bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies of the mechanism of bacterial resistance to complement-mediated killing. V. IgG and F(ab')2 mediate killing of E. coli 0111B4 by the alternative complement pathway without increasing C5b-9 deposition.
Authors: Joiner K A , Goldman R C , Hammer C H , Leive L , Frank M M 
Published: December 2022

Abstract
The mechanism of antibody-dependent complement-(C) mediated killing of Escherichia coli 0111B4, strain 12015 (12015), was examined. 12015 was resistant to serum killing when incubated in hypogammaglobulinemic serum (H gamma S) or pooled normal human serum (NHS) that had been previously adsorbed to remove specific antibody (Abs NHS). Presensitization with immune rabbit serum or purified immune rabbit IgG resulted in 1 to 3 log killing when 5 X 10(8) colony forming units (CFU)/ml were incubated in 10 to 40% Abs NHS. Binding of 125I-C3 and 131I-C9 to the bacterial surface of the presensitized and the nonpresensitized strain was quantitated when these organisms were incubated in 10, 20, and 40% Abs NHS. Stable binding of up to 3.0 X 10(5) molecules of C3 and 8.0 X 10(4) molecules of C9 to presensitized and nonpresensitized isolates occurred in the highest concentration of serum, but there was no killing without presensitization. Similar results were found when Abs NHS was chelated with ethylene bis glycoltetraacetic acid containing 2 mM MgCl2 (Mg EGTA) to block classical pathway activation, indicating that antibody mediated the bactericidal reaction through the alternative pathway. Deposition of C3 and C9 and killing of 120 15 in 10% Abs NHS or 10% H gamma S was measured after presensitization with increasing amounts of IgG, F(ab')2, or Fab'. There was a dose-dependent increase in C3 deposition and killing, but only minimal change in C9 binding when 1.0 X 10(3) to 3.2 X 10(4) IgG or F(ab')2/CFU were bound to the bacterial surface. In contrast, there was no increase in C3 or C9 binding and no bacterial killing when 1 X 10(3) to 3.4 X 10(4) molecules Fab'/CFU were bound to the bacterial surface. These experiments show that immune IgG and F(ab')2 can mediate killing of E. Coli 0111B4 by the alternative pathway without changing the extent of terminal C component attachment to the bacterial surface.
Recognition by cytotoxic T lymphocytes of cells expressing fragments of the SV40 tumor antigen.
Authors: Gooding L R , O'Connell K A 
Published: December 2022

Abstract
Recognition by cytotoxic T lymphocytes (CTL) of syngeneic cells transformed with simian virus 40 (SV40) was examined by using cells expressing known portions of the SV40 early region both as sensitizing cells for stimulation of CTL development and as targets for lysis by CTL. LMTK- cells transfected with a plasmid specifying a 33K amino-terminal fragment of the SV40 tumor (T) antigen served both to stimulate syngeneic CTL capable of lysing SV40 transformed cells and as target cells for CTL generated against syngeneic transformants. The same is true for cells infected with the adenovirus 2-SV40 hybrid viruses, Ad2+ND1 and Ad2+ND2, which produce proteins homologous with carboxy-terminal regions of the SV40 T antigen. These findings indicate that on cells transformed by SV40 virus, and expressing the entire T protein, determinants in both the amino- and carboxy-terminal regions of the molecule are exposed on the cell surface. Furthermore, determinants in both these regions are recognized independently in the polyclonal CTL response to SV40.
Defective B cell tolerance induction in New Zealand black mice. I. Macrophage independence and comparison with other autoimmune strains.
Authors: Goldings E A 
Published: December 2022

Abstract
B cell unresponsiveness was examined in vitro by using spleen cells from autoimmune NZB, BXSB/Mp male, MRL/Mp-Ipr/Ipr (MRL/l), and control mice, and the tolerogen trinitrophenyl human gamma-globulin (TNP-HGG). The B cell subset responsive to TNP-Brucella abortus in each autoimmune and control strain that was tested was highly susceptible to tolerance induction with the use of high epitope density conjugates (TNP30HGG and TNP32HGG). When a tolerogen with a lower epitope density was used (TNP7HGG), several control strains were all rendered tolerant in a thymic-independent and hapten-specific manner. NZB B cells were resistant to all concentrations of TNP7HGG tested, whereas B cells from BXSB/Mp male and MRL/1 mice were resistant to low concentrations of this tolerogen. NZB mice were resistant in addition to tolerance induction with TNP9HGG, TNP10HGG, and TNP12.7HGG. Experiments were performed to determine whether splenic macrophages played a role in resistance to tolerance in NZB mice. The mixing of NZB and control DBA/2J T cell-depleted splenocytes revealed no modulatory effects by the accessory cells in culture. Moreover, B cells rigorously depleted of macrophages by double Sephadex G-10 column passage exhibited characteristic patterns of resistance or susceptibility in NZB and control strains, respectively. These findings support the conclusion that resistance to tolerance in NZB mice is determined at the B cell level and are consistent with the hypothesis that diverse immunoregulatory disturbances contribute in varying degrees to the development of systemic lupus erythematosus in different inbred strains of mice.
B cell activation. II. Receptor cross-linking by thymus-independent and thymus-dependent antigens induces a rapid decrease in the plasma membrane potential of antigen-binding B lymphocytes.
Authors: Monroe J G , Cambier J C 
Published: December 2022

Abstract
We report the specific induction of B cell plasma membrane depolarization with the use of thymus-dependent and -independent antigens. We have utilized various trinitrophenol-carrier conjugates for the stimulation of isolated trinitrophenol-binding mouse B cells. Membrane depolarization was assessed by flow cytometric analysis of 3-3'-pentyloxacarbocyanine iodide (DiOC5[3])-stained cells. Entry into the cell cycle was determined by flow cytometric analysis of acridine orange-stained cells. The results indicate that polyvalent antigens, but not free hapten, induce B cell membrane depolarization by a large proportion of antigen-binding cells within 2 hr of stimulation. Although all polyvalent antigens induce membrane depolarization, only thymus-independent antigens induce the subsequent G0 to G1 transition, suggesting that the membrane Ig cross-linking signal alone, although sufficient to induce membrane depolarization and subsequent increased IA expression, is insufficient to drive the entry of B cells into the cell cycle. The G0 to G1 transition appears to be dependent on a second signal, perhaps mediated by the thymus-independent carrier or antigen-specific, Ia-restricted T cell helper.
Desensitization of contact allergy to DNFB in mice. I. Description of a model system.
Authors: Claman H N , Jaffee B D 
Published: December 2022

Abstract
We investigated the down-regulation of contact sensitivity (desensitization) in mice sensitized to DNFB. Mice were sensitized with DNFB, desensitized with antigen 2 wk later, and resensitized 2 wk after desensitization. Large doses of antigen (DNFB or DNBSO3) produced about 50% inhibition of the anamnestic response as measured by ear swelling after challenge with DNFB. Desensitization was antigen specific and long lasting. Lymph node cells from desensitized mice showed diminished antigen-induced proliferation in vitro. Although the anamnestic response can be inhibited by afferent- or efferent-acting suppressor cells, such suppressor cells were not demonstrated in desensitized animals. The most likely explanation is that antigen desensitizes by inactivating effector cells for contact sensitivity, although suppressor mechanisms have not been completely excluded.
Natural killer cells in mouse lung: surface phenotype, target preference, and response to local influenza virus infection.
Authors: Stein-Streilein J , Bennett M , Mann D , Kumar V 
Published: December 2022

Abstract
Natural killer (NK) and natural cytotoxic (NC) cells can be recovered from the spleens of mice. NK/NC cells are thought to serve as a first line of defense (before the development of immune responses) against tumor and virus infected cells; therefore organs such as the lung that are exposed to the environment may harbor NK/NC cells. Studies reported in this manuscript characterize a population of pulmonary cells (recovered from collagenase-treated lungs) that exhibited cytotoxic activity against 51Cr-labeled tumor targets in vitro. As with the spleen cell populations, the mononuclear cells from the lung lysed the NK-sensitive target YAC-1 as well as the NC-sensitive WEHI 164.1 tumor cells in vitro. By using flow cytometry, it was observed that 15 to 20% of nylon wool-passed (NWP) lung cells and 5 to 15% of NWP spleen cells from C57BL/6 mice could bind antibody for NK cell alloantigens (NK 1.2, defined by (CE X NZB)F1 anti-CBA sera). Treatment of lung and spleen cell populations with complement and antisera to NK 1.2, asialo GM1, and Ly-5 but not Thy-1 antigens significantly decreased lung and splenic NK (YAC-1) activity. Forty-eight hours after infection of mice by intratracheal inoculation of an infectious dose of influenza virus (PR/8/34) NK activity was stimulated in the lung and not the spleen. Therefore although NK cells in the lung and spleen are similar in antigenic phenotype and target preference there appears to be a pulmonary compartment of natural resistance cells the function of which can be modulated locally. These data are consistent with the hypothesis that the lung contains a separate compartment for NK/NC cells that may participate in the defense mechanisms of the lung.
Keratinocytes synthesize Ia antigen in acute cutaneous graft-vs-host disease.
Authors: Breathnach S M , Katz S I 
Published: December 2022

Abstract
Keratinocytes express la antigen (Ia) during cutaneous graft-vs-host disease (GVHD); it is, however, unclear whether this Ia is adsorbed from alloactivated donor lymphocytes or from Ia-bearing host Langerhans cells (LC), or whether it is actively synthesized by host keratinocytes. We therefore sought to determine the origin of keratinocyte Ia in a murine model of GVHD. Lethally irradiated C3H/He (H-2k) mice developed characteristic histopathologic changes of acute cutaneous GVHD 7 days after injection of BALB/c (H-2d) bone marrow and spleen cells, and expressed keratinocyte Ia of host (Iak) but not donor (Iad) origin in immunofluorescence studies. To determine whether the Ia was synthesized by keratinocytes or adsorbed from host LC, we investigated GVHD that was induced in chimeric mice. Parental strain A mice were made chimeric by lethal irradiation and reconstitution with (A X B)F1 bone marrow cells as follows: (BALB/c X C3H/He)F1 (H-2d,k) leads to C3H/He (H-2k), B6C3F1 (H-2b,k) leads to C57BL/6 (H-2b), and B6C3F1 (H-2b,k) leads to C3H/He (H-2k). After 3 mo, the LC in the skin of these chimeric mice were mainly of F1 haplotype. The chimeric mice were again lethally irradiated and injected with marrow and spleen cells from a third strain of mouse (C57BL/6, H-2b or BALB/c, H-2d) histoincompatible with both F1 parental strains. In the ensuing GVHD, the chimeric recipients only expressed keratinocyte Ia syngeneic to the original haplotype of the animal (strain A), despite the fact that the majority of their LC were derived from F1 marrow and expressed Ia of both F1 parental strain haplotypes (strains A and B). Together, these findings indicate that keratinocyte Ia in GVHD is synthesized by keratinocytes and is not derived from donor lymphocytes or adsorbed from host LC.
Characterization of a phenotypically distinct subpopulation of Leu-2+ cells that suppresses T cell proliferative responses.
Authors: Landay A , Gartland G L , Clement L T 
Published: December 2022

Abstract
Two new monoclonal antibodies (termed 2D2 and D12) have been used to identify and to analyze phenotypically distinct subpopulations of human T cells. The 2D2 antibody recognized an antigenic determinant closely related, if not identical, to that reactive with the anti-Leu-2 monoclonal antibody. The D12 antibody reacted with a variety of cell types, which included a subpopulation of Leu-2+ (2D2+) T cells. These antibodies were used to isolate four phenotypically distinct T cell populations by sequential cell sorter techniques. Functional analyses demonstrated that the 2D2+D12+ subset was unique in its ability to suppress the antigen-induced proliferation of T cells. These cells also suppressed the proliferative responses of other T cell subsets stimulated with mitogens. Pretreatment of 2D2+D12+ T cells with mitomycin C before culture abrogated the suppressor cell activity of these cells. We propose that the cells within the Leu-2+ cytotoxic/suppressor T cell subpopulation that suppress T cell proliferation are phenotypically distinct and express the 2D2+D12+ membrane antigenic phenotype.
Autoimmune encephalomyelitis (EAE) mediated or prevented by T lymphocyte lines directed against diverse antigenic determinants of myelin basic protein. Vaccination is determinant specific.
Authors: Holoshitz J , Frenkel A , Ben-Nun A , Cohen I R 
Published: December 2022

Abstract
Lines of T lymphocytes reactive against the basic protein of myelin (BP) were found in previous studies to mediate experimental autoimmune encephalomyelitis (EAE) in rats. Moreover, inoculation of rats with attenuated anti-BP line cells vaccinated them against subsequent attempts to induce active EAE by injection of BP in adjuvant. In the present study, we investigated the effects of T lymphocyte lines reactive to different antigenic determinants on the BP molecule, they are the major encephalitogenic peptide (EP) determinant present on guinea pig BP (G-BP), and minor, non-EP determinants present on bovine BP (B-BP). We found that both lines of T lymphocytes could mediate EAE. Resistance to active EAE acquired by spontaneous recovery from line mediated EAE or by vaccination with attenuated cells, however, was found to be specific for the particular BP determinant. Thus, EAE may be mediated by lines of T lymphocytes reactive to different determinants on the BP molecule, but the resistance to EAE acquired by exposure to line cells is determinant specific. This suggests that acquired resistance to EAE is directed by the receptor specificity of the autoimmune anti-BP T cells.
Inhibition of interleukin 2 production by factors released from tumor cells.
Authors: Hersey P , Bindon C , Czerniecki M , Spurling A , Wass J , McCarthy W H 
Published: December 2022

Abstract
In previous studies, cultured melanoma cells were shown to have a suppressive influence on the induction of cytotoxic T cells. Our investigation of the mechanism of these effects revealed that supernatants from certain cultures of melanoma cells contained inhibitory activity against the production of interleukin 2 (IL 2) from phytohemagglutinin (PHA)-stimulated cultures of lymphocytes. These supernatants did not inhibit interleukin 1 production, and also did not inhibit the mitogenic activity of performed IL 2 on IL 2-dependent target cells. Production of the inhibitory activity could be reduced by inhibitors of protein synthesis, but this activity was not inhibited by digestion with the proteolytic enzymes trypsin or pronase. Gel filtration analysis of tumor supernatants revealed that the majority of the inhibitory activity was detected in fractions of approximately 44 and 7 Kd. The addition of supernatants with inhibitory activity to PHA-stimulated cultures of lymphocytes was associated with reduced transition of cells from G1 to S phase of cell division, which could be reversed by the addition of IL 2. Preliminary studies suggest that the release of the factor(s) from melanoma cells may be related to rapid progression of tumor growth in patients, and therefore may be of prognostic significance in tumor host relationships.
IL 2 production by mitogen-stimulated T cell subsets: helper-precursors are predominantly Lyt-2-.
Authors: Miller R A 
Published: December 2022

Abstract
Although there is strong evidence that IL 2 can be secreted by at least some cells in both the Lyt-2- and Lyt-2+ T cell subsets, it is unclear whether lymphokine-secreting cells are present in equal frequencies in each population. We addressed this question by using a T cell mitogen, concanavalin A (Con A), that activates a large proportion of the cells of both subsets, as tested by their ability to grow in the presence of added conditioned medium. We found that, although Con A-responsive precursors of proliferating cells are at least as frequent in the Lyt-2+ set as in the Lyt-2- set, the frequency of Con A-responsive precursors of IL 2-secreting cells is much higher in the Lyt-2- population. Expressed as precursors per cell, lymphokine-secreting helpers are 17-fold more frequent in the Lyt-2- population. After adjusting for relative cell recoveries and for contamination, the data suggest that at least 97% (and more likely 99%) of the precursors for Con A-responsive IL 2-producing cells are in the Lyt-2- set. Thus, although the correlation between Lyt-2 surface antigen and helper function may not be absolute, our data support the idea that Lyt-2 does mark a functional distinction among T cells independent of antigen specificity.
Structural analysis of HLA-A2 antigen from immunoselected mutant 8.6.1: further definition of an HLA-A2-specific serological determinant.
Authors: Taketani S , Krangel M S , Pious D , Strominger J L 
Published: December 2022

Abstract
The HLA-A2 mutant cell line 8.6.1 was isolated previously from the lymphoblastoid B cell line T5-1 (HLA-A1, -A2, -B8, and -B27) by immunoselection with the mouse HLA-A2-specific monoclonal antibody BB7.2 and complement. The HLA-A2 molecules synthesized by 8.6.1 do not react with either the selecting antibody or with a second HLA-A2-specific monoclonal antibody, PA2.1. In this study, HLA-A2 heavy chains derived from 8.6.1 and those from the parent T5-1 cells have been analyzed by double-labeled tryptic peptide mapping by using reverse-phase HPLC, cation exchange chromatography, and microsequence analysis. We detect only a single difference between these molecules: 8.6.1 HLA-A2 differs from T5-1 HLA-A2 by the substitution of lysine for glutamic acid at position 161. This result is consistent with data derived from other immunoselected mutants, which implicate the second heavy chain domain (alpha 2) in the expression of the PA2.1 and BB7.2 epitopes, and suggests a crucial role for glutamic acid at position 161 in the formation of an HLA-A2-specific determinant.
The role of cyclic AMP in modulating cytotoxic T lymphocytes. II. Sequential changes during culture in responsiveness of cytotoxic lymphocytes to cyclic AMP-active agents.
Authors: Plaut M , Marone G , Gillespie E 
Published: December 2022

Abstract
Agents that increase cyclic AMP (cAMP) levels inhibited the activity of cytotoxic T lymphocytes (CTL) obtained from spleens of mice immunized with allogeneic cells. Cultured CTL, however, were desensitized to cAMP-active agents, in that the capacity of these agents to inhibit the activity of cultured CTL was markedly reduced. The capacity to inhibit CTL activity was reduced more rapidly for some agents than for others; the percent inhibition by histamine and PGE2 was reduced after 4 hr and was reduced more than 20% after 24 hr, whereas the percent inhibition by dibutyryl cAMP, theophylline, and cholera enterotoxin was reduced less than 6% after 24 hr, and was reduced significantly only after 48 hr. Culture in the presence of antigen accelerated desensitization to the latter three agents. CTL populations were also tested for their capacity to increase cAMP levels in response to agonists. The capacity of histamine to increase cAMP levels of the CTL was lost within 4 hr (i.e., as rapidly as its capacity to inhibit CTL activity) and was never restored, whereas the capacity of PGE2 to increase cAMP levels persisted throughout culture. These results suggest that culture induces multiple alterations in cAMP metabolism of CTL. These alterations, which result in dissociation of CTL activity from cAMP-mediated regulatory steps, may include loss of histamine receptors and/or histamine receptor-adenylate cyclase coupling, and also loss of one or more biochemical reactions that link elevated cAMP levels to inhibition of lysis.
Activation of granulocyte cytotoxic function by purified mouse colony-stimulating factors.
Authors: Lopez A F , Nicola N A , Burgess A W , Metcalf D , Battye F L , Sewell W A , Vadas M 
Published: December 2022

Abstract
Highly purified mouse colony-stimulating factors (CSF) were tested for their effect on neutrophil cytotoxic function in a homologous antibody-dependent cell-mediated cytotoxicity (ADCC) assay in which TNP-coupled mouse thymoma cells coated with mouse anti-TNP antibodies were used as targets, and purified normal mouse bone marrow neutrophils or induced peritoneal neutrophils were used as effector cells. Biochemically pure granulocyte-macrophage (GM)- and granulocyte (G)-CSF enhanced the cytotoxic activity of neutrophils obtained from both sources, allowing them to kill target cells at low antibody concentrations. Furthermore, GM- and G-CSF showed an additive effect, suggesting either the presence of separate receptors for GM- and G-CSF or of separate subsets of neutrophils. Induced peritoneal neutrophils showed a higher level of basal cytotoxic activity than did bone marrow neutrophils, suggesting neutrophil activation in vivo, but both reached similar levels of cytotoxicity upon maximal stimulation with CSF. In addition, CSF was found to be cross-reactive between mouse and human species in their enhancement of neutrophil cytotoxicity. By testing purified mouse CSF on human neutrophils, it could be shown that G-CSF and GM-CSF are functionally distinct molecules, because only G-CSF enhanced ADCC by human neutrophils. These experiments show that the purified factors that control the production of neutrophils by progenitor cells in vitro also activate differentiated neutrophils to carry out their cytotoxic activity in a more effective manner.
Humoral antibody response to individual viral proteins after murine cytomegalovirus infection.
Authors: Selgrade M K , Huang Y S , Graham J A , Huang C H , Hu P C 
Published: December 2022

Abstract
The purpose of this study was to identify viral proteins that played an important role in the humoral immune response to murine cytomegalovirus (MCMV). Viral proteins were separated from a purified virus preparation on polyacrylamide gels, were blotted onto nitrocellulose strips, and were reacted with antisera collected from mice on various days post infection. No antibody response was detected in serum obtained 5 days post infection, but by 10 days there was a faint response to five different proteins. Thereafter, the number of proteins eliciting an antibody response, as well as the intensity of the response, increased with time so that by 42 days post infection a response to 13 major antigens was detected. This method provides a means of separating out important immunogens from the more than 30 different MCMV proteins originally identified by polyacrylamide gel electrophoresis. Such information may improve our understanding of the pathogenesis of MCMV infection as well as host immune responses to the virus.
Effect of T cell-derived lymphokines containing B cell differentiation factor(s) for IgG (BCDF gamma) on gamma-specific mRNA in murine B cells.
Authors: Jones S , Chen Y W , Isakson P , Layton J , Pure E , Word C , Krammer P H , Tucker P , Vitetta E S 
Published: December 2022

Abstract
Cytoplasmic RNA was isolated from cells cultured with LPS and LPS plus a T cell-derived supernatant (SN) (PK 7.1) containing B cell differentiation factors. The steady state levels of isotype-specific mRNA were assessed by Northern blot analysis with gamma-specific CH3 probes. It was demonstrated that the SN induces an increase in the level of mRNA for gamma 1 and a concomitant decrease in the levels of mRNA for gamma 2b and gamma 3.