bluuebunny/crossref_metadata_2025_split huggingface dataset:
Moloney Virus-Induced Cell Surface Antigens and Histocompatibility Antigens Are Located on Distinct Molecules
Authors: Fox Robert I. , Weissman Irving L. 
Published: December 2022

Abstract
The Moloney lymphoma, LSTRA, is widely used as a target cell for cell-mediated lysis studies. This report further characterizes the antigenic structures that may be important in the cytotoxic T lymphocyte-target cell recognition. Anti-H-2 sera have been absorbed to remove contaminating antiviral activity. The results presented demonstrate that: a) no linkage between H-2 and viral antigens was detected with 1-dimensional (SDS-PAGE) or 2-dimensional (IEF followed by SDS-PAGE) gel electrophoresis; b) no molecule showing the antigenic properties of both viral and histocompatibility antigens was detected; c) H2-Dd and H2-Kd molecules on the LSTRA lymphoma appeared antigenically similar to the parental BALB/c cells based on inhibition of cytotoxicity experiments; d) with cell extracts made in the presence of iodoacetamide, no disulfide linkages could be demonstrated between viral and histocompatibility antigens; e) the Moloney viral antigen gp70 was found in large amounts on the cell surface of LSTRA cells; f) the p30 precursor (gag) was not detectable on the cell surface, although it was abundant in the cell cytoplasm.
Thus, these studies indicate that the LSTRA target cell appears to have H-2 and viral antigens present on separate molecules, which are dissociated during NP40 detergent extraction. No evidence was found of an “altered self” type molecule, in which either H-2 or viral antigens had been chemically altered as a consequence of viral transformation.
Differences in HLA Antigen Recognition by Human Influenza Virus-Immune Cytotoxic T Cells
Authors: Biddison William E. , Shaw Stephen 
Published: December 2022

Abstract
The specificity of in vitro induced human influenza-immune cytotoxic effector cells was analyzed with respect to recognition of HLA-A and -B-linked gene products. The influenza-immune cytotoxic activity observed on panels of virus-infected targets demonstrated that virus-immune effectors preferentially lyse targets with which they share HLA-A or -B specificities. Virus-immune effectors from certain donors recognized virus in conjunction with some, but not all, of their self HLA-A and -B antigens. Among donors who share a given HLA antigen (such as A2 or B7), there are differences in the ability of their virus-immune T cells to recognize the shared antigen. Virus-infected target cells from HLA-A2 or -B7 “nonresponder” donors could be lysed by virus-immune T cells obtained from other donors who shared only the HLA-A2 or -B7 antigen with these target cells.
These observations suggest that the absence of cytotoxic T cell responses by some donors to influenza virus in conjunction with HLA-A2 or -B7 is not due to control by the structural genes that code for these HLA antigens, but rather may result from control by regulatory genes that act at the level of the responder and/or stimulator cell. The results are discussed in the context of Ir gene regulation of human T cell responses.
Mechanisms of Mouse Mast Cell Activation and Inactivation for IgE-Mediated Histamine Release
Authors: Siraganian Reuben P. , Hazard Kimberley A. 
Published: December 2022

Abstract
The IgE-mediated histamine release from mouse mast cells requires Ca++, is optimal at 37°C, and is enhanced by phosphatidylserine. The rate of release is relatively slow. The mast cells can be activated to release histamine by either anti-IgE or anti-Fab antibodies and, in the case of cells from sensitized mice, by the immunizing antigen. The incubation of mast cells with antigen in the absence of Ca++ or phosphatidylserine fails to release histamine. Such cells are desensitized to the further addition under optimal conditions of the same antigen. Desensitization is antigen specific, requires optimal levels of antigen, and occurs at both 30° and 37°C. In contrast, anti-IgE desensitizes all IgE-mediated histamine release reactions.
The Structural Proteins of Murine Leukemia Virus and the Pathogenesis of Necrotizing Arteritis and Glomerulonephritis in SL/Ni Mice
Authors: Yoshiki Takashi , Hayasaka Takashi , Fukatsu Ryo , Shirai Toshikazu , Itoh Tetsuo , Ikeda Hisami , Katagiri Makoto 
Published: December 2022

Abstract
The analysis by immunofluorescent and electronmicroscopic studies of murine leukemia virus (MuLV), which could be of significance in the pathogenesis of necrotizng arteritis and glomerulonephritis in SL/Ni mice, yielded the following conclusions. The structural proteins, gp70, p30, and p15(E) of MuLV were granularly deposited along with bound immunoglobulins and C3, apparently as immune complexes, in the vessel walls of necrotizing arteritis. Just before or at the appearance of vascular lesions, C-type particles were found in greatest abundance around muscular cells and could be seen budding from the membrane of these cells. There was significant correlation between the presence of aggregated degenerating C-type particles and the presence of dense deposits in those vascular walls. In contrast, gp70 was the major viral protein deposited along with host immunoglobulins and C3 in the diseased kidney of mice. Electron dense deposits were demonstrated in the affected glomeruli.
In attempts to identify directly the molecule(s) bearing the antigenic determinants for Gross natural antibody (GNA), 125I-labeled E♂G2 MuLV proteins were subjected to immunoprecipitation with GNA-positive mouse sera. SDS-PAGE analysis of the precipitates revealed that the major molecule bearing antigenic determinants or GNA is p(85), the precursor polyprotein of the MuLV core structural proteins, p30, p15, and p10.
Shared Chemical Properties of Different Murine Thymus-Leukemia Antigens
Authors: Pischel Ken D. , Little J. Russell 
Published: December 2022

Abstract
Immunochemical studies of murine thymus-leukemia antigens (TLA) have confirmed that the subunit structure consists of a 45,000-dalton heavy chain and a β2 microglobulin (β2m) light chain. Similar structural features are exhibited by the TLA from thymocytes of Tlaa, Tlac, Tlad, and a leukemia cell derived from C57BL/6, a Tlab strain. In addition to the similar subunit structure from the four haplotypes, each TLA shows a similar pattern of trypsin proteolysis. This procedure yields a major heavy chain cleavage product of approximately 37,000 daltons that remains associated with β2m and retains most or all of the antigenic determinants of the intact TLA. Evidence is presented that TLA do not exhibit Fc receptor properties, nor do they adsorb to murine leukemia virus antigens under the conditions of isolation for analysis on polyacrylamide gel electrophoresis (PAGE) in sodium dodecyl sulfate (SDS). Taken together these findings strongly support the hypothesis that TLA comprise a family of chemically similar antigens belonging to a structurally and genetically related group that includes H-2D, H-2K, and Qa-2,3.
Antibody Penetration Into Living Cells
Authors: Alarcon-Segovia Donato , Ruiz-Arguelles Alejandro , Llorente Luis 
Published: December 2022

Abstract
We have previously shown that an anti-ribonucleoprotein (RNP) IgG can penetrate into live human mononuclear cells (MNC) having receptors for the Fc portion of IgG. Because T cells with such receptors (Tγ cells) seem to behave as suppressor cells in immune regulation and because this suppressor function is diminished in diseases where antinuclear antibodies appear, we considered the possibility that antinuclear IgG antibody could penetrate Tγ cells and affect them.
Herein we show that fluorescein-labeled anti-RNP IgG can penetrate into Tγ cells, enriched by either mitogenic stimulation or separation with a subpopulation of T cells with low affinity for sheep erythrocytes. Incubation of MNC with anti-RNP IgG before carrying out the separation procedures resulted in apparent loss of Tγ cells at the end of separation. To confirm that deletion had actually occurred, we performed a cytotoxicity assay using 51Cr-labeled T cells. Anti-RNP IgG had a significantly higher cytotoxic effect than normal IgG on T cells, particularly on those with low affinity for sheep erythrocytes that include most Tγ cells.
Suppressor cell function studied in a system where it was expanded, by either 7-day culture or incubation with concanavalin A, and detected in a reverse plaque-forming cell assay with rabbit anti-human immunoglobulin-developing antibody was found to be abrogated by the addition of anti-RNP IgG to the suppressor function-expanding cultures.
Controls in Ig-free medium, or medium supplemented with normal human IgG, aggregated normal human IgG, BSA-anti-BSA immune complexes, or F(ab′)2 fragments of the anti-RNP IgG, did not abrogate suppressor cell function. This indicates that the abrogation of suppressor cell function by anti-RNP IgG is due to its penetration into Tγ cells. Suppressor cell loss and/or dysfunction caused by penetration of antinuclear antibodies into Tγ cells may lead to the self-perpetuation of autoimmune disease.
Carboxymethyl Cellulose, a Nonimmunogenic Hapten Carrier with Tolerogenic Properties
Authors: Diner Uriel E. , Kunimoto Dennis , Diener Erwin 
Published: December 2022

Abstract
This communication reports on the tolerogenic properties of carboxymethyl cellulose (CMC) as a nonimmunogenic carrier for 2.4 dinitrophenyl (DNP) and the benzylpenicilloyl determinant (BPO). Either normal or primed mice, given an optimal dose of 250 µg per animal of DNP CMC, when challenged with an immunogenic form of the hapten as early as 30 min or as late as 21 days thereafter were completely and specifically unresponsive to it. Experimental evidence suggests that this unresponsiveness is not due to suppressor cells. Furthermore, DNP CMC induces tolerance in vivo but fails to do so in vitro under conditions at which other tolerogenic carbohydrate hapten conjugates such as DNP-dextran do. This together with comparative studies of tolerance induction kinetics by DNP CMC and DNP-dextran in vivo led us to conclude that molecular properties other than the epitope density must be attributed to CMC's tolerogenic potential. CMC may also be used as a tolerogenic carrier for BPO with respect to IgE antibody production. Thus, normal or primed mice injected with the BPO CMC conjugate were found specifically unresponsive to a challenge with an immunogenic form of penicillin.
Adaptive Differentiation of Murine Lymphocytes
Authors: Katz David H. 
Published: December 2022

Abstract
Responses to the synthetic terpolymer L-glutamic acid, L-lysine, L-phenylalanine (GLΦ) and hapten derivatives thereof are controlled by two complementing H-2-linked Ir genes in the mouse. F1 hybrids derived from two different nonresponder strains (one of which possesses the α and the other β Ir-GLΦ gene) are phenotypic responders to GLΦ and 2,4-dinitrophenyl (DNP)-GLΦ. Moreover, spleen cells from DNP-GLΦ-primed F1 mice can adoptively transfer secondary anti-DNP antibody responses to irradiated F1 recipients that have been challenged with DNP-GLΦ. When, however, GLΦ-primed F1 helper T cells are transferred together with the DNP-specific F1 B cells that had been primed in separate mice altogether by DNP coupled to an unrelated protein carrier, such mixtures failed to develop adequate adoptive secondary anti-DNP responses to DNP-GLΦ. This contrasted with the ability of the same GLΦ-primed F1 T cells to provide helper activity for DNP-primed B cells from responder recombinant B10.A (5R) mice. More important, the apparent defect of GLΦ-primed F1 T cells in providing help for DNP-primed F1 B cells (primed to a DNP-protein conjugate) could be readily overcome by using DNP-primed B cells from donor F1 mice primed with DNP-GLΦ. As discussed herein, these results suggest that interacting T and B lymphocytes pair off into partner cell sets, any pair of which interact optimally when a “best fit” reciprocal self-recognition occurs between them.
Mechanism of Immunosuppression of Progesterone on Maternal Lymphocyte Activation during Pregnancy
Authors: Clemens Louis E. , Siiteri Pentti K. , Stites Daniel P. 
Published: December 2022

Abstract
Lymphocyte reactivity was measured in human mixed lymphocyte (MLC) and mitogen-stimulated cultures in the presence of various steroids. When present during the entire culture period at concentrations between 1 and 20 µg/ml progesterone, estradiol, and testosterone blocked 3H-thymidine (3H-TdR) incorporation. Estriol and 16 α-hydroxy progesterone were without suppressive effects. The kinetics of steroid mediated suppression of thymidine incorporation and DNA synthesis was investigated at various times during lymphocyte activation. When progesterone was present only at the beginning of culture, subsequent DNA content, but not thymidine incorporation was suppressed. However, if added late during the activation process, progesterone reduced thymidine incorporation independent of cellular DNA content. If present during the entire culture period both were suppressed. Cortisol, but not progesterone irreversibly inhibited lymphocyte thymidine incorporation if added during the first 12 hr of culture. A reversible blockade of lymphocyte thymidine uptake could be observed with progesterone even during the final hours of mitogen or MLC cultures. Thus, effects of steroid hormones on cellular DNA synthesis and thymidine incorporation appear to be independent processes. Cell fractionation experiments demonstrated that progesterone blocked the uptake of 3H-TdR into the lymphocyte nucleoside pool thereby reducing its availability for incorporation into DNA. This study is consistent with the hypothesis that lymphocyte proliferation at the maternal fetal-interface during pregnancy may be under specific regulation by progesterone. The relatively high local concentrations of the hormone produced by trophoblast are immunosuppressive whereas the substantially lower peripheral steroid levels are entirely inadequate to suppress systemic immunity. We suggest that at least one important role of progesterone in maintaining pregnancy is its regulation of cellular immunity in the maternal-fetal bed.
Hyperthermia and Human Leukocyte Function
Authors: Roberts Norbert J. , Sandberg Kathryn 
Published: December 2022

Abstract
Fever has been shown by others to have a beneficial effect on the survival of animals challenged with bacteria. The febrile animals exhibited increased leukocyte accumulation at the site of bacterial inoculation. In order to investigate further these observations, as well as their possible relevance to human temperature elevation, human leukocytes were assayed in vitro for production of and response to leukocyte migration inhibition factor (LIF) at normal (37°C) and hyperthermic (38.5°C) temperatures. Leukocyte migration was assayed at both 37° and 38.5°C, by using an agarose plate technique, with exposure of the cells to supernatant fluids derived from stimulated and unstimulated leukocytes incubated at 37 or 38.5°C.
Hyperthermia (38.5°C) was consistently associated with greater spontaneous and stimulated LIF production by human mononuclear leukocytes. Hyperthermia was associated with decreased spontaneous leukocyte migration and greater inhibition of leukocyte migration by LIF-rich supernatant fluids. Migration at 38.5°C after exposure to LIF produced at 38.5°C was greatly reduced relative to migration at 37°C in response to LIF produced at 37°C (p &lt;0.005). Results were similar with mitogen- and antigen-stimulated LIF. The results suggest one possible mechanism by which hyperthermia may benefit the
Immunoregulation of Murine Myeloma: Isologous Immunization with M315 Induces Idiotype-Specific T Cells that Suppress IgA Secretion by MOPC-315 Cells in vivo
Authors: Rohrer James W. , Odermatt Bernhard , Lynch Richard G. 
Published: December 2022

Abstract
Previous studies demonstrated that MOPC-315 cells enclosed in peritoneal diffusion chambers (DC) in M315-immunized BALB/c mice did not secrete the 2,4,6-trinitrophenyl (TNP)-binding IgA paraprotein (M315). The secretory blockade was: i) idiotype (Id315)specific, ii) reversed in vitro after mild pronase treatment, and iii) independent of any effect on the cytologic differentiation of MOPC-315 from lymphocytoid to plasmacytoid cells. In addition to secretory blockade, MOPC-315 cells in M315-immunized hosts exhibited a marked reduction in expression of cell surface M315 (sIgA315). Since the alterations in M315 expression occurred across a 0.1-µ Millipore membrane, we proposed that Id315-specific, soluble factors contributed to the effector mechanism.
In the present studies, Id315-specific suppression of M315 secretion was adoptively transferred to normal mice with spleen cells from M315-immunized donors, and the transfer could be abrogated by treatment of the immune spleen cells with heterologous anti-ϑ serum plus complement. Furthermore, in contrast to actively immunized mice, adoptively immunized mice neither developed anti-Id315 antibodies nor suppressed sIgA315 expression.
These findings: i) establish that idiotype-specific suppression of M315 secretion is a process distinct from inhibition of sIgA315 expression, ii) demonstrate that secretory blockade of MOPC-315 cells is dependent on Id315-specific T cells, and iii) suggest that inhibition of sIgA315 expression is dependent on anti-Id315 antibodies.
The results presented here establish that immunoglobulin expression by MOPC-315 cells is responsive to idiotype-specific T cell regulation as well as the antigen-specific T cell regulation we described earlier. These studies provide further insight into the mechanisms of idiotype-specific regulation of myeloma and may contribute to more complete understanding of T cell-mediated regulation of idiotype expression in non-neoplastic B cells.
Genetic Control of in vivo Sensitivity to Lipopolysaccharide: Evidence for Codominant Inheritance
Authors: McGhee Jerry R. , Michalek Suzanne M. , Moore Robert N. , Mergenhagen Stephan E. , Rosenstreich David L. 
Published: December 2022

Abstract
The genetic control of several endotoxin-induced in vivo effects, specifically, immunogenicity, adjuvanticity, interferon production, and lethality, was studied. Lipopolysaccharide (LPS) responder (C3H/HeN or C57BL/6J) mice produced high levels of anti-LPS antibody in response to an optimal dose (10 µg) of a phenol-water extracted LPS from Escherichia coli K235 (Ph-LPS), whereas nonresponder (C3H/HeJ) mice did not demonstrate significant antibody responses. The F1 progeny of responder C3H/HeN × C3H/HeJ parents exhibited low to intermediate responses. C3H/HeN, F1 and C3H/HeJ mice produced equivalent amounts of antibody in response to endotoxin prepared by butanol-water extraction. Adjuvanticity was studied by measuring the immune response to trinitrophenyl group (TNP) coupled to homologous erythrocytes (MRC). Ph-LPS was a good adjuvant for TNP-MRC in C3H/HeN mice, whereas no response was observed with C3H/HeJ mice; the adjuvant response in F1 hybrid mice was intermediate. Similarly, interferon production induced by optimal doses of Ph-LPS followed the same pattern. Finally, F1 hybrid mice were clearly intermediate in sensitivity to LPS-induced lethality. The results of this study demonstrate that the in vivo responses of mice to LPS, like the in vitro sensitivity of lymphoid cells, are under codominant gene control.
In vitro Stimulation of Natural Killer (NK) Cells by Soluble Factor(s) Generated in Antigen-Stimulated Rhesus Monkey Peripheral Blood Lymphocyte Cultures
Authors: Lazda Velta A. , Baram Peter 
Published: December 2022

Abstract
Peripheral blood lymphocytes from rhesus monkeys (Macaca mulatta) sensitized to keyhole limpet hemocyanin (KLH), when stimulated in vitro with KLH, developed natural killer (NK) cell activity that was assayed with Rous Sarcoma virus-transformed marmoset fibroblasts as targets in a 4-hr 51Cr-release assay. The supernatant fluids from 24- to 25-hr KLH-activated cultures were capable of stimulating NK development in nonsensitive lymphocyte cultures. The effector cells were neither macrophages nor B cells (plastic and nylon-wool nonadherent) and did not form E-rosettes with neuraminidase-treated sheep red blood cells. Cultures depleted of EA-rosetting cells, i.e., Fc-receptor-bearing lymphocytes, were incapable of generating NK activity when stimulated in vitro. Kinetic studies showed that peak DNA synthesis, as measured by 3H-T incorporation, preceded maximum cytotoxicity. Elimination of dividing cells by 5-bromo-2′-deoxyuridine (BrdU) and light treatment during the interval from day 1 to day 4 inhibited the development of cytotoxicity on day 7. Cell replication was required for the induction of NK cells with KLH as well as with antigen-activated culture supernatant fluids. When cultures were left unstimulated for 4 days, NK activity could not be developed subsequently either by adding antigen, mitogen (PHA), or supernatant fluids from activated cultures.
Effect of Purified Protein SAA on Immune Response in vitro: Mechanisms of Suppression
Authors: Benson Merrill D. , Aldo-Benson Marlene 
Published: December 2022

Abstract
Studies were done to characterize the immunosuppressive effect of the serum α-globulin SAA. The in vitro antibody response of CBA/J murine spleen cells was studied in the Marbrook culture system. Addition of 10% SAA-containing serum from casein-treated CBA/J mice suppressed the primary antibody response to SRBC as measured by the hemolytic plaque assay by up to 90%. This suppression was reversed by addition of rabbit anti-amyloid protein AA. Addition of SAA 24 hr or longer after initiation of cultures failed to give suppression, showing that the suppression by SAA occurs in the early recognition phase of the in vitro antibody response. Extensive washing of spleen cells reversed the suppression, suggesting an effect at the level of the cell membrane. A lack of suppression of the response to DNP-Ficoll (a T-independent antigen) indicated that there was no direct effect of SAA on B lymphocytes.
Purified SAA (100 µg/ml) isolated from the serum of casein-treated mice gave 95% suppression of SRBC response, and concentrations as low as 10 µg/ml gave significant suppression. This is much lower than the serum levels of SAA attained in humans and experimental animals after antigen challenge or immunization. It is suggested that a normal function of SAA may be to regulate immune response to certain foreign antigens or altered autologous antigens.
Slow Reacting Substance (SRS) from Ionophore A23187-Stimulated Peritoneal Mast Cells of the Normal Rat
Authors: Yecies Lewis D. , Johnson Stephen M. , Wedner H. James , Parker Charles W. 
Published: December 2022

Abstract
The generation of slow reacting substance (SRS) from ionophore A23187-stimulated rat peritoneal mast cells was enhanced by arachidonic acid (AA). This SRS generation was inhibited by 5,8,11,14-eicosatetraynoic acid (ETYA), an acetylenic analogue of AA and an inhibitor of both fatty acid cyclooxygenase and lipoxygenase. Indomethacin, a fatty acid cyclooxygenase inhibitor, had an enhancing effect upon SRS generation. This suggests SRS generation occurred through an ETYA sensitive step—perhaps a lipoxygenase. Radiolabel from [14C]-AA was incorporated into SRS with comigration of radio-activity and bioreactivity in silicic acid and thin layer chromatographies. Upon silicic acid chromatography, the active principle was eluted in the methanol fraction. Two-dimensional thin layer chromatography revealed chromatographic separation from other known spasmogenic substances and phospholipids. Mast cell SRS was found to display physiochemical properties similar to those of rat basophilic leukemia cell SRS, namely: that mast cell SRS generation was 1) enhanced by arachidonic acid; 2) inhibited by ETYA but not by indomethacin; 3) incorporation of [14C]-AA into the active principle; and 4) similar behavior during purification in silicic acid and thin layer chromatographies.