bluuebunny/crossref_metadata_2025_split huggingface dataset:
HLA-B27 antigenicity: antibodies against the chemically synthesized 63-84 peptide from HLA-B27.1 display alloantigenic specificity and discriminate among HLA-B27 subtypes.
Authors: Rojo S , López de Castro J A , Aparicio P , Van Seventer G , Bragado R 
Published: December 2022

Abstract
A chemically synthesized peptide with an amino acid sequence identical to that of the segment spanning residue 63-84 of the major HLA-B27.1 subtype antigen has been obtained. Specific antibodies were raised in rabbits against this peptide, coupled to keyhole limpet hemocyanin carrier. These antibodies lysed lymphoblastoid cell lines expressing HLA-B27.1 in a complement-mediated cytotoxicity assay. They lysed neither B27-negative target cells, nor B27-positive cells expressing other B27 subtype antigens. Complement-mediated lysis of B27.1-positive targets was inhibited by free peptide and by peptide coupled to an unrelated carrier. In addition, the lytic action of the rabbit antiserum was blocked by a monoclonal antibody with no complement-activating capacity that under the conditions of the assay, was specific for HLA-B27. These results indicate that rabbit antibodies against the 63-84 peptide recognize the native HLA-B27.1 antigen; this antiserum is allospecific in character; and it discriminates among B27 subtypes. Thus the data provide direct evidence on the contribution of the hypervariable region spanning residues 63-84 to the alloantigenic specificity of HLA-B27.
Structural relationships between the DR beta 1 and DR beta 2 subunits in DR4, 7, and w9 haplotypes and the DRw53 (MT3) specificity.
Authors: Matsuyama T , Schwenzer J , Silver J , Winchester R 
Published: December 2022

Abstract
The class II molecules of DR4, DR7, and DRw9 haplotypes were analyzed by immunoprecipitation, followed by two-dimensional gel electrophoresis and N-terminal amino acid sequencing. By using HLA-DR chain-specific monoclonal antibodies, two distinct DR beta-chains were identified. One beta-chain, designated DR beta 2, had a characteristic acidic mobility. In all three DR types the DR beta 2-chains were indistinguishable by two-dimensional gel electrophoresis and partial N-terminal sequencing. A second DR beta-chain designated beta 1 had a more basic mobility on two-dimensional gel electrophoresis, and differed from the DR beta 2-chains by the consistent presence of phenylalanine at position 18. In contrast to the DR beta 2-chains, the DR beta 1-chains were clearly polymorphic, with specific amino acid sequence differences characteristic of each DR type. The monoclonal antibodies 109d6 and 17-3-3S, recognizing distinct polymorphic epitopes similarly correlated with the DRw53 allospecificity, were found to react with different DR beta-chains. The epitope recognized by monoclonal antibody 109d6 was identified on the DR beta 2-chain in the prototypic DR4, DR7, and DRw9 cell lines. However, the DR7, Dw11, DQw3 cell line BEI was unreactive with antibody 109d6 by either immunofluorescence or immunoprecipitation despite the presence of the DRw53 allodeterminant on this cell line. The other DRw53-like monoclonal antibody, 17-3-3S, reacted with the DR beta 1-rather than the DR beta 2-chain in all DR4 and DR7 cell lines tested, including the cell line BEI. However, antibody 17-3-3S did not react with the DRw53-positive DRw9 cell line ISK. These studies suggest that the DRw53 allospecificity is more complex than previously thought and may comprise a number of distinct epitopes encoded by two different DR beta loci.
Heterogeneity among T cells in intracellular free calcium responses after mitogen stimulation with PHA or anti-CD3. Simultaneous use of indo-1 and immunofluorescence with flow cytometry.
Authors: Rabinovitch P S , June C H , Grossmann A , Ledbetter J A 
Published: December 2022

Abstract
Measurement of intracellular ionized calcium concentrations ([Ca2+]i) has been indispensable in elucidating the central role of [Ca2+]i as a trigger of cellular responses to activating stimuli. Such studies have employed the dye quin2, which has not been readily adapted to analysis of individual small cells. We show here that the calcium response of large numbers of single cells can be analyzed with the use of flow cytometry and the recently described dye, indo-1. Such analyses demonstrate for the first time the heterogeneous nature of the [Ca2+]i response to mitogenic stimuli within populations of peripheral blood lymphocytes (PBL). By simultaneous quantitation of one- or two-color surface immunofluorescence labels, some of this heterogeneity of [Ca2+]i response in PBL is shown to be related to cellular immunophenotype. Almost all T cells responded to anti-CD3 antibody; however, the response is greater among CD4+ than CD8+ cells, and within the CD4+ population the rate of response to stimulation by antibody to CD3 differed between subpopulations defined by expression of the common leukocyte marker p220. In contrast, not all T cells responded to phytohemagglutinin (PHA), even at very high doses. As with anti-CD3, after stimulation with PHA, CD4+ cells showed a larger proportion of responding cells than did CD8+ cells. In separate experiments, indo-1 was found not to impair reproductive viability of PBL, thereby providing the potential for analysis of functional activity after the separation of cells by sorting on the basis of the [Ca2+]i response to stimuli. Mixing experiments indicated that a response of a subpopulation representing as little as 0.3% of total cells could be readily detected. Thus, the flow cytometric assay with indo-1 is the first technique that allows the quantitative analysis of response differences of small subpopulations of cells and intercellular variation in [Ca2+]i.
Functional modifications of alloreactive T cell clones infected with HTLV-I.
Authors: Suciu-Foca N , Rubinstein P , Rohowsky-Kochan C , Cai J , Popovic M , Gallo R C , King D W 
Published: December 2022

Abstract
Two alloreactive T cell clones with anti-HLA-DR1 specificity showed significant alterations of cognitive and functional characteristics after infection with human T cell leukemia virus (HTLV-I). Similar to HTLV-I-infected lines derived from immunologically uncommitted lymphocytes, the transformed clones displayed blastogenic mixed lymphocyte culture (MLC) responses to cells carrying any of the allelic variants of human HLA-D/DR antigens, including self. Although these two clones were originally able to provide allospecific help only to B cells expressing the DR1 antigen, after infection with HTLV-I they stimulated B cells of any HLA-D/DR phenotype to produce immunoglobulin in cultures. The helper inducer activity of the transformed clones remained susceptible to the effect of monoclonal antibody anti-LDA1 that inhibits the helper function of normal human T cells. One of these clones (207TK), which before infection specifically killed DR1-positive target cells, lost its killing ability. The other clone (19TK) although originally noncytotoxic, acquired natural killer-like function after transformation. Study of the rearrangement of the genes coding for the beta-chain of the T cell antigen receptor revealed no differences between the wild (noninfected) and mutant (infected) clones. There was, however, an increased level of this message, as well as of the message encoded by the beta-chain gene of HLA-DR in the mutant clones. Such changes may be related to transacting transcriptional effects induced by the human T cell lymphotropic virus HTLV-I.
Mitogenic activation of B cells in vitro: the properties of adherent accessory cells as revealed by partition analysis.
Authors: Kettman J R , Soederberg A , Lefkovits I 
Published: December 2022

Abstract
The requirement of B cells activated by mitogen (dextran sulfate plus lipopolysaccharide) for accessory cells was studied by partition analysis. Small numbers of splenic B cells were activated to clonal growth, as determined by visual inspection, and to immunoglobulin (Ig) synthesis, as determined by release of Ig into the culture fluid. By placing irradiated adherent cells in the periphery of the microculture wells and forcing responding cells to different areas of the well (slant experiments), it was observed that no cell contact was necessary for B cell activation, and that "promoted" contact ("Rock and Roll" experiments) does not increase the efficiency of activation. Sequential microcultures suggest that only some irradiated adherent cells act as accessory cells, but they can perform this function to more than one B cell. Attempts to perform limiting dilution analysis by varying irradiated adherent cell input showed non-single-hit behavior. When the data were rearranged, taking into account the distribution of irradiated adherent cells, then single-hit behavior with about 1 to 5% of irradiated adherent cells acting as an accessory cells for B cell clonal activation was observed. The evidence suggests that an uncommon irradiated adherent cell releases a soluble factor necessary for B cell activation and/or clonal proliferation.
Mechanism of defective NK cell activity in patients with acquired immunodeficiency syndrome (AIDS) and AIDS-related complex. I. Defective trigger on NK cells for NKCF production by target cells, and partial restoration by IL 2.
Authors: Bonavida B , Katz J , Gottlieb M 
Published: December 2022

Abstract
Peripheral blood from patients with acquired immunodeficiency syndrome (AIDS) or AIDS-related complex (ARC) exhibits poor NK activity in the 51Cr-release assay. The present studies were undertaken to investigate the mechanism underlying the observed defective NK cytotoxic activity. On the basis of our studies on the mechanism of natural killer cell-mediated cytotoxicity (NKCMC), a defective NK cell can result from lack or decreased frequency of effector cells, inability to recognize and bind the target cell, failure to be activated for the release of NK cytotoxic factors (NKCF), and/or failure to synthesize or secrete NKCF. Each of these various possibilities was examined. Single cell analysis revealed that the frequency of NK cells was comparable to controls, and although the NK cells bind to the NK-sensitive target, the bound target is not lysed. These results suggested that the defect in NK cells was not due to depletion of NK cells or to a defect in recognition structures, but that it was located at the postrecognition event. We previously demonstrated that after binding to target, the NK cell is stimulated to release NKCF in the supernatants and NKCF lyse specifically NK-sensitive targets. Accordingly, we investigated the activation of NK cells from AIDS and ARC patients for release of NKCF. After coculture with the stimulator cell, the patients' NK cells failed to release active NKCF in the supernatant. However, the cells released NKCF after stimulation with the lectin Con A or a mixture of TPA and ionophore, albeit to a lesser extent than controls. These results suggested that AIDS and ARC NK cells are defective in the trigger involved in release of NKCF. Further studies were done to investigate whether the immunomodulator IL 2 can restore the functional activity of the defective NK cells. Treatment with IL 2 resulted in augmented NK cytolytic activity, but did not reach control levels of activated cells from normal controls. Furthermore, the patients' IL 2-treated cells recover partially the ability to be stimulated by NK cells and to release NKCF. These results suggest that the trigger for NKCF production and the cytolytic function of the patients' NK cells are regulated by IL 2. By delineating the stage at which the AIDS and ARC NK cells are defective, it is now possible to monitor their recovery and to investigate the effect of various biologic response modifiers in restoring NK activity.
Concentrations of glandular kallikrein in human nasal secretions increase during experimentally induced allergic rhinitis.
Authors: Baumgarten C R , Nichols R C , Naclerio R M , Proud D 
Published: December 2022

Abstract
We have previously demonstrated that a mixture of bradykinin and lysylbradykinin is generated in nasal secretions during the immediate allergic response to allergen. The present studies were performed to determine whether glandular kallikrein plays a role in kinin formation during the allergic reaction. Allergic individuals (n = 7) and nonallergic controls (n = 7) were challenged intranasally with appropriate allergen, and nasal lavages obtained before and after challenge were assayed for immunoreactive glandular kallikrein as well as for histamine, kinins, and N-alpha-tosyl-L-arginine methyl esterase (TAME-esterase) activity. The increase in postchallenge immunoreactive glandular kallikrein levels above baseline was significantly greater (p less than 0.01) for the allergic group (16.3 +/- 14 ng/ml; means +/- SD) than for the nonallergic controls (1.0 +/- 1.9 ng/ml). Increased levels of immunoreactive glandular kallikrein correlated with increases in kinins, histamine, and TAME-esterase activity and with the onset of clinical symptoms. Characterization of immunoreactive glandular kallikrein purified from postchallenge lavages by immunoaffinity chromatography confirmed the identity of this material as an authentic glandular kallikrein on the basis of its inhibition by protease inhibitors and by monospecific antibody to tissue kallikrein, its chromatographic behavior on gel filtration, and its ability to generate lysylbradykinin from highly purified human low m.w. kininogen. The specific activity of this purified material, in terms of kinin generation from kininogen, was very similar to that for authentic glandular kallikrein, suggesting that most if not all of the immunoreactive material purified from nasal lavages represented active enzyme. Inhibition studies by using pooled postchallenge lavages suggest that the majority of the kinin generating activity in these samples was due to glandular kallikrein. We conclude, therefore, that glandular kallikrein is secreted during the allergic response and can contribute to the formation of the lysylbradykinin produced during the allergic reaction.
Tumor dormancy. I. Regression of BCL1 tumor and induction of a dormant tumor state in mice chimeric at the major histocompatibility complex.
Authors: Siu H , Vitetta E S , May R D , Uhr J W 
Published: December 2022

Abstract
The growth of the BCL1 tumor in murine H-2 chimeras was studied. Lethally x-irradiated BALB/c mice were reconstituted with C57BL/6 bone marrow that had been depleted of T cells. When chimerism was established 90 to 120 days later, large doses of BCL1 cells were injected. The tumor grew progressively, reaching a peak level of as many as 10(9) tumor cells per animal by 40 days after inoculation. After that time, the tumor regressed in all the chimeric animals, and by 100 days after inoculation, virtually all the animals appeared disease free as judged by an absence of BCL1-idiotype-positive cells in the spleen and peripheral blood, a normal spleen size, and absence of an elevated white blood cell count. Such animals were followed for as long as 8 mo after tumor inoculation and remained disease free. However, transfer of graded numbers of splenocytes from these animals into normal BALB/c recipients resulted in development of tumor in recipients receiving 100 or more spleen cells. These results indicate a large tumor burden in the spleen of each donor, namely, 10(6) to 10(7) BCL1 cells. The present model should facilitate characterization of the mechanisms underlying tumor dormancy.
The effects of hexose 6-O-sulfate esters on human natural killer cell lytic function.
Authors: Chambers W H , Oeltmann T N 
Published: December 2022

Abstract
Natural cell-mediated cytotoxicity (NCMC) is inhibited by some neutral hexoses and hexose phosphates at 25 to 100 mM concentrations. In this study we describe the effects of hexose 6-O-sulfate esters on NCMC against K-562 target cells. Mannose 6-sulfate, galactose 6-sulfate, N-acetylglucosamine 6-sulfate, and N-acetylgalactosamine 6-sulfate inhibit NCMC in a dose-dependent manner at concentrations of 10 mM and below. Inhibitory effects of mannose 6-sulfate and galactose 6-sulfate were evident at concentrations as low as 1.25 mM. The neutral forms of these sugars, glucose and glucose 6-sulfate, did not inhibit NCMC over this range of concentrations. Comparison of the inhibitory effects of sulfated and phosphorylated forms of mannose and galactose indicated that the sulfated forms are much more potent inhibitors. Formation of effector cell:target cell conjugates was unaffected by the presence of sugar sulfates. Calcium pulse experiments demonstrated that inhibitory effects of sugar sulfates were exerted after the Ca++-dependent triggering step in the NK lytic process. Kinetic studies showed that addition of sugars as long as 60 min after initiation of cultures yielded potent inhibitory effects. Sugar sulfates were not toxic for effector cell populations and effectors were not refractory for lytic function after removal of sugars. Sugar sulfates were inhibitory against multiple tumor types in both human and murine NK lytic assays. These results suggest that the sugar sulfates inhibit NK cells at a postconjugation, posttriggering step involving lectin-like receptors or lectin-like molecules.
Depletion of donor Ia+ cells before transplantation does not prolong islet allograft survival.
Authors: Gores P F , Sutherland D E , Platt J L , Bach F H 
Published: December 2022

Abstract
Culture of pancreatic islets reduces their immunogenicity and results in prolonged graft survival after allotransplantation. The mechanism by which immunogenicity is reduced by culture is not known, but it has been suggested that prolonged graft survival is the result of the depletion of Ia+ cells from the graft. We studied the effect of eliminating Ia+ cells from islets before allotransplantation. Freshly isolated islets were incubated with anti-Ia serum plus complement or with monoclonal antibody to IAk plus complement or were left untreated before transplantation beneath the renal capsule of diabetic recipients. Incubation with anti-Ia serum plus complement eliminated intra-islet IA+ cells as demonstrated by indirect immunofluorescence staining. Incubation with monoclonal antibody to IAk plus complement significantly reduced but did not eliminate IA+ cells. Neither pretreatment regimen influenced survival of islet allografts placed beneath the renal capsule. However, untreated islets injected into the portal circulation were rejected in a low percentage of cases. We conclude that decreased immunogenicity observed after culture is not due solely to the depletion of Ia+ cells and that the site of engraftment has an important impact on graft survival.
Studies of experimental allergic encephalomyelitis by using encephalitogenic T cell lines and clones in euthymic and athymic mice.
Authors: Sakai K , Namikawa T , Kunishita T , Yamanouchi K , Tabira T 
Published: December 2022

Abstract
The role of T-T cell interactions in the clinical course of acute experimental allergic encephalomyelitis (EAE) in mice was investigated. Myelin basic protein (MBP)-reactive and encephalitogenic T cell clones were established from long-term lines derived from susceptible strain SJL/J mice and resistant strain DDD/1 mice. The lines and clones from DDD/1 mice were obtained by immunization of congenitally athymic mice of DDD/1 origin, which had been reconstituted with syngeneic Lyt-2+-depleted splenic T cells. The clones derived from both strains bore surface phenotypes of Lyt-1+, 2- and L3T4+, and proliferated well in response to rat, rabbit, bovine, and guinea pig MBP in the presence of antigen-presenting cells with I-As. Passive EAE could be induced in syngeneic normal recipients by these clones as well as by the lines from which the clones were derived. The clinical features of the clone-induced EAE were essentially the same as those of the line-induced EAE. Furthermore, DDD/1 athymic recipients developed signs of acute EAE by the adoptive transfer of I-A-compatible syngeneic and allogeneic T cell clones, in which there was no significant difference in time of onset, maximum severity, or prognosis. These results indicate that the entire clinical course of acute EAE can be elicited by a single population of MBP-reactive T cells in the absence of the thymus and other populations of primed or unprimed T cells.
Construction of rat-mouse T cell hybridomas that express regulatable rat interleukin 2 receptor.
Authors: Kohda H , Uede T , Yuasa H , Yamaki T , Osawa H , Diamantstein T , Yodoi J , Kikuchi K 
Published: December 2022

Abstract
Spleen cells obtained from Lewis rats were cultured with 4 micrograms/ml Con A for 96 hr, and activated cells were fused with BW5147 mouse T lymphoma cells. Seven clones obtained by fusion expressed rat IL 2R. The expression of rat IL 2R on those hybrid cells could be up-regulated by IL 2 itself, ATL-derived factor, and TPA and CA++ ionophore. Those IL 2R could be down-regulated by murine MoAb ART-18 that detects rat IL 2R. All hybrid clones produced IL 2 constitutively. IL 2 produced by hybrid cells bound to its receptor and promoted the proliferation of hybrid cells in some clones. Incubation of cells with exogenous IL 2 resulted in the proliferation of hybrid cells, whereas the proliferation of some clones was inhibited by exogenous IL 2, indicating that IL 2 had bifunctional properties on cell growth. Rat IL 2R from 6H2-F9 hybrid cells was studied by both one- and two-dimensional SDS-PAGE with ART-18. The IL 2R derived from 6H2-F9 cells had 72,000 to 77,000 and 40,000 to 48,000 m.w. major components under nonreducing conditions, and had 50,000 to 56,000 m.w. major and 35,000 to 38,000 m.w. minor components under reducing conditions. The 110,000 m.w. component, the third component of IL 2R, was constantly observed in 6H2-F9 hybrid cells.
Role of specific IgE antibodies in peroxidase (EPO) release from human eosinophils.
Authors: Khalife J , Capron M , Cesbron J Y , Tai P C , Taelman H , Prin L , Capron A 
Published: December 2022

Abstract
After the demonstration of cytophilic IgE immunoglobulins (Ig) on human blood and lung eosinophils, their role in cell activation was studied by eosinophil peroxidase (EPO) assay. Hypodense human eosinophils from filariasis-infected patients were activated by anti-human Ig or various antigens. A selective release of EPO occurred after incubation with anti-human IgE, but not with anti-human IgG. The activation by antigens showed a strict antibody specificity of cytophilic IgE antibodies. The direct involvement of IgE antibodies in activation by the specific antigen was evidenced by inhibition experiments with aggregated human IgE myeloma protein. Circulating IgE antibodies exhibiting the same specificity and able to induce EPO release were detected in the sera from filariasis patients by a passive sensitization assay. Only the hypodense eosinophils were able to release EPO after IgE-dependent activation both in the direct assay and in the passive sensitization test, confirming the functional heterogeneity of human eosinophils. These results suggest that the interaction between IgE antibodies and human eosinophils can play a role both in protective immunity and pathology by releasing active pharmacologic mediators.