bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibodies to human immunodeficiency virus in human sera induce cell-mediated lysis of human immunodeficiency virus-infected cells.
Authors: Ojo-Amaize E A , Nishanian P , Keith D E , Houghton R L , Heitjan D F , Fahey J L , Giorgi J V 
Published: December 2022

Abstract
The capacity of human immunodeficiency virus (HIV) antibody-positive sera from homosexually active men without acquired immune deficiency syndrome to lyse the HIV-infected T cell lines MOLT-4f and CCRF-CEM (CEM) in cooperation with lymphocytes from normal donors was investigated. Twenty-seven HIV antibody-positive sera, most of which enhanced the killing of HIV-infected MOLT-4f and CEM target cells by normal mononuclear cells were studied in detail. HIV antibody-positive sera resulted in lysis at dilutions as high as 1/10,000. HIV antibody-negative sera did not augment lysis of infected target cells. In addition, lysis of uninfected targets was not enhanced in the presence of HIV antibody-positive sera. Because fractionation of the HIV antibody-positive sera on a protein A affinity column resulted in recovery of the activity from the IgG fraction, the extra cytotoxic activity mediated by nonimmune cells in the presence of immune sera appears to be antibody-dependent. Furthermore, the cytotoxic effector cells were in the nonrosetting fraction of lymphocytes and expressed Leu-11 (cluster designation (CD)15) antigens, which is characteristic of cells participating in antibody-dependent cellular cytotoxicity reactions. The antibody specificity of the sera, determined by radioimmunoprecipitation, provides evidence that antibody-dependent cellular cytotoxicity can occur even when there are no detectable antibodies directed against gag proteins. Sera which lacked detectable antibodies to the envelope protein gp120 by radioimmunoprecipitation did not mediate antibody-dependent cellular cytotoxicity.
Schistosoma mansoni polypeptides immunogenic in mice vaccinated with radiation-attenuated cercariae.
Authors: Dalton J P , Strand M 
Published: December 2022

Abstract
We compared the humoral immune response of mice protected against Schistosoma mansoni by vaccination with radiation-attenuated cercariae to that of patently infected mice, and we identified antigens that elicit a greater, or unique, immune response in the vaccinated mice. These comparisons were based upon radioimmunoprecipitations and immunodepletion of [35S]methionine-labeled schistosomular and adult worm polypeptides, followed by one- and two-dimensional polyacrylamide gel analyses. The humoral responses of patently infected mice and of mice vaccinated once were remarkably similar and were directed against schistosome glycoproteins ranging in molecular size from greater than 300 to less than 10 kDa. Exposing mice to a second vaccination resulted in a marked change in the immune response, to one predominantly directed toward high molecular size glycoproteins. Sequential immunodepletion techniques identified five schistosomular and seven adult worm antigens that showed a greater or unique immunogenicity in vaccinated mice as compared with patently infected mice. These adult worm antigens were purified by preparative sequential immunoaffinity chromatography and used to prepare a polyclonal antiserum, anti-irradiated vaccine. This antiserum bound to the surface of live newly transformed and lung-stage schistosomula, as assessed by immunofluorescence assays, and was reactive with a number of 125I-labeled schistosomular surface polypeptides, including a doublet of 150 kDa that was also recognized by sera of vaccinated mice but not by sera of patently infected mice.
Purification and partial sequence analysis of murine B cell growth factor II (interleukin 5).
Authors: McKenzie D T , Filutowicz H I , Swain S L , Dutton R W 
Published: December 2022

Abstract
Murine B cell growth factor II (BCGF-II/interleukin 5) was purified from the conditioned media of the helper T cell line D10 . G4 . 1. The purification scheme consisted of sequential batch adsorption onto trimethylsilyl-controlled pore glass beads, high pressure ion exchange chromatography, and reverse phase high pressure liquid chromatography. The purified BCGF-II had a relative molecular weight of 45,000 when analyzed by sodium dodecyl sulfate-polyacrylamide gel electrophoresis under nonreducing conditions. Identical analysis of BCGF-II under reducing conditions yielded a m.w. of 22,500, suggesting that native BCGF-II exists as a homodimer. The NH2-terminal amino acid sequence of the purified lymphokine was determined by automated Edman degradation. A single amino acid sequence of 24 residues was obtained that, upon comparison, was contained within the cDNA pSP6K-mTRF23 recently described as encoding murine BCGF-II/T cell-replacing factor. The NH2-terminal methionine in mature BCGF-II is found at position 21 of the amino acid sequence predicted from the cDNA pSP6K-mTRF23. This finding supports the contention of Kinashi et al. (Kinashi, T., N. Harada, E. Severinson, T. Tanabe, P. Sideras, M. Konishi, C. Azuma, A. Tominaga, S. Bergstedt-Lindqvist, M. Takahashi, F. Matsuda, Y. Yaoita, K. Takatsu, and T. Honjo. 1986. Nature 324:70) that amino acids 1-20 serve as the signal sequence for the BCGF-II gene. The ability of BCGF-II to stimulate the proliferation of the B cell lymphoma BCL1 was used to assess the potency of the lymphokine. BCGF-II at 13.5 pM induced 50% of the maximal proliferative response in the BCL1 cells; concentrations as low as 2 pM were still effective in stimulating the growth of the cells. Assuming that the amount of BCGF-II necessary to mount a 50% response in the BCL1 assay is defined as one unit of activity, then the purified BCGF-II has a specific activity of 16.5 U/ng of protein.
Thymic stroma-derived T cell growth factor (TSTGF). I. Functional distinction of TSTGF from interleukins 2 and 4 and its preferential growth-promoting effect on helper T cell clones.
Authors: Ogata M , Sato S , Sano H , Hamaoka T , Doi H , Nakanishi K , Asano Y , Itoh T , Fujiwara H 
Published: December 2022

Abstract
A recently established thymic stroma-derived cell line (TSCL) supported the growth of the interleukin (IL) 2-dependent, antigen-specific helper T cell (Th) clone, 9-16, without requirement for IL-2 and antigen, and such growth was substituted by a factor produced into cultures by this established TSCL. This substance, thymic stroma-derived T cell-growth factor (TSTGF), was capable of inducing the proliferation of various Th clones including 9-16 Th clone, but not of cytotoxic T cell clones. TSTGF-induced growth promotion was obtained in a dose-dependent fashion and in maintaining antigen specificity of Th clones. The culture supernatant from the TSCL did not contain detectable level of IL-1, IL-2, IL-3, IL-4, or interferon activity. The proliferation of 9-16 Th clone was stimulated by recombinant IL-2 and IL-4 as well as TSTGF, but not by IL-1, IL-3, or interferons. However, the proliferation of this Th clone by IL-2 or IL-4 was almost completely inhibited by anti-IL-2 receptor or anti-IL-4 monoclonal antibody, respectively, whereas TSTGF-induced growth of 9-16 Th clones was not affected by either type of antibody, demonstrating that TSTGF is functionally distinct from IL-2 and IL-4. In addition, TSTGF activity was also obtained from the culture supernatant of the primary thymic explant, which was freshly prepared. These results indicate that the primary thymic explant as well as an established TSCL produce factors capable of promoting the growth of helper but not cytotoxic type of T cells in the absence of T cell growth factors thus far defined.
Differential regulatory role of monomorphic and polymorphic determinants of histocompatibility leukocyte antigen class I antigens in monoclonal antibody OKT3-induced T cell proliferation.
Authors: De Felice M , Turco M C , Giarrusso P C , Corbo L , Pizzano R , Martinelli V , Ferrone S , Venuta S 
Published: December 2022

Abstract
Monoclonal antibodies (mAb) to monomorphic and polymorphic determinants on the heavy chain of histocompatibility leukocyte antigen (HLA) class I antigens inhibit mAb OKT3-induced T cell proliferation, whereas the anti-beta 2-microglobulin mAb NAMB-1 does not affect it. The inhibitory effect of anti-HLA class I mAb is specific, is not an Fc-mediated phenomenon, does not require accessory cells, and does not involve early stages of T cell activation. Distinct determinants of HLA class I antigens regulate T cell proliferation by different mechanisms, because the anti-HLA-A2, A28 mAb CR11-351, and the mAb W6/32 to a framework determinant of HLA class I antigens block interleukin 2 (IL-2) secretion and IL-2 receptor expression, whereas the mAb CR10-215 to a monomorphic determinant blocks only IL-2 receptor expression. The mAb CR10-215 and W6/32 induced a 50% of maximal inhibition of T cell proliferation, when added after 27 and 12 hr, respectively, of incubation of peripheral blood mononuclear cells with mAb OKT3. On the other hand, the mAb CR11-351 inhibited T cell proliferation even when added after 38 hr of incubation of peripheral blood mononuclear cells with mAb OKT3 and was the only one to inhibit proliferation of cycling T lymphocytes. It is suggested that HLA class I antigens regulate T cell proliferation by interacting with cell-surface molecules involved in T cell activation. The differential inhibitory activity of the anti-HLA class I monoclonal antibodies tested may reflect the different ability of the corresponding determinants to interact with activation molecules.
Serologic cross-reactivity of T11 target structure and lymphocyte function-associated antigen 3. Evidence for structural homology of the sheep and human ligands of CD2.
Authors: Tiefenthaler G , Dustin M L , Springer T A , Hünig T 
Published: December 2022

Abstract
T11 target structure (T11TS) and lymphocyte function-associated antigen (LFA) 3 are the cell-surface glycoproteins on sheep and human erythrocytes (E) binding to cluster differentiation 2 (the E-receptor) on T cells in E rosette formation. Here we show that this functional cross-reactivity is most likely due to a structural homology of these molecules. A rabbit antiserum to sheep T11TS is shown to cross-react with LFA-3 in several independent assays: (a) rabbit anti-T11TS antiserum blocks the formation of E rosettes by human T cells with both autologous and xenogeneic (sheep) E by binding to the respective E; (b) the antiserum blocks the binding of anti-LFA-3 monoclonal antibody to human E; and (c) it reacts with purified LFA-3 in Western blotting. Together, these findings demonstrate that T11TS on sheep E and LFA-3 on human E are serologically related, providing further support for the notion that T11TS and LFA-3 are the sheep and human forms of the same cell interaction molecule.
Modulation of the murine immune response to streptococcal group A carbohydrate by immunization with monoclonal anti-idiotope.
Authors: Monafo W J , Greenspan N S , Cebra-Thomas J A , Davie J M 
Published: December 2022

Abstract
Using monoclonal anti-idiotopes with previously defined specificities for the variable (V) domain of HGAC 39, a monoclonal antibody against streptococcal group A carbohydrate (GAC), we have studied the effect of anti-idiotope on an anticarbohydrate immune response. Anti-IdI-3a and anti-IdI-3b are anti-idiotopes which recognize binding site-associated determinants, whereas anti-IdX recognizes a framework-associated determinant on the HGAC 39 V kappa domain. Each of three anti-idiotopes elicited a specific idiotope response, as measured by inhibition radioimmunoassay, in A/J and C57BL/6J mice. A single immunization with conjugated anti-IdI-3a elicited an idiotope(+), GAC-binding(+) response in C57BL/6J and (BALB/c X CBA/N)F1 male mice, but not in A/J or (CBA/N X BALB/c)F1 male, X-linked immunodeficient mice. When C57BL/6J mice immunized initially with anti-idiotope were further treated with group A vaccine, those receiving anti-IdX had the greatest increase in anti-GAC activity. Stimulation of an anticarbohydrate response with anti-idiotope may therefore be enhanced by selecting anti-idiotopes against both binding site- and framework-associated determinants.
Immunosuppression by succinylacetone. II. Prevention of graft-vs-host disease.
Authors: Hess R A , Tschudy D P , Blaese R M 
Published: December 2022

Abstract
Succinylacetone is a seven-carbon organic ketoacid that we have previously shown to inhibit tumor allograft rejection as well as the primary antibody response to sheep erythrocytes in rats. Because it appeared to be such a potent immunosuppressive agent in our initial studies, we evaluated succinylacetone for its ability to block graft-vs-host disease (GVHD) in adult F1 rats injected with parental strain spleen cells. Untreated ACE X Lewis F1 rats given Lewis strain spleen cells died of GVHD, with a mean survival of 24 days. By contrast, 62% of F1 rats in the group treated with succinylacetone survived, and the deaths that occurred in this group occurred significantly later. To confirm this observation and determine whether succinylacetone would interfere with bone marrow engraftment, lethally irradiated adult Wistar-Furth rats were reconstituted with syngeneic or totally allogeneic Fisher 344 lymphohemopoietic cells consisting of equal numbers of bone marrow and spleen cells. All animals given allogeneic cells without additional immunosuppressive treatment developed severe GVHD and died by day 42. By contrast 92% of the allogeneic cell recipients that had been treated with succinylacetone were long term survivors. Cytotoxicity typing of peripheral lymphocytes demonstrated greater than 90% donor-type lymphocytes persisting in the succinylacetone-treated recipients as long as 255 days post-transplantation. No chronic or late developing acute GVHD was observed even though the animals received succinylacetone as the sole immunosuppressant for only 28 days after transplantation. Furthermore, hemopoietic reconstitution in recipients of syngeneic cells was essentially identical between the control group and the group treated with succinylacetone. In addition, no gross or histologic evidence for renal, hepatic, cardiovascular, endocrine, or neurologic toxicity was observed in the long term transplant survivors treated with succinylacetone. These data indicate that succinylacetone treatment is effective in preventing lethal GVHD in this allogeneic bone marrow transplantation system while permitting normal hemopoietic reconstitution in the absence of significant chronic toxicity to other major organ systems.
Protein kinase C required for cytotoxic T lymphocyte triggering.
Authors: Nishimura T , Burakoff S J , Herrmann S H 
Published: December 2022

Abstract
The role of protein kinase C (PK-C) in triggering the lytic response of cytotoxic T lymphocytes (CTL) has been examined. Both target cell lysis and the release of CTL-associated serine esterase (SE), a marker for cytotoxic granules, were used as indicators of the CTL lytic response. We found triggering of the CTL lytic response occurred when both a PK-C activator, phorbol 12-myristate 13-acetate (PMA), and a calcium ionophore, ionomycin, were added to CTL. The previously described inactivation of the CTL lytic response by long term treatment (24 hr) with PMA was also investigated. CTL cultured with PMA for 24 hr were unable to mediate target cell lysis or release SE; this inability to respond correlated with an absence of PK-C activity. Incubation of the PMA-treated CTL in the absence of PMA for an additional 24 hr resulted in recovery of PK-C activity, SE release, and the lytic response. These experiments strongly suggest that PK-C is involved with the transmembrane signaling required for SE release which is a necessary event in CTL-mediated target cell lysis.
Role of natural killer cells, in comparison with T lymphocytes and monocytes, in the regulation of normal human megakaryocytopoiesis in vitro.
Authors: Gewirtz A M , Xu W Y , Mangan K F 
Published: December 2022

Abstract
Natural killer (NK) cells are thought to play an important role in host defense against virus-infected and neoplastic cells. Recent reports suggest that these cells may also influence developmental events in the course of normal erythropoiesis and granulopoiesis. The role of NK cells in the regulation of normal human megakaryocytopoiesis has not been reported, but clinical observations suggest that NK cell effects on megakaryocyte progenitors might differ from those of other cell lineages. We therefore carried out in vitro studies designed to assess the influence of NK cells on the growth of autologous megakaryocyte colony-forming units (CFU-Meg). To provide a frame of reference for these experiments, the effect of T lymphocytes, and monocyte-macrophages (M luminal diameter) on autologous CFU-Meg cloning efficiency was also studied. Purified immune effector cells were co-cultured in plasma clots with both unseparated, and progenitor cell-enriched marrow mononuclear cells (MNC) at target to effector cell ratios varying from 100:1 to 1:1. Resulting megakaryocyte colonies were enumerated by indirect fluorescence microscopy by using a rabbit anti-human platelet glycoprotein antiserum as probe for cells of the megakaryocyte lineage. The addition of NK cells to both unseparated (n = 12), and progenitor-enriched (n = 3) MNC at target to effector cell ratios of 2:1 and 1:1 resulted in a significant (p less than 0.05) augmentation in CFU-Meg-derived colony formation. Augmentation of colony formation was blocked by incubating the NK cells in Leu-11b monoclonal antibody. Stimulation appeared to be carried out by the production of a soluble growth factor which was detectable in NK cell-conditioned medium. Exposure of NK cells for 18 hr to highly purified or recombinant gamma-interferon (500 U/10(6) cells), a putative NK cell stimulator, neither increased nor abrogated the stimulatory effect. The latter could be accomplished, however, by centrifuging (200 X G for 5 min), and then preincubating the target and effector cells together for 3 hr before plating. At no time was significant inhibition of CFU-Meg demonstrated. In contrast to these results, when tested at the same ratios, and under the same conditions, no consistent effect on CFU-Meg cloning efficiency could be demonstrated by the addition of whole T cells, T cell subsets, or M luminal diameter. These results suggest that NK cells could play a role in the basal regulation of megakaryocytopoiesis.(ABSTRACT TRUNCATED AT 400 WORDS)
Human monoclonal IgG rheumatoid factor has structural homology with bacterial Fc receptor proteins.
Authors: Weisbart R H , Noritake D T , Colburn K K , Saxton R E 
Published: December 2022

Abstract
A cloned lymphoblast cell line, hRF-1, that secreted human monoclonal IgG4 rheumatoid factor autoantibody was produced by Epstein-Barr virus transformation of lymphocytes from rheumatoid arthritis synovium. The binding of hRF-1 rheumatoid factor to IgG globulins of different mammalian species was similar to the binding specificity of Staphylococcus aureus protein A (SpA) and to antibodies found in the sera from patients with rheumatoid arthritis. hRF-1 also had the same binding pattern to human IgG subclasses as SpA. Direct competition was observed between SpA and hRF-1 in binding IgG Fc. These results provide evidence for structural homology between a bacterial Fc receptor protein (SpA) and the monoclonal IgG rheumatoid factor.
Cyclosporine-induced tolerance requires antigens capable of initiating an immune response.
Authors: Haug C E , Gill R G , Babcock S K , Lafferty K J , Bellgrau D , Weil R 
Published: December 2022

Abstract
We studied two example where indefinite graft survival could be obtained in rats. In the first, strain DA hearts were permanently accepted in allogeneic PVG rats if the recipients were treated for at least 7 consecutive days with cyclosporine A (CsA) after transplantation. In the second, DA pancreatic islets were permanently accepted in PVG rats if the islets were cultured in vitro for 14 days in high oxygen. When cultured islet-grafted PVG rats were injected with lymphocytes from other PVG rats previously sensitized to DA alloantigens, the islet grafts were destroyed within 14 days. By contrast, it was difficult to cause the DA heart allografts to cease beating with the same adoptive transfer protocol; approximately two-thirds of the heart-grafted animals maintained their grafts. This difference was not due to the CsA as cultured islets transplanted in the presence of CsA were still susceptible to rejection by sensitized lymphocytes. However, islets that had not been cultured in high oxygen prior to transplantation and that were maintained with CsA were not rejected after the injection of sensitized lymphocytes. These results suggest that CsA can most readily induce a state of tolerance when the graft is capable of initiating an immune response.
Enhancement of human B cell proliferation and differentiation by tumor necrosis factor-alpha and interleukin 1.
Authors: Jelinek D F , Lipsky P E 
Published: December 2022

Abstract
The role of tumor necrosis factor-alpha (TNF-alpha) in human B cell responses was examined and compared with that of interleukin (IL) 1 by assessing the ability of each cytokine to support proliferation and differentiation. Recombinant TNF-alpha (rTNF-alpha) and recombinant IL-1 (rIL-1) each enhanced the generation of immunoglobulin-secreting cells (ISC) in cultures of pokeweed mitogen-stimulated B cells incubated with T cells. To examine the direct effect of rTNF-alpha and rIL-1 on the responding B cell, highly purified peripheral blood B cells were stimulated with Cowan I Staphylococcus aureus (SA). In the absence of T cell factors, proliferation was minimal and there was no generation of ISC. Recombinant IL-2 (rIL-2) supported both responses. Although rTNF-alpha alone did not support SA-stimulated generation of ISC, it did increase SA-stimulated B cell DNA synthesis by two- to eightfold. In addition, rTNF-alpha augmented B cell proliferation in rIL-2 supported SA-stimulated cultures. Moreover, rTNF-alpha enhanced the generation of ISC stimulated by rIL-2 alone or rIL-2 and SA. rIL-1 also augmented DNA synthesis and generation of ISC by B cells stimulated with SA and rIL-2. However, rTNF-alpha enhanced proliferation and ISC generation in SA + rIL-2-stimulated cultures even when they were supplemented with saturating concentrations of rIL-1. Utilizing a two-stage culture system, it was found that the major effect of rTNF-alpha was to enhance responsiveness of SA-activated B cells to rIL-2, whereas it exerted only a minimal effect during initial stimulation. These results indicate that TNF-alpha as well as IL-1 augment B cell responsiveness. Moreover, the ability of rTNF-alpha to enhance B cell responsiveness was not an indirect effect resulting from the induction of Il-1 production by contaminating monocytes, but rather resulted from the delivery of a signal by rTNF-alpha directly to the responding B cell that promoted both proliferation and differentiation after initial activation. The data therefore indicate that human B cell responsiveness can be independently regulated by the action of two separate monocyte-derived cytokines.
Recombination between DQ alpha and DQ beta genes generates human histocompatibility leukocyte antigen class II haplotype diversity.
Authors: Song Q L , Gregersen P K , Karr R W , Silver J 
Published: December 2022

Abstract
Two major DR7 haplotypes have been defined on the basis of serologic typing: those that type as DQw2 and others that type as DQw3. In order to define the molecular basis for these serologic differences we have isolated and sequenced DQ alpha, DR beta I, and DQ beta cDNA clones from both representative haplotypes. These studies reveal that although the DQ alpha and DR beta I genes of both haplotypes are identical, the DQ beta genes are very different. These data suggest that the serologic differences of these two DR7 haplotypes are the result of a recombinational event that occurred between the DQ alpha and DQ beta genes. In addition, they emphasize the role of DQ recombination in generating "hybrid" HLA-DQ heterodimers.