bluuebunny/crossref_metadata_2025_split huggingface dataset:
Ontogeny and postnatal persistence of a strong suppressor activity in man.
Authors: Unander A M , Olding L B 
Published: December 2022

Abstract
We report here on the ontogeny and postnatal persistence of an inhibited human immune response in which lymphocytes from human newborns strongly suppress the proliferation of adults' lymphocytes stimulated by phytohemagglutinin (PHA) or alloantigens in vitro. For this research we used a 2-way mixed lymphocyte culture (MLC) supplemented with PHA, with sex chromosomes acting as markers for dividing male and female cells, or alternatively a double chamber system. The proliferation of maternal lymphocytes was significantly suppressed by fetal lymphoid cells from the liver as early as the 8th week of gestation and by those from fetal blood at the 14th week or later during gestation. This strong suppressor activity persisted in 11-mo-old infants but usually disappeared after that time.
Sequential production of IFN-alpha and immune-specific IFN-gamma by human mononuclear leukocytes exposed to herpes simplex virus.
Authors: Green J A , Yeh T J , Overall J C 
Published: December 2022

Abstract
Both viral-induced interferon (IFN-alpha) and immune interferon (IFN-gamma) were produced in cultures of human peripheral mononuclear leukocytes (PML) exposed to ultraviolet (UV) light-inactivated herpes simplex virus (HSV). Comparable IFN titers (100 to 300 U) were present in supernatant media from PML of HSV-seropositive and -seronegative donors maintained for 2 days in culture. This "early" IFN was not immunologically specific and had the characteristics of IFN-alpha. In contrast, PML from 20 of 21 (95%) seropositive donors, but only 2 of 22 (9%) seronegative subjects, produced IFN in day-5 cultures that had been washed on day 2 followed by the addition of fresh media without UV-HSV (p &lt; 0.0001). In addition,the geometric mean IFN titer of 35 U present in media from day 5 cultures of seropositive donors was significantly higher (p &lt; 0.0001) than those from seronegative subjects (&lt;10 IFN U). This "late" IFN was defined as immunologically specific by virtue of its being present almost exclusively in PML cultures from seropositive donors. Late-appearing, HSV-induced, immunospecific IFN-gamma had antigenic characteristics of both viral-induced IFN-aand mitogen-induced IFN-gamma. A considerable degree of overlapping sensitivity to anti-IFN-alpha and anti-IFN-gamma antibody existed in late IFN, but was not seen in standard, control specimens. The latter finding suggests that the possible existence of an IFN of antigenic character intermediate to IFN-alpha and IFN-gamma. Late IFN was not induced in PML cultures by UV-inactivated Newcastle disease virus (NDV). NDV did, however, induce high titers of early IFN-alpha in PML cultures of both HSV-seropositive and HSV-seronegative donors. HSV-stimulated lymphocyte blastic transformation occurred only in cultures of seropositive individuals, whereas none occurred in response to NDV. Delayed appearance of antiviral activity with the characteristics of IFN-gamma in HSV-stimulated PML cultures is a sensitive and specific measure of the human immune IFN response. Sequential synthesis of IFN-alpha and IFN-gamma in individual PML cultures provides an opportunity to examine regulation of IFN production in response to virus with intrinsic IFN-inducing properties.
A mouse IgM allotypic determinant (Igh-6.5) recognized by a monoclonal rat antibody.
Authors: Kung J T , Sharrow S O , Sieckmann D G , Lieberman R , Paul W E 
Published: December 2022

Abstract
Two monoclonal rat anti-mouse IgM antibodies, Bet 1 and Bet 2, are described in this paper. Bet 1 defines a new allotypic determinant, Igh-6.5, expressed on IgM molecules in serum and on B lymphocytes, whereas Bet 2 recognizes a determinant on IgM molecules of all mouse strains tested. Both reagents bind to the IgM myeloma protein MOPC104E, but not to IgG myeloma proteins, including FLOPC21, MOPC21, and UPC10. Using serum from various mouse strains to inhibit the binding of Bet 1 to MOPC104E, 3 distinct inhibition patterns were found. BALB/c, DBA/2, and CBA sera inhibited strongly, C56BL/6 (B6), SJL, AKR, and NZB sera inhibited weakly, and A and AL sera showed no inhibition of binding of BET 1 to MOPC104E. All sera tested were equivalent in their inhibition of the binding of Bet 2 to MOPC104E. When spleen cells from different mouse strains were reacted with fluorescein-conjugated Bet 1 (F-Bet 1) and subjected to flow microfluorometry analysis, 3 types of staining patterns, corresponding to those obtained with the serum inhibition assay, were also found. The determinant recognized by Bet 1 is controlled by a gene linked to the Igh-C gene complex. C.AL20 behaved like AL, and C.B20 and BAB/14 behaved like B6, both in the serum inhibition assay and in flow microfluorometry analysis of spleen cells stained with F-Bet 1. In addition, the capacity of serum from individual (BALB/c X B6) X B6 backcross progeny to inhibit the binding of Bet 1 to MOPC104E was linked to the expression of the Ig-1a marker.
Changes in lectin receptor lateral mobilities accompany lymphocyte stimulation.
Authors: Leuther M D , Peacock J S , Krakauer H , Barisas B G 
Published: December 2022

Abstract
Changes in lateral mobilities of rabbit lymphocyte membrane components in response to succinyl concanavalin A (S Con A) have been studied by fluorescence photobleaching recovery (FPR). During hrs 0 to 3 after exposure to S Con A, lectin receptor mobilities on both T and B cells fall about 2-fold. Reduced mobility of T cell lectin receptors persists until hr 18. From hr 18 to 24 rapid recovery of original mobility occurs if and only if lectin is present. In contrast, nonresponding B cells recover original receptor mobility gradually over hr 4 to 48. Metabolic inhibitors added at hr 3 restore original receptor mobilities, but cytoskeletal disruptors have this effect on T cells only. From hr 0 to 15, washing lectin from the cell surface is decreasingly effective in restoring T cell receptor mobility. After hr 15, mobility cannot be enhance by lectin removal. Parallel DNA synthesis studies show that, for T cell stimulation, lectin must be present on the cell surface during hr 0 to 3 and 18 to 24. These are the periods when FPR measurements show lectin receptor mobilities being restricted and released, respectively. Stimulation of B cells by anti-Ig shows several interesting features. First, stimulation by intact anti-Ig fails to reduce the mobilities of Con A receptors in a manner similar to that produced by S Con A. Second, S Con A does reduce mobility of surface Ig. Thus, Con A receptors would appear to exert a unique anchorage modulation of mobilities of other membrane molecules.
Induction of immunoglobulin-secreting cells in the allogeneic mixed leukocyte reaction: regulation by helper and suppressor lymphocyte subsets in man.
Authors: Kotzin B L , Benike C J , Engleman E G 
Published: December 2022

Abstract
The existence of functionally distinct T lymphocyte subsets in man, initially demonstrated with heteroantisera, has been confirmed with monoclonal reagents. Two major subsets have been defined: Leu-2 cells, which effect cell mediated lymphocytotoxicity (CML), and Leu-3 cells, which amplify CML and other T cell functions. This study is an effort to determine the effects of these subsets on the immunoglobulin secretion induced in the human mixed leukocyte reaction (MLR). T cells were separated from non-T cells by rosetting with sheep erythrocytes and were fractionated into Leu-2 and Leu-3 subsets by solid phase immunoabsorption with monoclonal antibodies. T cell subsets were cultured with autologous non-T cells and irradiated allogeneic stimulator non-T cells. Secretion of IgM and IgG was measured by a reverse hemolytic plaque assay. MLR-induced antibody secretion was specifically dependent on the Leu-3 T lymphocyte subset. The Leu-2 subset was incapable of generating large numbers of IgM- or IgG-secreting cells, and, in fact, suppressed the Leu-3-induced response. Exposure of Leu-3 cells to a dose of irradiation sufficient to prevent their proliferation in MLR did not reduce induced immunoglobulin secretion. Leu-2-mediated suppression, however, was sensitive to low dose irradiation. Thus Ig secretion in human MLR is regulated by a balance of helper activity from the Leu-3 subset and suppressor activity from the Leu-2 subset.
Inhibition of IgE-mediated histamine release from rat basophilic leukemia cells and rat mast cells by inhibitors of transmethylation.
Authors: Morita Y , Siraganian R P 
Published: December 2022

Abstract
This study evaluated the effect of inhibitors of transmethylation on histamine release from rat mast cells and rat basophilic leukemia cells. IgE-mediated histamine release from rat basophilic leukemia cells (RBL-2H3 cells) was inhibited by 3-deazaadenosine (DZA) in the presence of L-homocysteine thiolactone (Hcy) or the combination of adenosine, erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA), and Hcy in a dose-dependent fashion. There were no significant changes in the cellular cAMP levels by these inhibitors. Histamine release induced by anti-IgE or dextran from normal rat mast cells was also blocked by DZA plus Hcy in a dose-dependent manner. DZA at 10(-3) M in the presence of 10(-4) M Hcy or the combination of 10(-3) M adenosine, 10(-4) M EHNA, and 10(-3) M Hcy inhibited lipid (perhaps phospholipid) methylation into RBL-2H3 cells without affecting choline incorporation. In the presence of 10(-3) M DZA plus 10(-4) M Hcy there was a 170-fold increase in [35S]AdoHcy with the concomitant appearance of 3-deaza-AdoHcy when the cells were incubated with [35S]methionine, thus indicating that these drugs inhibited methylation reaction(s) through the intracellular accumulation of AdoHcy and 3-deaza-AdoHcy. In contrast, histamine release from rat mast cells induced by the calcium ionophore A23187, compound 48/80, polymyxin B, or ATP was not inhibited by these compounds. These results suggest that IgE- or dextran-mediated histamine release involves methylation reactions(s), whereas the other secretagogues bypass this early step.
Characterization of the human complement (c3b) receptor with a fluid phase C3b dimer.
Authors: Arnaout M A , Melamed J , Tack B F , Colten H R 
Published: December 2022

Abstract
The interaction of C3b receptor with C3b, the major cleavage product of C3, elicits important biologic functions, such as enhanced phagocytosis and release of cellular enzymes. We determined the binding kinetics and binding isotherm of C3b-receptor interaction by using human cells and fluid phase C3b generated by trypsin cleavage of purified native C3. 125I labeled C3b was separated into 2 molecular species, a dimer and a monomer by column chromatography. We found that dimeric C3b bound to human erythrocyte C3b receptors with an affinity that was more than 25 times that of the monomer. 125I dimeric C3b did not bind to sheep red blood cells, which lack the C3b receptor, nor to trypsinized or 2-mercaptoethanol treated normal human red blood cells, 2 methods for abrogating the immune adherence activity. Binding of 125I fluid phase C3b dimer to the C3b receptor was specific, saturable (about 90 ng of C3b dimer bound maximally per 1 X 10(9) red blood cells), reversible (in the presence of a 100-fold molar excess of unlabeled ligand), and of moderate affinity (Kd about 9.53 nM). The equilibrium binding constants were similar with the various cells tested. Binding was characterized by rapid on and off rates and did not exhibit ligand cooperativity. This specific interaction reached a steady state within 10 to 15 min at 0 degrees C; 50% of specifically bound ligand dissociated from its binding site on human red blood cells in approximately 1 min at 0 degrees C. The density of C3b receptors on human red blood cells, polymorphonuclear leukocytes, monocytes, and B lymphocyte-enriched preparations was 360, 20,000, 30,000, and 21,000 receptors/cell, respectively.
A new possible regulatory system for protein phosphorylation in human peripheral lymphocytes. II. Possible relation to phosphatidylinositol turnover induced by mitogens.
Authors: Ku Y , Kishimoto A , Takai Y , Ogawa Y , Kimura S , Nishizuka Y 
Published: December 2022

Abstract
Ca++-activated, phospholipid-dependent protein kinase present in human peripheral lymphocytes requires a small amount of diacylglycerol in addition to phospholipid, particularly at lower concentrations of Ca++. It is necessary that such diacylglycerol contain unsaturated fatty acid at least at position 2. Saturated diacylglycerols such as dipalmitin and distearin are far less effective. Kinetic analysis indicates that unsaturated diacylglycerol greatly increases the apparent affinity of the enzyme for phospholipid, and sharply decreases the Ca++ concentration to the micromolar range that gives rise to the maximum enzyme activation. Among various phospholipids tested, phosphatidylserine is most active in supporting enzymatic activity. Phosphatidylinositol and phosphatidylethanolamine are less effective. Phosphatidylcholine, phosphatidic acid, sphingomyelin, and lysophosphatidylcholine are inert. It is most likely, therefore, that various lymphocyte mitogens induce specific hydrolysis of phosphatidylinositol to produce such an active unsaturated diacylglycerol, which in turn serves as a second messenger for the selective activation of this unique protein kinase. Dibucaine and chlorpromazine appear to interact with phospholipid and thereby inhibit the activation process of this enzyme. Cyclic nucleotide-dependent protein kinases are not susceptible to these phospholipid-interacting drugs.
Helper cells active in the generation of cytotoxicity to a syngeneic tumor.
Authors: Hancock E J , Kilburn D G , Levy J G 
Published: December 2022

Abstract
We have examined a population of thymic lymphocytes that augment the generation in vitro of specific cytotoxic T cells against P815.X2, a syngeneic tumor in DBA/2 mice. These helper cells are evident in the thymus of DBA/2 mice 5 to 7 days after subcutaneous injection of live P815 cells. They are Thy-1 positive, resistant to gamma radiation, antigen specific, and appear to exert their influence most effectively when added at the beginning of the culture.
Virus-immune and alloreactive response characteristics of thymocytes and spleen cells from young mice.
Authors: Schwartz D H , Doherty P C 
Published: December 2022

Abstract
Thymocytes from 3-day-old mice generate a strong, virus-immune cytotoxic T lymphocyte (CTL) response when primed in irradiated, vaccinia-infected recipients. Effector potential is not detected in spleen until day 4 or 5, when alloreactive precursors may also be present. Mice of 8 days or older survive inoculation with large doses of vaccinia virus, and generate significant CTL activity in spleen. There is, unlike the situation described by others for Listeria antigens, no major defect in stimulator function for spleens of 1-wk-old mice. This is true for both the virus-specific and alloreactive CTL responses.
Establishment of unresponsiveness in primed B lymphocytes in vivo.
Authors: Nelson-Rampy P A , Parks D E , Weigle W O 
Published: December 2022

Abstract
As an approach to examine the influence of the state of cellular activation on the ability to tolerize B cells, the induction of unresponsiveness in human gamma-globulin-(HGG) primed B lymphocytes was studied in an adoptive transfer system. In contrast to transferred normal spleen cells, spleen cells from HGG-primed mice are not readily rendered unresponsive when exposed to the tolerogen, deaggregated HGG (DHGG), in irradiated recipients. A kinetic study showed that unfractionated primed spleen cells do not respond to an antigenic challenge given between 6 and 10 days after cell transfer and injection of DHGG, indicating that they are transiently depressed. In contrast, isolated primed B cells are tolerized when transferred to recipients and treated with DHGG in the absence of T cells. Furthermore, primed B cells exposed to tolerogen in the recipients do not recover the ability to respond to HGG either after a secondary challenge with AHGG given up to 14 days after transfer, or after 2 consecutive challenges given on days 14 and 24 after transfer. The presence of primed T cells at the time of tolerization interferes with the induction of unresponsiveness in these primed B cells. These studies suggest that the presence of primed T cells is responsible for the inability to tolerize unfractionated primed spleen cells populations and that primed B cells themselves are not intrinsically resistant to the induction of unresponsiveness.
A C1-inhibitor-complex assay (INCA): a method to detect C1 activation in vitro and in vivo.
Authors: Hack C E , Hannema A J , Eerenberg-Belmer A J , Out T A , Aalberse R C 
Published: December 2022

Abstract
A radioimmunoassay (the C1-inhibitor-complex assay, INCA) is described for the detection of complexes that are composed of at least C1s and C1-inhibitor. This INCA is based on demonstrating that C1s and C1-inhibitor (C1-In) are linked: after an incubation with anti-C1s-Sepharose, bound C1sC1-In complexes are detected by 125I-anti-C1-In. C1sC1-In complexes were prepared by the addition of a slight excess of C1s to normal human serum (NHS). As little as 2 ng C1-In bound to C1s was detected. Additional free C1s in serum hardly influenced the detection of C1sC1-In complexes. Complexes presumably composed of C1rC1s(C1-In)2 were generated by the addition of aggregated IgG to NHS. This generation was inhibited by lowering the temperature to 0 degrees C, and by EDTA, and depended on the concentration of aggregated IgG. These complexes had a sedimentation value of approximately 9S. Complexes of C1s and C1-In were also generated in NHS by the addition of DNP-albumin and protein A, but not by zymosan. The INCA was applied to blood samples from normal donors and patients. Sixteen out of 19 samples from patients with acute glomerulonephritis contained increased amounts of C1rC1s(C1-In)2 complexes as compared with the amounts in blood samples from normal donors. The INCA provides a useful tool to assess the activation of C1 in the presence of C1-In, both in vitro and in vivo.
Differential glycosylation of murine B cell and spleen adherent cell Ia antigens.
Authors: Cullen S E , Kindle C S , Shreffler D C , Cowing C 
Published: December 2022

Abstract
Examination of I-A and I-E molecules from purified B cells and splenic adherent cells from various haplotypes revealed a consistent difference in isoelectric focusing (IEF) that has been localized to the alpha-chain. alpa-Chains from B cells appeared heterogeneous and contained acidic IEF bands absent from the adherent cell I-A molecules. No difference in Ia beta-chain or H-2 IEF patterns was observed when B cell and adherent cell preparatios were compared when B cell and adherent cell preparations were compared. I-A alpha-chain preparations from the 2 cell sources showed no differences in 3H-leucine-labeled tryptic peptides separated by reverse-phase high-pressure liquid chromatography. Digestion with neuraminidase, kinetics of labeling, and subcellular distribution indicated that the extra acidic IEF bands in B cell Ia represent a mature, more heavily sialated form of alpha-chain that is not present in adherent cells. The selective differential glycosylation of B cell and adherent cell Ia could have some relation to the function of those cell types or to cell type-specific recognition of those cells.
The metabolic relationships of the immunoglobulins in fish serum, cutaneous mucus, and bile.
Authors: Lobb C J , Clem L W 
Published: December 2022

Abstract
Passive administration of homologous, radioiodinated, purified high m.w. (HMW) or low m.w. (LMW) serum immunoglobulin (Ig) into the sheepshead, a marine teleost, showed that the LMW Ig was neither an extracellular precursor nor a degradation product of the HMW Ig. These studies also showed that the half-lives of the HMW and LMW Ig were statistically identical, i.e., approximately 16 days. Furthermore, this work demonstrated that the Ig found in cutaneous mucus and bile were not due to transudation or active transport of either the serum HMW or LMW Ig. The implications of these later findings, coupled with previous physicochemical characterizations of the Ig in fish secretions, support the hypothesis that fish, similar to higher vertebrates, have a secretory immune system.
Effects of prostaglandin D2 and theophylline on rat serosal mast cells: discordance between increased cellular levels of cyclic AMP and activation of cyclic AMP-dependent protein kinase.
Authors: Holgate S T , Winslow C M , Lewis R A , Austen K F 
Published: December 2022

Abstract
Previous studies have shown that perturbation of the mast cell IgE-Fc receptor activates adenylate cyclase so as to raise cellular levels of cyclic AMP and to activate cyclic AMP-dependent protein kinase. Theophylline, an inhibitor of cytoplasmic cyclic nucleotide phosphodiesterase, raises cellular cyclic AMP levels, activates Type I and Type II cytoplasmic cyclic AMP-dependent protein kinase isoenzymes, and inhibits immunologic mediator release in a dose-dependent fashion. Since the EC50 values for each of these effects are similar (8 to 9.5 mM), it seems likely that a relationship exists between the activation of cyclic AMP-dependent protein kinase and the inhibition of mediator release. Such inhibition could be due to either to the uncovering of an inhibitory protein by phosphorylation or to the depletion of cyclic AMP-dependent protein kinase holoenzyme, which is essential for productive IgE-Fc receptor-induced activation-secretion coupling. PGD2, which also raises mast cell cyclic AMP levels in a dose-dependent fashion and interacts synergistically with theophylline in this regard, fails to suppress mediator release alone or to add to the inhibitory effect of theophylline. The finding that PGD2 also fails to activate cyclic AMP-dependent protein kinase suggests that the adenylate cyclase stimulated by this agonist is not linked to the mast cell activation-secretion response.
An antigenic determinant of human beta 2-microglobulin masked by the association with HLA heavy chains at the cell surface: analysis using monoclonal antibodies.
Authors: Liabeuf A , le Borgne de Kaouel C , Kourilsky F M , Malissen B , Manuel Y , Sanderson A R 
Published: December 2022

Abstract
Four anti-human beta 2-microglobulin monoclonal antibodies were produced against whole lymphoid cells or against urinary beta 2-microglobulin. Their reactivity was fully inhibited by purified soluble beta 2-microglobulin. The B1.1G6, C23.24.2, and B2.62.2 antibodies bound either to free or to HLA-complexed beta 2m. They recognized the same or very close determinants, since they achieved mutual blocking. In contrast, the C21.48A1 antibody did not bind to the cell surface and did not recognize the same determinant on the purified beta 2-microglobulin molecule as the others. It was able to bind and to form a specific complex with membrane beta 2-microglobulin only, once separated from the HLA heavy chain. These data strongly suggest that the C21.48A1 antigenic determinant might be hidden when the beta 2-microglobulin is complexed with the HLA heavy chains at the cell surface.