bluuebunny/crossref_metadata_2025_split huggingface dataset:
Interaction of monoclonal anti-peptide antibodies with lysozyme.
Authors: Hirayama A , Takagaki Y , Karush F 
Published: December 2022

Abstract
The interaction of monoclonal anti-peptide antibodies with the free peptide and its protein counterpart has been evaluated for hen egg white lysozyme and the peptide constituting residues 38 to 45. Fluorescence methodology has been developed for the measurement of association constants based on resonance energy transfer between the excited tryptophan of antibody and bound peptide ligand conjugated to a fluorescent probe. Five antibodies, four IgM and one IgG, have been assayed by ELISA, and have demonstrated binding to the adsorbed peptide alone, to the adsorbed lysozyme alone, or to both. Multivalent interaction with the adsorbed ligand is a key factor in the efficacy of binding. Measurement of binding constants in homogeneous solution, by equilibrium dialysis and energy transfer, demonstrated that lysozyme was bound to an IgG antipeptide antibody with an association constant (4 X 10(2) M-1) 200-fold less than that for the free peptide (8 X 10(4) M-1). It was also inferred for IgM that an association constant of the order of 10(2) M-1 was sufficient to effect selective interaction in a system providing multivalent interaction. The shared conformations between protein and peptide, implied by the specific reactivity of the anti-peptide antibody with the protein, points to structural fluctuations of the surface regions and residues of globular proteins.
The human lymphocyte function-associated (HLFA) antigen and a related macrophage differentiation antigen (HMac-1): functional effects of subunit-specific monoclonal antibodies.
Authors: Hildreth J E , August J T 
Published: December 2022

Abstract
The structural and functional relations between the alpha- and beta-subunits of the human lymphocyte function-associated antigen (HLFA) and the human Mac-1 antigen (HMac-1) have been analyzed with the use of five monoclonal antibodies that react with these proteins. The specificities of these antibodies were examined by immunoprecipitation of proteins from 125I-labeled cells and purified HLFA and HMac-1 antigens. Three antibodies reacted with the Mr 95,000 common beta-subunit of the proteins, and also co-precipitated the Mr 175,000 HLFA alpha-subunit, the Mr 165,000 HMac-1 alpha-subunit, and a third polypeptide alpha-subunit of Mr 150,000. The other antibodies were specific to noncross-reactive epitopes present on the alpha-subunits of HLFA or HMac-1. These specificities were confirmed in sequential immunoprecipitation studies. Peptide mapping showed that the beta-subunits of HLFA and HMac-1 were identical, whereas the two alpha-subunits differed considerably. The HLFA alpha-subunit-specific monoclonal antibody inhibited phytohemagglutinin stimulation, the mixed lymphocytes reaction, cytolytic T lymphocyte-mediated killing, and tetanus toxoid stimulation, but did not affect natural killer cell-mediated killing or complement receptor type 3 function. The HMac-1 alpha-subunit-specific monoclonal antibody inhibited complement receptor type 3 function but had no effect on T cell or natural killer cell functions. Three monoclonal antibodies to the beta-subunit inhibited all functions tested, including T cell, natural killer cell, and complement receptor type 3 activities. The results suggest that the functions of the HLFA and HMac-1 molecules may be determined by the alpha-subunit, and that the common beta-subunit also bears functionally important epitopes.
The majority of human monoclonal IgM rheumatoid factors express a "primary structure-dependent" cross-reactive idiotype.
Authors: Chen P P , Goñi F , Fong S , Jirik F , Vaughan J H , Frangione B , Carson D A 
Published: December 2022

Abstract
Genetic studies of human immunoglobulin variable regions have been hampered by the lack of anti-idiotypic antibodies that recognize specific heavy and light chain variable region sequences. Sixty percent of human monoclonal IgM anti-IgG autoantibodies (rheumatoid factors [RF]) from unrelated individuals share a cross-reactive idiotype (CRI) termed Wa. In previous experiments in which we used an enzyme-linked immunosorbent assay, we reported that a synthetic peptide (PSL2), corresponding to the second hypervariable region in the kappa light chain of a monoclonal IgM-RF (Sie), induced rabbit antibodies reactive with several RF paraproteins. In the present experiments, to avoid interference due to the human IgM-RF binding toward rabbit IgG, the reactivity of the anti-PSL2 antibody to the separated heavy and light chains of multiple IgM proteins and Bence-Jones proteins was assessed by the Western blot technique. The PSL2-induced anti-CRI reacted well with the separated kappa chains from 10 out of 12 IgM-RF, zero out of four light chains from IgM proteins lacking anti-IgG activity, and one out of six kappa Bence-Jones proteins. The results show that the PSL2-CRI is associated with RF and is not a kappa subgroup marker. Furthermore, a comparison of the reported light chain sequences of the PSL2-CRI-positive IgM-RF suggests that the majority of human IgM-RF light chains derive from a single germ-line VK gene or from a family of closely related VK genes that is highly conserved in the human population. Synthetic peptide-induced anti-CRI provide a potent tool for analyzing the genetic basis of CRI and abnormal autoantibody production in humans.
Clearance of IgE from serum of normal and hybridoma-bearing mice.
Authors: Haba S , Ovary Z , Nisonoff A 
Published: December 2022

Abstract
The half-life of IgE in the mouse was investigated by using radiolabeled and unlabeled monoclonal antibodies of the IgE class. Quantitative serologic assays were used for the unlabeled antibodies. IgE was cleared rapidly upon i.v. inoculation; after 48 hr, less than 0.2% of the initial concentration remained in the serum. The IgE was cleared initially with a half-life of 1 to 2 hr, attaining a relatively constant value of 5 to 8 hr. The corresponding values for IgG1, determined as a control, were 11 to 12 hr and 9 to 11 days, respectively. The initial stage probably reflects equilibration with extravascular spaces. This is supported by experiments with mice in which IgE-secreting tumors were implanted and then resected; IgE was cleared from such mice with an average initial half-life of about 5 hr. The rates of clearance of inoculated IgE were approximately the same in mice bearing an IgE-secreting tumor and in normal mice. This suggests that the initial rapid clearance of IgE from normal mice is not due to adherence of IgE to saturable sites; such sites might be expected to be occupied in mice expressing high serum concentrations of IgE. This conclusion was supported by experiments in which 1-mg quantities of IgE were inoculated i.v. into normal mice daily for 6 days. Additional IgE injected on day 7 was cleared normally. The results obtained with tumor-bearing mice indicate that the reported failure to elicit an IgE response to an antigen in mice bearing IgE-secreting hybridomas cannot be attributed to rapid clearance of newly synthesized IgE in such mice, as compared with normal mice.
Antibody-induced suppression and postsuppression stimulation of complement in vitro. II. Intracellular and extracellular changes in C4 during long-term C4 suppression in guinea pig splenic fragments.
Authors: Goldman M B , O'Rourke K S , Becker D S , Goldman J N 
Published: December 2022

Abstract
Suppression of the synthesis of the fourth component of complement in vitro was originally accomplished by exposing cultured guinea pig peritoneal cells to anti-C4 alloantisera. When guinea pig splenic fragments were used instead of peritoneal cells, equivalent antibody treatment produced C4 suppression of significantly longer duration, lasting weeks instead of days after removal of antibody. As with peritoneal cell monolayers, antibody treatment induced specific suppression of C4 followed by nonspecific stimulation of C4 and other proteins such as C2. Although IgG2 is more readily sequestered by splenic tissue, both IgG1 and IgG2 antibodies were effective in inducing and maintaining suppression. Experiments with radiolabeled antibody demonstrated that a small amount (less than 5%) of the original dose of antibody was retained by the splenic fragments. Because there was no continuous slow release of that antibody, long-term suppression of C4 cannot be explained as a fluid-phase neutralization reaction. Because antibody treatment might induce production of aberrant C4 molecules with no functional activity, C4 antigens was also studied. Tissue culture supernatants were assayed by using an ELISA for C4. In none of these experiments was extracellular C4 antigen detectable immediately after antibody treatment. Extracellular and intracellular C4 were immunoprecipitated from biosynthetically labeled tissue cultures and analyzed by SDS-PAGE. Antibody treatment suppressed intracellular C4 as well as extracellular C4. Although extracellular C4 levels of antibody-treated cultures eventually returned to levels comparable to untreated cultures, intracellular C4 levels of treated fragments remained lower than controls for the full period of observation (22 days). Therefore, a short (4-day) exposure to anti-C4 antibody induced long-term effects that profoundly altered regulation of C4 synthesis and secretion by cultured splenic macrophages.
Antibody-mediated alternative complement pathway activation resists inhibition by sialoglycolipids.
Authors: Okada N , Yasuda T , Okada H 
Published: December 2022

Abstract
Although sialoglycolipids on liposome membranes were able to inhibit the activation of the alternative complement pathway (ACP) of guinea pigs mediated by trinitrophenylaminocaproyldipalmitoylphosphatidylethanolamine, they scarcely inhibited the ACP activation mediated by natural antibody to paragloboside (PG) inserted into the liposome membranes. Therefore, ACP activation was able to proceed regardless of the presence of sialoglycolipids on heterologous cell membranes when antibodies to constituents of the membranes were available. On the other hand, sialoglycolipids effectively inhibit undesirable ACP activation on self cell membranes, because little if any antibody is reacting on the self cell surface. Thus, the natural antibody reaction may effectively discriminate between self and non-self cell surface by cooperation with complement inhibitors on cell membranes such as sialoglycolipids.
Chemotactic responses of human peripheral blood monocytes to the complement-derived peptides C5a and C5a des Arg.
Authors: Marder S R , Chenoweth D E , Goldstein I M , Perez H D 
Published: December 2022

Abstract
We examined responses of human peripheral blood polymorphonuclear leukocytes (PMN) and monocytes to the highly purified human complement-derived peptides C5a and C5a des Arg. As reported previously, C5a proved to be approximately 10- to 20-fold more potent than C5a des Arg as a chemoattractant for human PMN. C5a also was more potent than C5a des Arg in causing PMN to acquire a polarized morphology. In contrast, we found that human monocytes do not distinguish between C5a and C5a des Arg when these peptides are used as chemoattractants. In two different assay systems, both peptides acted at identical concentrations to stimulate suboptimal and optimal migration of monocytes. Human monocytes also did not distinguish between C5a and C5a des Arg when these peptides were used as inducers of polarization. Studies performed with functionally active, [125I]-labeled C5a and C5a des Arg, however, demonstrated that binding of C5a des Arg to monocytes differed from binding of C5a. Although [125I]-C5a des Arg appeared to bind to the same receptor as [125I]-C5a, binding of labeled C5a des Arg occurred with an affinity that was approximately 100-fold less than that observed with labeled C5a. These results indicate that leukocyte chemotactic and polarization responses to C5a and C5a des Arg vary, depending on the target cell type.
Characterization of a soluble form of the C3b/C4b receptor (CR1) in human plasma.
Authors: Yoon S H , Fearon D T 
Published: December 2022

Abstract
A radioimmunoassay with the use of soluble 125I-Fab monoclonal anti-CR1 and rabbit IgG anti-CR1 bound to Staphylococcus aureus particles was employed to detect and quantitate CR1 antigen in human plasma. Among 16 normal individuals the concentration of soluble CR1 in plasma ranged from 13 to 81 ng/ml, and a similar range of concentration was found in plasma from 15 patients having systemic lupus erythematosus (SLE). The amount of plasma CR1 in normal donors, but not in SLE patients, significantly correlated with the number of CR1 sites on erythrocytes (r = 0.90, p less than 0.001), and was 7.1% of the amount of receptor that was present on erythrocytes in blood. The concentration of soluble CR1 was not diminished by ultracentrifugation or ultrafiltration of plasma, was not affected by various modes of anti-coagulation or even by clotting of blood, and did not change during incubation of blood at 4 degrees C for up to 4 hr. On sucrose density gradient ultracentrifugation of plasma the CR1 was distributed as a broad peak that overlapped the plasma protein profile. The Mr of plasma CR1 was identical to that of erythrocyte CR1 when assessed by polyacrylamide gel electrophoresis in the presence of sodium dodecyl sulfate and immunoblotting. In addition, the plasma form of CR1 exhibited the same structural phenotype as did receptor from erythrocytes of the same individual. CR1 antigen purified from plasma was as active as CR1 from erythrocytes in promoting the cleavage by factor I of C3b to iC3b, C3c, and C3dg. Therefore, a functionally and structurally intact form of soluble CR1 resides in plasma.
D-Penicillamine: analysis of the mechanism of copper-catalyzed hydrogen peroxide generation.
Authors: Starkebaum G , Root R K 
Published: December 2022

Abstract
Recent studies have suggested that the inhibition of lymphocyte mitogenesis by D-penicillamine in the presence of copper could be mediated by the formation and action of hydrogen peroxide. To explore this possibility further, we first sought evidence of H2O2 generation by D-penicillamine in a cell-free system by a) measurement of copper-catalyzed D-penicillamine oxidation and the requirement for oxygen in this process; b) direct measurement of H2O2 formation during D-penicillamine oxidation by the peroxidase-mediated oxidation of fluorescent scopoletin; and c) evaluation of the possible synthesis of O2- during D-penicillamine oxidation. The addition of copper to D-penicillamine in physiologic buffer catalyzed D-penicillamine oxidation in a dose-dependent fashion. D-penicillamine oxidation was accompanied by O2 consumption with a molar ratio of approximately 2:1, but did not occur under anaerobic conditions. Furthermore, D-penicillamine oxidation resulted in the formation of amounts of H2O2 stoichiometrically equivalent to oxygen consumption (i.e., 1:1). Copper-catalyzed D-penicillamine oxidation caused reduction of nitroblue tetrazolium in a reaction blocked by superoxide dismutase, suggesting the formation of O2-. Additional studies confirmed that D-penicillamine inhibited PHA-induced mitogenesis of lymphocytes in the presence of copper, and that catalase protected the cells from this action. Furthermore, when polymorphonuclear leukocytes were incubated with D-penicillamine plus copper, hexose monophosphate shunt activity increased up to threefold with abrogation of this stimulation by catalase. None of the effects of D-penicillamine plus copper on cells were diminished by hydroxyl radical scavengers mannitol or benzoate. These results are consistent with oxygen-dependent copper-catalyzed oxidation of D-penicillamine in aqueous solutions leading to the formation of O2- and H2O2. H2O2 produced by this reaction can inhibit lymphocyte mitogenesis and stimulate neutrophil hexose monophosphate shunt activity in vitro and may be relevant to the therapeutic effects of D-penicillamine in vivo.
Suppression of cytotoxic T lymphocyte activation by L-ornithine.
Authors: Dröge W , Männel D , Falk W , Lehmann V , Schmidt H , Nick S , Häcker-Shahin B , Jänicke R 
Published: December 2022

Abstract
The effect of L-ornithine on several types of immune reactions was analyzed. L-ornithine was found to suppress the activation of cytotoxic T lymphocytes (CTL) in vivo and in vitro. This suppressive effect was not observed with the structural analogues D-ornithine, L-lysine, or putrescine or with the amino acids L-histidine or L-alanine. The concentration of 9 X 10(-3) M L-ornithine was found to mediate a practically complete suppression of the cytotoxic response in vitro if applied on day 0 or day 1 of the culture, but a comparably weak suppression if applied on day 3. The same concentration of L-ornithine had no effect on the production of the lymphokines interleukin 2 (IL 2) and gamma-interferon (IFN-gamma). This concentration of ornithine had also no substantial effect on several types of proliferative responses, including the allogeneic mixed lymphocyte reaction, the concanavalin A-activated IL 2-dependent proliferation of thymocytes, and IL 2-dependent proliferation of the T cell clone W-2. These observations suggest that L-ornithine inhibits selectively the differentiation of CTL effector cells. By the criteria tested, the immunosuppressive effect of L-ornithine is more selective than that of cyclosporine A, which was previously found to suppress not only the activation of cytotoxic activity but also proliferative responses and the production of the lymphokines IL 2 and IFN-gamma.
Germline VH genes in an a3 rabbit not typical of any one VHa allotype.
Authors: Bernstein K E , Alexander C B , Mage R G 
Published: December 2022

Abstract
We have undertaken investigations in the rabbit of VH genes that may be responsible for the observations of VHa allotypes unexpected from an animal's pedigree (latent allotypes). A short cDNA probe was prepared and shown to be specific for VHa2 mRNA. Southern analyses with short and large probes were unrevealing but screening of a lambda phage library from a VHa3-expressing animal identified a number of unusual genes. These VH genes are remarkable in that they are far closer to one another in the genome (in one case 3085 bps) than VH genes reported in mouse or man, they are highly homologous over long stretches of sequence, and they encode proteins not typical of any one VHa allotype. Proteins similar to the sort encoded by these genomic V-regions may explain some of the observations of latent allotype. Our data suggest that the allelic behavior of VHa allotypes is not due to allelism of a regulatory mechanism that acts upon identical VH genes in rabbits of different VHa phenotypes.
Proliferation of human malignant lymphocytes induced by anti-IgM independent of B cell growth factor.
Authors: Baeker T R , Rothstein T L 
Published: December 2022

Abstract
Human malignant B lymphocytes were identified that proliferate in response to small doses of anti-immunoglobulin. Proliferation was induced by monoclonal mouse anti-HIgM, polyclonal goat anti-HIgM, and F(ab')2 fragments thereof, in vitro, and was not accompanied by immunoglobulin secretion. Proliferation was found to be unaffected by T cell depletion and was not enhanced by supplementation with B cell growth factor. Culture fluids from unstimulated malignant lymphocytes as well as from malignant lymphocytes stimulated with anti-HIgM contained no measurable B cell growth factor activity. Thus, proliferation of these malignant lymphocytes was not dependent on the presence of T lymphocytes and was independent of the presence of B cell growth factor. These results imply that B cell stimulatory factors may not be required for proliferation of all human B lymphocytes. Moreover, these results imply that treatment with anti-immunoglobulin reagents may be inappropriate for some B lymphocyte malignancies.
Decrease in HLA-DR-positive monocytes in patients with systemic lupus erythematosus (SLE).
Authors: Shirakawa F , Yamashita U , Suzuki H 
Published: December 2022

Abstract
Monocyte populations expressing HLA-DR antigens were studied in SLE patients by flow cytofluorometry with indirect immunofluorescence. Both the number of HLA-DR-positive monocytes and the expression of HLA-DR antigens on monocytes were markedly decreased in active SLE patients and were recovered to the normal level in inactive SLE patients. Because Ia-positive monocytes play a regulatory role for several immune responses, the decrease in HLA-DR-positive monocytes will result in abnormal regulations of immune responses and will play some critical role in the pathogenesis and the process of SLE.
Participation of class II alloantigens in in vivo regulation of K/D region disparate thyroid graft rejection in mice.
Authors: Isakov N , Bach F H 
Published: December 2022

Abstract
Class I and II molecules preferentially activate cytotoxic T cells and helper T cells, respectively, in primary in vitro alloactivation of T lymphocytes. Collaboration between these subpopulations leads to an efficient anti-class I specific cytotoxic response. We tested whether the presence of class II, in addition to class I, alloantigens on thyroid allografts in vivo induces augmentation of anti-class I antigen immune response and leads to rejection of K/D region disparate grafts which otherwise would have been accepted. Different pairs of K or D region disparate mouse strains were selected in which transplantation across a class I antigen disparity alone resulted in long-term graft acceptance. In some pairs of mouse strains, co-transplantation of recipient mice with a second thyroid graft sharing the K/D region of the first, but additionally expressing an allo class II molecule, led to accelerated K/D region disparate thyroid graft rejection. Transplantation of thyroid allografts expressing both class II and I alloantigens did not induce increased host anti-class I antigen cytotoxic response, or affect the frequency of specific precursor cytotoxic T cells. In one pair of congenic mouse strains, acute rejection of K/D region disparate thyroid grafts occurred in the absence of class II alloantigen stimulation; in other strains, co-transplantation of class I and II alloantigen disparate thyroid allografts was not sufficient to induce K/D region disparate graft rejection. The results thus demonstrate that a class II alloantigen on a thyroid graft may augment the rejection response directed against the graft class I alloantigens. The class II alloantigen stimulation was not always essential or sufficient for induction of class I antigen disparate thyroid graft rejection, and was dependent on the specific I region and/or K/D region gene allele.
The proliferative response of cloned Peyer's patch switch T cells to syngeneic and allogeneic stimuli.
Authors: Kawanishi H , Ozato K , Strober W 
Published: December 2022

Abstract
We previously defined a concanavalin A (Con A)-induced cloned T cell population in Peyer's patches (PP) that causes sIgM-bearing B cells to switch to sIgA-bearing B cells. In the present study we show that such IgA-specific switch T cells proliferate when exposed to syngeneic stimulator cells, i.e., the switch T cells are autoreactive. Detailed study of this phenomenon disclosed that both B cells and macrophages were capable of causing switch T cell proliferation, and in both cases, stimulation was enhanced by preactivation of the stimulator cells with lipopolysaccharide (LPS). In addition, fresh T cells can act as stimulators, but only if preactivated with Con A. Finally, it was clearly shown in blocking studies with the use of various antibodies directed at class II MHC specificities that class II MHC antigens were the stimulatory determinants. These studies suggest that IgA-specific switch T cells arise in PP as a result of autologous cell-cell interactions with activated (antigen-stimulated) B cells, macrophages, or T cells.