibodies to a 140,000-m.w. protein on Plasmodium knowlesi merozoites inhibit their invasion of rhesus erythrocytes.
Authors: Miller L H , David P H , Hudson D E , Hadley T J , Richards R L , Aikawa M 
Published: December 2022

Abstract
Merozoites are the invasive stage of the malaria parasite, which are released from infected erythrocytes to invade other erythrocytes. Antibody to surface antigens on merozoites may prevent invasion by agglutinating merozoites as they are released from infected erythrocytes or by blocking receptors before contact of merozoites with the host erythrocyte. Monoclonal antibodies were produced to a 140,000-m.w. protein on the merozoite surface. The protein was synthesized by the mature intraerythrocytic parasite, the schizont, as a 143,000-m.w. protein and had a m.w. of 140,000 on the surface of free merozoites. The monoclonal antibodies were shown to bind to the surface of merozoites by immune electron microscopy. Ascitic fluid containing four of 11 anti-140,000 monoclonal antibodies partially blocked invasion of erythrocytes by merozoites released from schizont-infected cells. The low invasion rate was always associated with a high frequency of multiply infected erythrocytes (two or more rings per erythrocyte). Monoclonal antibodies purified by (NH4)2SO4 precipitation and diethylaminoethyl column fractionation also blocked invasion and caused multiple invasion of individual erythrocytes. The monoclonal antibodies, incubated with free merozoites, did not block invasion, indicating that the antibodies did not bind to merozoite receptors for erythrocytes. We propose that the reduced rate of invasion and the multiple invasion of erythrocytes, the characteristic of these monoclonal antibodies, was caused by weak agglutination of merozoites as they were released from infected erythrocytes.
The cytolytic T lymphocyte response to the murine cytomegalovirus. I. Distinct maturation stages of cytolytic T lymphocytes constitute the cellular immune response during acute infection of mice with the murine cytomegalovirus.
Authors: Reddehase M J , Keil G M , Koszinowski U H 
Published: December 2022

Abstract
Limiting dilution (LD) analysis with two modifications, the expansion and the restimulation LD assay, led to the detection and quantification of two distinct in vivo maturation stages within the lineage of virus-specific self-restricted CTL after infection of mice with the murine cytomegalovirus (MCMV). A low frequency set, representing an average of 15% of the specifically activated CTL-P in a draining lymph node, generated virus-specific lytic activity in the absence of antigen, solely under expansion conditions provided by growth and differentiation interleukins. These cells were considered to be active and were denoted antigen-independent or interleukin-receptive CTL-P (IL-CTL-P). A high frequency set required additional antigen in vitro to generate functionally active clones, and therefore the cells were termed antigen-dependent. Both sets are present in vivo simultaneously at the peak of the acute immune response and represent antigen-activated cells because their existence strictly depends on a preceding priming event. IL-CTL-P disappear quickly after acute infection and are absent during the memory state. It is proposed that the isolation of IL-CTL-P could serve to detect viral antigen expression during persistent and/or recurrent herpes virus infections.
High frequency of splenic anti-class I cytotoxic T lymphocyte precursors correlates with in vivo rejection of K/D region disparate thyroid and islet grafts in mice.
Authors: Isakov N , Bach F H 
Published: December 2022

Abstract
The relationship between the ability of different recombinant mouse strains to reject thyroid and pancreatic islet grafts that differ in class I antigens and the frequencies of the recipients' cytolytic T lymphocyte precursors (CTL-P) directed against donor antigens was examined. We analyzed three different pairs of D region histoincompatible recombinant mouse strains in which unidirectional thyroid graft rejection occurred. Frequency analysis of their splenic CTL-P demonstrated that the mouse strains that rejected the grafts exhibit a relatively high CTL-P frequency against the donor D region-encoded alloantigens at a magnitude similar to that directed against a third party, which differ in the entire H-2 complex. Mouse strains that did not reject thyroid grafts exhibited a relatively low CTL-P frequency against the donor alloantigens, but a normal high frequency against alloantigens encoded by the entire H-2 complex of a third party strain. The effect of different routes of immunization on the two parameters was tested in B10.S(7R) mice, which accept B10.S thyroid grafts permanently. Immunization of B10.S(7R) mice by injection of 50 X 10(6) B10.S spleen cells i.p. did not confer the ability to reject B10.S thyroid grafts and did not affect the low splenic anti-B10.S CTL-P frequency. By contrast, B10.S(7R) mice that were immunized by transplantation of B10.S skin rejected a subsequent B10.S thyroid graft and at the same time demonstrated a fourfold increase in the specific CTL-P frequency. We found that the ability to reject thyroid and pancreatic islet grafts always correlated with high CTL-P frequency against the donor alloantigens; however, acceptance of allografts was not always correlated with low CTL-P frequency. We assume, therefore, that the high frequency of CTL-P against donor alloantigens may be a prerequisite (but is not always sufficient) for rejection of K/D region disparate thyroid and pancreatic islet grafts.
In vitro reeducated T helper cells from sarcoma-bearing mice inhibit sarcoma growth in vivo.
Authors: Forni G , Giovarelli M 
Published: December 2022

Abstract
Spleen cells from BALB/c mice bearing a small, but already clinically evident transplantable methylcholanthrene-induced sarcoma (CE-2) are not able to release interferons, proliferate and perform a cytotoxic response against CE-2 cells, nor able to inhibit their growth in vivo in a Winn-type neutralization assay. They can, however, be reeducated to be efficiently active against the tumor. Spleen cells (25 X 10(6) ) and 10(6) mitomycin C-treated CE-2 cells were cultured in 20 ml of medium for 6 days. The surviving spleen cells were then cultured for another 5 days under the same conditions plus 10% interleukin 2-rich supernatant from a clone of EL-4 thymoma cells stimulated with phorbol-12-myristate-13-acetate. Reeducated spleen cells were then able to inhibit the growth of a 100% lethal dose of CE-2 tumor cells in a Winn-type assay, even when the lymphocyte to tumor cell ratio was 5:1. In vitro, they released interferon-gamma when restimulated by CE-2 cells, and displayed a marked cytotoxicity in an 18-hr assay. Their in vivo tumor-neutralizing activity was not affected by the removal of Lyt-2.2+ lymphocytes, nor by the absorption of cytolytic cells on CE-2 monolayers. The absorbed cell population no longer contained cytotoxic cells nor cytotoxic cell precursors, but still contained CE-2-specific helper cells, which assist the in vitro induction of cytotoxic cells by normal thymocytes. Lyt-2.2-, noncytotoxic, reeducated spleen cells from tumor-bearing mice thus play an important role in tumor neutralization in vivo.
Establishment and functional analysis of a cloned, antigen-specific suppressor effector T cell line.
Authors: Nakauchi H , Ohno I , Kim M , Okumura K , Tada T 
Published: December 2022

Abstract
A long-term cultured suppressor T cell line (3D10) was established from the spleen cells of KLH hyperimmunized C3H mice. The cells of 3D10 suppressed the secondary antibody response against dinitrophenylated KLH both in vitro and in vivo. The 3D10 cells were capable of directly suppressing the antibody response mounted by B cells and Lyt-1+2-helper T cells without participation of Lyt-1+2+ cells, which indicates that 3D10 is an effector rather than an inducer-type suppressor T cell. The cell line was unable to suppress the response against DNP-FGG even in the presence of free KLH. By analysis with a fluorescence-activated cell sorter, 3D10 was found to bear determinants detectable by conventional anti-Ia as well as rabbit anti-VH. The Ia locus was mapped in the I-J subregion and was detected by either conventional or monoclonal anti-I-J antibodies. The I-J determinants detected by monoclonal antibodies were different from those expressed on inducer-type suppressor T cells. The cell line also bears an antigenic determinant detected by a monoclonal SJL anti-SJA/9 antibody (HA16) that recognizes an allotypic determinant on T cells linked to the immunoglobulin heavy chain locus. The results indicate that the cell line 3D10 represents a suppressor effector T cell that acts directly on carrier-specific helper T cells.
Loss of specificity in cytolytic T lymphocyte clones obtained by limit dilution culture of Ly-2+ T cells.
Authors: Shortman K , Wilson A , Scollay R 
Published: December 2022

Abstract
Nonspecific cytotoxicity developed reproducibly and with high frequency in limit dilution cultures consisting of low numbers of murine cells stimulated with concanavalin A in the presence of growth factors and irradiated filler cells. The individual clones in cultures showing nonspecific killing were all derived from single, Thy-1+, Ly-2+ cells. At early times of culture (day 5 or 6), clones appeared to be specific in their lytic activity, as expected of cytolytic T lymphocytes (CTL). On continued culture (day 8 or 9), most of the originally specific CTL clones became nonspecific, killing a range of murine target cells, both syngeneic and allogeneic. The lack of specificity was observed at all effector cell doses. The effector cells responsible for the nonspecific cytolysis were Thy-1+ and Ly-2+, as were most cells in the cultures. The effector cells had the normal DNA content for a dividing T cell population, and most cells in the cultures had a normal chromosome complement. In mixed cultures in which the responder cells and the irradiated filler cells were from different mouse strains, the nonspecific killers displayed the Thy-1 and H-2 allotypes of the responder, and not of the filler cells. The development of a broad cytotoxic potential appears to be a normal and rapid event when Ly-2+ T cell-derived CTL-clones are grown under these conditions; this is a caveat for the use of limit dilution cultures to determine the T cell specificity repertoire. The relationship between these nonspecific CTL, activated lymphocyte killers, and natural killer cells is discussed.
Soluble antigen-primed inducer T cells activate antigen-specific suppressor T cells in the absence of antigen-pulsed accessory cells: phenotypic definition of suppressor-inducer and suppressor-effector cells.
Authors: Damle N K , Mohagheghpour N , Engleman E G 
Published: December 2022

Abstract
This study was undertaken to characterize interactions among human T cell subpopulations involved in the generation of suppressor T cells specific for a soluble antigen. Purified PPD-primed Leu-3+ cells, when co-cultured for 7 days with fresh autologous Leu-2+ cells, induced differentiation of Leu-2+ but not Leu-3+ cells into specific suppressor T cells, which subsequently inhibited the proliferative response of fresh Leu-3+ cells to PPD but not to tetanus toxoid or allogeneic non-T cells. The PPD-specific suppressor effect of activated Leu-2+ cells was not due to altered kinetics of the PPD response and also extended to the secondary response of PPD-primed Leu-3+ cells. Furthermore, only those Leu-2+ cells that lacked the 9.3 marker, an antigen present on the majority of T cells including the precursors of cytotoxic T cells, differentiated into suppressor T cells. To analyze the inducer population, fresh Leu-3+ cells were separated into Leu-3+,8- and Leu-3+,8+ subpopulations with anti-Leu-8 monoclonal antibody, activated with PPD, and then were examined for inducer function. Although both Leu-3+,8- and Leu-3+,8+ cells proliferated in response to PPD and upon activation expressed comparable amounts of HLA-DR (Ia) antigens, the Leu-3+,8+ subpopulation alone induced Leu-2+ cells to become suppressor-effectors in the absence of PPD-pulsed autologous non-T cells. Once activated, however, Leu-2+ suppressor cells inhibited the PPD response of both Leu-3+,8- and Leu-3+,8+ cells. These results indicate that antigen-primed Leu-3+,8+ inducer cells can directly activate Leu-2+, 9.3- precursors of antigen-specific suppressor T cells in the absence of antigen-pulsed autologous non-T cells.
Modulation of mononuclear phagocyte function by intravenous gamma-globulin.
Authors: Kimberly R P , Salmon J E , Bussel J B , Crow M K , Hilgartner M W 
Published: December 2022

Abstract
To assess the effects on mononuclear phagocyte function of i.v. gamma-globulin treatment in idiopathic thrombocytopenic purpura, we examined in vivo and in vitro mononuclear phagocyte function in 11 patients before and after therapy. All patients, both splenectomized and non-splenectomized, demonstrated a prolongation of in vivo clearance of autologous IgG-sensitized erythrocytes (p less than 0.01). Concurrent in vitro assessment of blood monocyte function showed decreased IgG-sensitized erythrocyte (EA) rosette formation (mean +/- SD: 31.6% +/- 8.2 vs 24.5% +/- 9.5; p less than 0.03) and decreased affinity of Fc receptor-specific IgG oligomer binding (9.9 +/- 16.3 vs 1.8 +/- 2.1 X 10(8) M-1; p less than 0.008), but no consistent change in the estimate of the maximum number of binding sites. Phagocytosis of two different EA probes was decreased (EhuA:0.49 +/- 0.26 vs 0.25 +/- 0.14 erythrocyte/monocyte/hr; p less than 0.02, EoxA: 1.76 +/- 0.66 vs 1.27 +/- 0.67 erythrocyte/monocyte/hr, p less than 0.05). The change in in vivo mononuclear phagocyte system clearance was significantly correlated with the change in the association constant for oligomer binding (r = 0.98, p less than 0.05). These data demonstrate that i.v. gamma-globulin infusions induce alterations of mononuclear phagocyte function that are not dependent on the presence of autologous serum containing infusate. The change in apparent Fc receptor affinity rather than receptor number may reflect an altered Fc receptor population with different binding properties.
Reactivity of antisera to endogenous primate retrovirus with a human T cell membrane protein: recognition of a nonviral glycoprotein by antibodies directed only against carbohydrate components.
Authors: Markenson J A , Snyder H W 
Published: December 2022

Abstract
A glycosylated protein of approximately 70,000 daltons (gp70) from the surface of human peripheral blood T cells was immunoprecipitated by antisera to the baboon endogenous retrovirus (BEV-M7) and the serologically related feline endogenous retrovirus (RD114) but not by antisera to other retroviruses. Whereas preliminary absorption experiments were consistent with a possible viral specificity for this reaction, detailed biochemical and serologic characterization of the purified cellular protein suggested that it was not related to the gp70 of either M7 or RD114 viruses. The specificity of the reaction was further analyzed by assays of cellular gp70 antigenicity after exposure to exo- and endoglycosidases or trypsin and carbohydrate hapten inhibition studies. The results of these experiments were consistent with the interpretation that the glycoprotein was being recognized by antibody binding to the carbohydrate moiety of the molecule. These results provide an example of an antibody activity that could lead to inappropriate conclusions when sensitive radioimmunoprecipitation techniques are used for the biochemical analysis of antigenic systems. They emphasize the necessity of purifying cellular antigens as a prerequisite to determining the exact basis for a serologic reaction.