bluuebunny/crossref_metadata_2025_split huggingface dataset:
Contact hypersensitivity reactions to dinitrofluorobenzene mediated by monoclonal IgE anti-DNP antibodies.
Authors: Ray M C , Tharp M D , Sullivan T J , Tigelaar R E 
Published: December 2022

Abstract
Several studies have suggested a possible role for IgE antibodies in the pathogenesis of cutaneous hypersensitivity reactions that reach maximum intensity 24 to 48 hr after antigen challenge. The recent availability of murine monoclonal IgE anti-hapten antibodies has made possible the direct examination of the range of cutaneous inflammatory reactions that can be mediated by such antibodies. We have examined the effects of passively sensitizing BALB/c mice with monoclonal IgE anti-dinitrophenyl (DNP) antibody 48 hr before antigen challenge. Inflammatory responses were assessed by measuring ear swelling in mice challenged on the ears with the reactive hapten 2,4-dinitrofluorobenzene (DNFB). Compared with unsensitized controls, the ears of mice passively sensitized with IgE anti-DNP displayed a biphasic pattern of ear swelling after DNFB challenge. An early, transient response (present within 15 to 30 min of challenge and returning to control levels within 4 to 9 hr) was followed by a second, more persistent increase in ear swelling that peaked 24 to 48 hr after challenge. This biphasic pattern of ear swelling seen in IgE-sensitized mice was temporally indistinguishable from that observed in mice conventionally sensitized for allergic contact dermatitis reactions by epicutaneous application of DNFB 5 days before DNFB ear challenge. Antigen specificity of the IgE-mediated contact hypersensitivity reactions was demonstrated by the failure of mice passively sensitized with IgE anti-DNP to display early or delayed ear swelling greater than unsensitized controls when challenged with either of two noncross-reacting haptens, fluorescein isothiocyanate or oxazolone. Mice passively sensitized with a monoclonal IgA anti-DNP antibody (MOPC 315) 48 hr before DNFB challenge failed to display early or delayed ear swelling greater than unsensitized controls. Heat inactivation of the IgE anti-DNP ascitic fluid at 56 degrees C for 30 min completely abolished its capacity to passively sensitize mice for contact hypersensitivity reactions after DNFB challenge. These results document the existence of an antigen-specific, IgE-mediated, delayed-in-time cutaneous hypersensitivity response that can be elicited by epicutaneous challenge (contract) with a reactive hapten.
A partial characterization of suppressor cells in the spleens of mice conditioned with fractionated total lymphoid irradiation (TLI).
Authors: May R D , Slavin S , Vitetta E S 
Published: December 2022

Abstract
Total lymphoid irradiation (TLI) is a highly effective modality for inducing immunosuppression and transplantation tolerance. The cellular basis for this immunosuppression is not clear, although T cells have been implicated. To study further the effect of TLI on the immune system, we have examined the B cells and suppressor cells in the spleens from TLI-conditioned mice. Our results indicate that after TLI, the spleen is rapidly repopulated with many large, immature cells. The probable source of these cells is the shielded bone marrow (BM). The B cells from TLI-conditioned mice are transiently immature and hyporesponsive in vitro to a T-independent antigen. Spleen cells from TLI-conditioned mice nonspecifically suppress the in vitro T-independent anti-TNP response of normal B cells. The suppressor cells lack both B and T cell markers and adhere to Sephadex G-10. The suppressor cells in spleens from TLI-treated mice bear a number of similarities to those present in normal BM. When normal BM cells were analyzed by indirect immunofluorescence for the presence of the Mac-1 antigen, two populations of suppressor cells could be identified: one was Mac-1+ and the other was Mac-1-. These data are consistent with the possibility that a subpopulation of the suppressor cells found in normal BM and in the spleens from TLI-conditioned mice are immature cells of the monocytic/granulocytic lineage.
Monoclonal antibodies to streptococcal group A carbohydrate. II. The VK1GAC light chain is preferentially associated with serum IgG3.
Authors: Fulton R J , Nahm M H , Davie J M 
Published: December 2022

Abstract
A kappa-light chain variable region (V kappa) dominantly employed in the serum antibody response of A/J mice to streptococcal group A carbohydrate (GAC) has been termed VK1GAC. Examination of in vitro recombinants between the isolated heavy and light chains of VK1GAC+ and VK1GAC-anti-GAC hybridomas and non-GAC-binding myeloma proteins indicated that two antisera (anti-Id5 and anti-Id20) recognized the VK1GAC light chain when it was free in solution or paired with several heterologous heavy chains. Screening of a panel of A/J anti-GAC monoclonal antibodies with these antisera showed almost complete concordance between Id5 and Id20 expression and the presence of VK1GAC light chain as detected by its unique isoelectric focusing spectrotype. These antisera were used to examine serum expression of the VK1GAC light chain in normal and hyperimmune serum of A/J mice. Normal A/J serum contained from 20 to 100 micrograms Id5/ml serum, whereas only 1 to 10 micrograms Id20/ml serum was detected. The levels of both VK1GAC idiotypes increased dramatically 10- to 20-fold after hyperimmunization of mice with group A vaccine. When serum IgG from normal and immune mice was fractionated into the IgG subclasses (IgG1, IgG2a, and IgG3), it was found that the VK1GAC light chain does not pair randomly with heavy chains of the IgG subclasses, but rather is associated preferentially with heavy chains of the IgG3 subclass whether or not it is associated with antibodies to GAC. These results suggest that the heavy chain pairing exhibited by this VK product may not be random.
Serologic relatedness between Thy-1.2 and actin revealed by monoclonal antibody.
Authors: Dales S , Fujinami R S , Oldstone M B 
Published: December 2022

Abstract
Monoclonal antibodies with affinity for Thy-1.2 on thymocytes also can bind to actin within marsupial, murine, and human cells. A similar cross-reactivity between Thy-1.1 and vimentin was revealed by Dulbecco and co-workers employing monoclonals. A computer-assisted analysis of the amino acid composition provided suggestive evidence for the occurrence of sequence homology between Thy-1.1 or Thy-1.2, actin, and vimentin that likely accounts for the serologic relatedness detected by hybridoma antibodies.
Description of a new Qa antigenic specificity, "Qa-m9," whose expression is under complex genetic control.
Authors: Sutton V R , Hogarth P M , McKenzie I F 
Published: December 2022

Abstract
The "Qa-m9" specificity has been defined by a monoclonal antibody, and evidence for three-gene control of its expression has been demonstrated. The Qa allocation was made on the basis of H-2 linkage (H-2 congenic strains, Rl lines), differential reaction with B6.K1 and B6.K2, and biochemical analysis (two chains: 39,000 Mr and 12,000 Mr). "Qa-m9" is expressed on T and B cells in spleen and lymph node; it is present on a small population of bone marrow cells but is absent from thymocytes. The three genes involved in the expression of the antigen are: a) an H-2 linked Qa gene (possibly encoded by a gene different from Qa-2-6); b) an H-3 linked gene--probably beta 2m; and c) an H-2D linked gene that controls the amount of antigen present. It is likely that the determinant is of the "combinatorial" or conformational type, whereby the C57BL/6-type Qa heavy chain and the appropriate beta 2m light chain must both be in association. Thus, the study provides evidence for a multi-gene control of antigen expression and demonstrates the potential for generating new antigens with diversity at a post-translational level.
Elimination of complement channels from the plasma membranes of U937, a nucleated mammalian cell line: temperature dependence of the elimination rate.
Authors: Ramm L E , Whitlow M B , Koski C L , Shin M L , Mayer M M 
Published: December 2022

Abstract
We have studied the release of radiolabeled small markers from nucleated cells carrying complement channels in order to determine the life-span of these channels at various temperatures. U937 cells, a human histiocytic cell line, were labeled with 14C-aminoisobutyric acid or 86RbCl, and treated with sublytic doses of C to form transmembrane channels. The cells were then incubated at various temperatures, and the persistence of channels was evaluated by measuring the release of the intracellular markers through the remaining channels. The results indicate that the life-span of the C channels in the plasma membranes of these cells varies markedly with temperature. Thus, at 2 degrees C, the half-life of the channels was about 2 hr, whereas at 37 degrees C, the half-life was estimated to be approximately 1 min. The rapid elimination of the transmembrane channels from the plasma membranes of these nucleated cells contrasts sharply with the long persistence of C channels in the membranes of erythrocytes or erythrocyte ghosts. It is likely that the multi-hit requirement recently reported for lysis of nucleated mammalian cells by C is due, at least in part, to the rapid disappearance of channels.
Immunologic response of athymic rats to Schistosoma mansoni infection. II. Antibody-dependent mechanisms of resistance.
Authors: Capron M , Capron A , Abdel-Hafez S K , Bazin H , Joseph M , Phillips S M 
Published: December 2022

Abstract
The responses of congenitally athymic rats to Schistosoma mansoni were compared to thymic reconstituted, heterozygous littermate controls, and inbred Fischer rats. The mechanisms of the impaired resistance of athymic rats to initial exposure and re-exposure to S. mansoni were investigated by the study of various parameters of antibody response. The uninfected athymic animals demonstrated normal levels of total IgM but reduced levels of total IgG2a and IgE. After infection with S. mansoni, the immunoglobulin increases in athymic rats were less than those observed in heterozygote control rats. In addition, the level of anti-S. mansoni IgG antibody, utilizing ELISA assay, was reduced. Furthermore, the functional avidity of the IgG2a antibody, which was produced by the athymic animals, was significantly lower than that of control heterozygote and Fischer animals. Similarly, the levels of IgE and IgG2a anaphylactic antibodies were reduced in the congenitally athymic animals. After thymic reconstitution and exposure to S. mansoni of the congenitally athymic animals, all of these parameters became similar to the analogous value obtained from exposed heterozygous and homozygous animals. In vitro studies of antibody-dependent cell-mediated cytotoxicity (ADCC) activity indicated that the antibody response of the congenitally athymic animals was characterized by significant reductions in IgE-macrophage-mediated, IgG-eosinophil-mediated, and IgE-eosinophil-mediated cytotoxicity directed against schistosomula. These results, coupled with previously reported in vivo observations, that athymic animals produced antibody that was less capable of transferring resistance in adoptive-challenge experiments, suggest that the mechanisms of impaired resistance in the congenitally athymic rat may involve the failure to develop adequate, functional ADCC mechanisms. As such, these studies suggest a relationship between in vivo resistance and possible in vitro mechanisms of that resistance.
Infection with vaccinia favors the selection of hybridomas synthesizing autoantibodies against intermediate filaments, one of them cross-reacting with the virus hemagglutinin.
Authors: Dales S , Fujinami R S , Oldstone M B 
Published: December 2022

Abstract
Immunization of mice with lysates from infected cells and pure vaccinia virus generated hybridomas, a large fraction of which make autoantibodies binding to intermediate filaments (greater than IF) and vimentin. Antibodies that can be detected in preimmune mice as weakly binding to the cytoskeleton (greater than CS) are elevated in potency after immunization with either active or UV-inactivated pure vaccinia, suggesting that virus replication may not be obligatory for activation of greater than CS lymphocyte clones. Demonstration of a cross-reactivity of one IF monoclonal antibody with virally coded hemagglutinin, expressed at the surface, raises questions about the development of pathologic conditions associated with virus-mediated autoimmunity.
Monoclonal antibodies to murine leukemia virus gp 70 recognize the same T lymphoma cell surface molecules as anti-immunoglobulin.
Authors: Baird S , Lesley J , Majda J , Raschke W 
Published: December 2022

Abstract
Chicken antisera to mouse immunoglobulin (anti-Ig) detect molecules on T lymphocytes of mice consisting of "heavy chains" similar in size to IgM mu chains and "light chains" similar in size to lambda or kappa chains. Because these T cell-derived proteins react with anti-Ig and are composed of Ig-like heavy and light chains, these molecules have been viewed as candidates for "IgT," the putative T lymphocyte receptor for antigen. We have demonstrated, by immunoprecipitation and two-dimensional gel analysis, that the lymphoma surface molecule precipitated by chicken anti-Ig is identical to the viral 70,000 dalton glycoprotein (gp 70) expressed by that lymphoma and is unassociated with any "light chain" or equivalent. For each of the three lymphomas analyzed, the gp 70 two-dimensional gel pattern was individually distinctive, and, in each case, the molecules precipitated by anti-Ig exhibited the same pattern as the gp 70. The viral gp 70 does have cross-reacting determinants with mouse IgM as seen by the chicken antiserum. We have substantiated these results by demonstrating that monoclonal antibodies to viral gp 70 precipitate the same molecules as chicken anti-Ig. These findings demonstrate that these T lymphoma cell surface molecules do not represent the T cell immunoglobulin receptor for antigen unless gp 70 itself is an antigen receptor.
Gangliotriaosylceramide (asialo GM2), a glycosphingolipid marker for cell lines derived from patients with Hodgkin's disease.
Authors: Kniep B , Monner D A , Burrichter H , Diehl V , Mühlradt P F 
Published: December 2022

Abstract
Three cell lines, isolated from different patients with Hodgkin's disease, were analyzed for their neutral glycosphingolipids by high performance liquid chromatography. On two of these lines gangliotriaosylceramide (asialo GM2) was identified by the comparison of retention time to authentic standards and by degradation with specific glycosidases. This glycosphingolipid was also serologically detected with a specific monoclonal antibody of the IgM class. The third line, which according to other criteria such as the Epstein Barr virus nuclear antigen differs phenotypically from the first two, did not exhibit gangliotriaosylceramide. This glycosphingolipid is an unusual marker for human cells and could not be detected on the peripheral blood leukocytes of healthy donors.
Specific stimulation of human T lymphocytes by substance P.
Authors: Payan D G , Brewster D R , Goetzl E J 
Published: December 2022

Abstract
Substance P (SP) and SP(4-11) stimulated significantly the proliferation of human T lymphocytes in vitro at respective concentrations of 10(-11) M to 10(-7) M and 10(-9) M to 10(-7) M, as assessed by the uptake of [3H]thymidine and [3H]leucine. The proliferative response of human T lymphocytes to PHA was augmented by 10(-9) M to 10(-8) M SP and 10(-10) M to 10(-7) M SP(4-11). The inactive analogue [D-Pro2, D-Phe7, D-Trp9]-SP inhibited the effects of SP on T lymphocytes. The specific stimulation of T lymphocytes by SP suggests a unique mechanism for the regulation of immunologic responses by peripheral nerve-derived factors.
An IL 2-secreting T cell hybridoma that responds to a self class I histocompatibility antigen in the H-2D region.
Authors: Endres R O , Marrack P , Kappler J W 
Published: December 2022

Abstract
A self-reactive T cell hybridoma that secretes IL-2 in response to H-2d haplotype cells resulted from a fusion of BALB/cBy lymph node cells with the AKR thymoma BW5147. The lymph node cells used had been enriched for cells reactive to (TG)-A--L, but neither this antigen nor fetal calf serum were required for stimulation of the hybridoma designated 3DT52.5. The gene product responsible for stimulation mapped to the H-2D region. Allogeneic cells of the b, f, k, q, and s haplotypes failed to stimulate. Not all H-2d haplotype cells were effective stimulators of 3DT52.5. Peritoneal cells and splenic B cells were much more stimulatory than splenic T cells. Most tumor cell lines of H-2d derivation and of B cell or macrophage/monocyte lineage were stimulatory, whereas H-2d T cell lines were not. The capacity to stimulate 3DT52.5 did not correlate with the ability to stimulate I region-restricted hybridomas, or with the ability to be induced to stimulate such hybridomas. Stimulatory cell lines did not apparently produce a soluble factor required for stimulation, and negative cell lines were not inhibitory. The monoclonal antibody 27-11-13, which reacts with H-2D of the b, d, and q haplotypes, inhibited stimulation of 3DT52.5 but did not inhibit stimulation of the sibling hybridoma 3DT18.11, which responds to (TG)-A--L plus I-Ad. Conversely, the monoclonal anti-I-Ad antibody MK-D6 inhibited stimulation of 3DT18.11 but not 3DT52.5. Although it is clear that 3DT52.5 recognizes a class I antigen coded for in the H-2D region, the precise molecular nature of the antigen is unknown. The structure of the antigen receptor on this hybridoma may prove to be of interest when it can be compared with receptors found on T cell hybridomas restricted by class II histocompatibility antigens.
Unresponsiveness in hapten-specific cytotoxic T lymphocytes. IV. Functional deletion of T cell subsets required for trinitrophenyl (TNP)-specific cytotoxic T cell generation after acute or chronic treatment with trinitrobenzene sulfonic acid (TNBS).
Authors: Butler L D , Chiller J M 
Published: December 2022

Abstract
The generation of cytotoxic T cell responses requires the interaction of a network of immunocompetent cells. Within this network, a dynamic balance of positive and negative immunoregulatory cells and their products modulate the cytotoxic T cell response. We have developed protocols which shift the balance to favor negative immunoregulation and thus result in antigen-specific unresponsiveness. In this report, a variety of approaches have been utilized to examine the effects of acute and chronic tolerance protocols on specific T cell subsets, namely amplifier helper T cells and precursor cytotoxic T cells. The results to be detailed show differential effects on these T cell subsets which are related to the tolerance protocol employed and the strains of mice tested.
T cell proliferative responses to a mitogen derived from Mycoplasma arthritidis are controlled by the accessory cell.
Authors: Lynch D H , Gurish M F , Cole B C , Daynes R A 
Published: December 2022

Abstract
Cell-free supernatants from broth cultures of Mycoplasma arthritidis (MAS) induce vigorous proliferative responses in thymus-derived T lymphocytes from H2k or H2d strains of mice. Populations of lymphoid cells from mice of H2b, H2q, or H2s haplotypes do not respond to this stimulus. Previous studies with lymphoid cells from congenic and recombinant strains of mice indicate that the T cell proliferative response induced by MAS is controlled by a gene(s) that maps to the I-E/C subregion of the murine major histocompatibility complex (MHC). The T cell proliferative response induced by MAS is dependent upon the presence of a population of la+, radioresistant accessory cells (AC). Data presented here demonstrates that responder strain AC that have been pulsed with MAS (followed by extensive washing) induced vigorous proliferative responses in subsequently added T cell populations. Pulsing of T cells with MAS, followed by the addition of AC, however, did not result in T cell proliferation. MAS was found to stimulate (responder X nonresponder) F1 T cells to proliferate if the MAS was presented in the context of either responder or (responder X nonresponder) F1 AC; nonresponder strain AC were ineffective in this regard. Nonresponder strain T cells were found to be capable of responding to MAS if it was presented in the context of responder strain AC, even if the T cells and AC were completely allogeneic. Thus, nonresponder strain T cells mounted vigorous proliferative responses if the MAS was presented in the context of responder strain AC. Conversely, responder strain T cells did not respond to MAS presented in the context of nonresponder strain AC. In addition, lymphoid cells from a B10 leads to B6AF1 radiation bone marrow chimera were also found to be capable of responding to MAS, but only in the presence of AC that expressed cell surface determinants controlled by the I-E/C subregion. The data presented here indicate that MAS-induced T cell proliferative responses are controlled at the level of the AC by a gene(s) that maps to the I-E/C subregion of the MHC.
Evidence for a nonoxidative mechanism of human natural killer (NK) cell cytotoxicity by using mononuclear effector cells from healthy donors and from patients with chronic granulomatous disease.
Authors: Kay H D , Smith D L , Sullivan G , Mandell G L , Donowitz G R 
Published: December 2022

Abstract
In vitro natural killer (NK) activity expressed by blood mononuclear cells from patients with chronic granulomatous disease of childhood (CGD) was equivalent to that expressed by cells from normal, healthy volunteers. Because neutrophils and monocytes from these same donors exhibited extremely depressed oxidative functions, our data could be interpreted to show that a) NK cells derived from a unique and separate cellular lineage unaffected by the disease-related oxidative defect, or b) the in vitro cytolytic mechanism(s) of NK cells were not dependent on oxygen metabolites. These hypotheses were examined by using as NK effector cells large granular lymphocytes (LGL) from healthy donors whose monocytes and neutrophils had normal oxidative functions. Such functions were measured in the nitroblue tetrazolium dye reduction assay, which is a qualitative measurement of superoxide anion production; by reduction of ferric cytochrome c, a more specific and quantitative measurement of superoxide anion production; and in the luminol-enhanced chemiluminescence assay, an extremely sensitive measure of several reactive oxygen radicals, including superoxide anion, hydroxyl radical, and singlet oxygen. Whereas monocytes and neutrophils from healthy donors were readily stimulated with zymosan or phorbol myristate acetate (PMA) in each of these assays. LGL produced no detectable amounts of oxygen metabolites when co-incubated either with K562 erythroleukemia cells, PMA, E. coli endotoxin, or the calcium ionophore A23187. Thus, because NK cell activity is normal in CGD patients with major oxidative defects, and because no reactive oxygen metabolites could be detected in LGL that simultaneously exhibited potent NK activity, we conclude that in vitro NK activity by human mononuclear cells involves a lytic mechanism(s) independent of oxygen metabolites.