bluuebunny/crossref_metadata_2025_split huggingface dataset:
Control of lipopolysaccharide-high density lipoprotein binding by acute phase protein(s).
Authors: Tobias P S , Ulevitch R J 
Published: December 2022

Abstract
When Salmonella minnesota R595 lipopolysaccharide (LPS) is mixed with serum, the LPS eventually forms a complex with high density lipoprotein (HDL). Complex formation is conveniently followed by CsCl equilibrium density gradient centrifugation. When mixing 10 micrograms LPS with normal rabbit serum (NRS) at 37 degrees C in the presence of 20 mM EDTA, the half-life for LPS binding to HDL is typically 2 to 3 min. When the same experiment is performed with the use of acute phase rabbit serum (APRS; collected 24 hr post-induction with silver nitrate), the half-life for LPS binding to HDL is typically 40 to 100 min. Thus LPS binding to HDL occurs some 20- to 40-fold slower in APRS than in NRS. Two other phenomena have been found, the time dependencies of which correlate well with the time dependency of LPS binding to HDL in APRS. If LPS-APRS reaction mixtures are cooled to 4 degrees C shortly after mixing and are dialyzed against 2.5 mM HEPES, 15 mM NaCl, pH 7.4 buffer, LPS is recovered in the washed precipitates ("euglobulin precipitate") if, and only if, the LPS-HDL binding reaction is not complete. The amount of LPS in the precipitate correlates well with the amount of LPS that has not bound to HDL. The second phenomenon we observe is that the LPS-containing euglobulin precipitate prepared from LPS-acute phase serum reaction mixtures shortly after mixing also contains a protein, gp60, the concentration of which in the euglobulin precipitate correlates well with the amount of LPS in the precipitate. Thus three phenomena are kinetically well correlated in APRS: the degree of binding of LPS to HDL, the degree of appearance of LPS in a euglobulin fraction, and the concentration of protein gp60 in the euglobulin fraction. We were unable to precipitate gp60 from APRS in the absence of LPS, from APRS after the LPS has fully bound to HDL, or from normal serum in the presence or absence of LPS. The known properties of gp60 are not reminiscent of any other known acute phase reactant. These data demonstrate that APRS contains acute phase reactants that interact with LPS to modify its buoyant density, its solubility, and the rate of its binding to HDL.
C3b deposition during activation of the alternative complement pathway and the effect of deposition on the activating surface.
Authors: Pangburn M K , Schreiber R D , Müller-Eberhard H J 
Published: December 2022

Abstract
Examination of C3b deposition on the surface of activators during alternative pathway activation revealed three temporal phases: a lag phase, an amplification phase, and a heretofore uncharacterized plateau phase. During the plateau phase no C3b deposition appeared to occur even in the presence of an excess of alternative pathway components. Double label experiments, however, revealed that the plateau was a steady state between continued C3b deposition and release of C3b or C3bi from the activator. Under conditions of excess complement it was found that deposition of increasing numbers of C3b molecules caused a gradual increase in the ability of Factors H and I to inactivate newly deposited C3b; i.e., the deposited C3b converted the activator into a nonactivator. The data indicate that the surface of rabbit erythrocytes is rendered completely nonactivating when 2.4 X 10(6) molecules of C3b plus C3bi are bound per cell. The plateau of C3b deposition appears to represent the maximum steady state level maintainable by a given concentration of complement components, and it also reflects conversion of an activating surface to one resembling a nonactivator.
Cellular mechanisms of genetically controlled host resistance to Mycobacterium bovis (BCG).
Authors: Gros P , Skamene E , Forget A 
Published: December 2022

Abstract
Multiplication of Mycobacterium bovis (BCG) in the reticuloendothelial tissues of the mouse is controlled by the Chromosome 1 locus (Bcg), which exists in two allelic forms, resistant (Bcgr) and susceptible (Bcgs). We have investigated the phenotypic expression of this locus at the cellular level in vivo. No significant differences were observed in the early clearance of BCG from the bloodstream and peritoneal cavity, nor in the uptake of the infectious inoculum in spleen and liver of the mice of Bcgr and Bcgs strains. Inflammatory response to an i.p. injection of live BCG, with respect to both the cell populations involved and the kinetics of their appearance, was comparable in Bcgr and Bcgs mice. A kinetic study of BCG infection in congenitally athymic mice that carried the "nude" mutation on Bcgr (AKR/J) or Bcgs (BALB/c) background showed that the functional absence of T lymphocytes did not influence the expression of the Bcg gene. The population expressing the Bcg gene seems to be a mature cell of the mononuclear phagocyte lineage: it was resistant to a 950-rad dose of x-irradiation; it was susceptible to a prolonged exposure to silica; and, as demonstrated in radiation chimeras, it originated from bone marrow-derived precursors.
Humoral immune response in experimental syphilis to polypeptides of Treponema pallidum.
Authors: Hanff P A , Bishop N H , Miller J N , Lovett M A 
Published: December 2022

Abstract
The ontogeny of the IgG response in rabbits with experimental syphilis to individual polypeptides of Treponema pallidum, Nichols strain, was examined. The polypeptides of motile, virulent T. pallidum, purified from host tissue by Percoll density gradient centrifugation, were separated on SDS-polyacrylamide gels and were electrophoretically transferred to a solid-phase matrix of nitrocellulose for antigen analysis. Serum from rabbits early in infection at day 3 post-infection showed a weak but detectable IgG response to two polypeptides of 60,000 and 46,000 m.w. This was followed on days 11, 17, and 19 by an apparent quantitative increase in antibody to other treponemal protein antigens. By day 19, 21 of the 22 detectable polypeptides could be identified. A similar set of antigens was detected by serum from patients with human secondary and early latent syphilis. A close correlation was found between the presence of IgG antibody to T. pallidum polypeptides at day 9 and 1, 4.5, 13.5, and 17 mo post-infection and the immune status of the rabbit to symptomatic reinfection. Serum from rabbits that were partially immune to challenge at day 9 detected three polypeptides of 60,000, 46,000, and 36,000 daltons. By 1 mo post-infection, at a time when a more complete immunity had developed, the number of detectable antigens increased to 21 polypeptides ranging in m.w. from 94,000 to 14,400 daltons. IgG antibody to 22 treponemal antigens persisted in animals that were solidly immune to symptomatic reinfection at 3, 4.5, 13.5, and 17 mo post-infection. Serum neutralizing activity was not demonstrable at day 9 or 1 mo post-infection, however, but was present at 3, 4.5, 13.5, and 17 mo. The results suggest that after intratesticular challenge a vigorous IgG response to T. pallidum polypeptides can be detected. The potential role of humoral immune mechanisms in the development and maintenance of immunity is discussed.
The mechanism of retrovirus suppression of human T cell proliferation in vitro.
Authors: Copelan E A , Rinehart J J , Lewis M , Mathes L , Olsen R , Sagone A 
Published: December 2022

Abstract
Immunosuppression is commonly associated with retrovirus-induced animal tumors. Studies in the murine and feline retrovirus systems suggest that the 15,000-dalton envelope protein (p15E) of the virion may contribute to immunosuppression by interfering with normal lymphocyte function. We examined the effect of inactivated feline leukemia virus (UV-FeLV) and p15E derived from this virus on concanavalin A (Con A) driven human T cell proliferation. Virus and p15E markedly suppressed mononuclear cell proliferative response to Con A. Suppression was not due to inhibition of monocyte accessory cell function, or interleukin 1 (IL 1) secretion. In fact, the presence of monocytes partially protected T cells from UV-FeLV suppression. UV-FeLV, however, suppressed T cell secretion of and response to interleukin 2 (IL 2). We conclude that UV-FeLV and derived p15E inhibit T cell proliferation by direct inhibition of T cell function. These findings, extended to the in vivo situations, suggest that retrovirus-associated suppression of the immune response involves the induction of T cell but not monocyte dysfunction.
The binding of tumor cells by murine mononuclear phagocytes can be divided into two qualitatively distinct types.
Authors: Somers S D , Mastin J P , Adams D O 
Published: December 2022

Abstract
Peritoneal macrophages from C57BL/6N mice infected with BCG have a greater capacity for tumor cell binding than do inflammatory macrophages elicited by several agents. To determine if these quantitatively distinct types of binding were qualitatively distinct as well, we compared them in several ways. Scanning electron microscopy of macrophage-tumor cell interactions reveals clustering of 2 to 5 tumor targets on the central portion of BCG-activated macrophages, in contrast to the very few tumor cells found at the periphery of inflammatory macrophages. Tumor cell binding to BCG-activated macrophages required divalent cations and trypsin-sensitive surface structures on the macrophages, but the low-level binding to inflammatory macrophages required neither. The ability of trypsinized BCG-activated macrophages to bind P815 tumor targets was recovered with time in culture. BCG-activated macrophages required intact energy metabolism, microfilaments, and microtubules to complete augmented tumor cell binding, whereas inflammatory macrophages did not. Targets bound to BCG macrophages could be competitively removed by addition of large excesses of unlabeled tumor cells, but targets bound to inflammatory macrophages could not be so removed. Tumor cells labeled with 111Indium oxine were used to estimate the specific (i.e., competitively inhibitable) and nonspecific (noncompetitively inhibitable) components of binding. Binding of P815 tumor cells to BCG-activated macrophages was predominantly specific, whereas their binding to inflammatory macrophages was predominantly nonspecific. Binding by activated or inflammatory macrophages of lymphocytes or by transformed 3T3 cells of neoplastic or non-neoplastic targets was also nonspecific. Binding by BCG-elicited macrophages from A/J mice, previously demonstrated to be quantitatively deficient in binding ability, was qualitatively similar to that to inflammatory macrophages and was not competitively inhibitable. The data suggest that tumor cell binding by activated macrophages is qualitatively as well as quantitatively distinct from binding to inflammatory macrophages.
Lyb-5- B cells of CBA/N mice can be induced to synthesize DNA by culture with insolubilized but not soluble anti-Ig.
Authors: Mond J J , Schaefer M , Smith J , Finkelman F D 
Published: December 2022

Abstract
The use of anti-immunoglobulin (anti-Ig) antibodies to stimulate B cell proliferation (1-4), and to stimulate B cell differentiation in the presence of T cell derived-lymphokines (5-8), has simplified investigations into the mechanisms of B cell growth and maturation that are dependent on the cross-linking of surface Ig (sIg). It is only the ontogenetically late appearing Lyb-5+ murine splenic B cells, however, that proliferate in response to anti-Ig antibodies, whereas B cells of the Lyb-5- phenotype obtained from neonatal mice or from mice with the xid immune defect cannot be induced to proliferate in response to this stimulus (1, 9, 10). Thus, the analysis of B lymphocyte physiology of the Lyb-5- B cell population has been hampered by the unavailability of B cell stimulants that mimic an antigen-induced sIg cross-linking event that leads to B cell activation. The inability of soluble anti-Ig antibodies to induce the proliferation of Lyb-5- cells has been particularly difficult to explain because these cells can be induced to increase in size (11) and to show an increase in their expression of surface Ia (sIa) after exposure to anti-Ig (12). Apparently, therefore, these cells are not entirely refractory to this stimulus but are simply unable to progress to the latter stages of cell activation. In view of our observations that the cells of CBA/N mice cannot respond to soluble trinitrophenyl-(TNP) dextran or TNP-polyacrylamide (13) but can respond to insolubilized forms of these antigens, we evaluated their ability to respond to insolubilized anti-Ig. In this paper we report that B cells from CBA/N mice can be stimulated to proliferate in response to anti-Ig conjugated to Sepharose beads, but in contrast to normal B cells they need to be stimulated with beads expressing a high-epitope density of anti-Ig antibodies.
Inhibition of macrophage tumoricidal activity by immune complexes and altered erythrocytes.
Authors: Esparza I , Green R , Schreiber R D 
Published: December 2022

Abstract
Engagement of the macrophage membrane by biologic particles including insoluble immune complexes inhibited the development of lymphokine-mediated nonspecific tumoricidal activity by murine macrophages. The degree of inhibition was dependent on the dose of particles and the lymphokine concentration. Inhibition was not due to macrophage cell death or to diminution of cell adherence after ingestion of the immune complexes. Soluble immune complexes were not inhibitory, although approximately 10% of the complexes became cell-associated. Monomeric or heat-aggregated IgG was also not inhibitory. IgG-opsonized erythrocytes (EA) were inhibitory and inhibition was dependent on the degree of opsonization. In contrast, nonopsonized erythrocytes (E), which did not bind to macrophages, were not inhibitory. Phagocytosis of glutaraldehyde-treated E or E carrying IgM antibody and complement (EAC) also led to a reduction of tumorilytic activity. Insoluble immune complexes were inhibitory when added either before or after lymphokine. Phagocytosis was neither sufficient nor necessary to cause inhibition because 1) ingestion of polystyrene latex beads did not diminish tumoricidal activity, and 2) macrophages plated on IgG-coated surfaces were inhibited with respect to the tumoricidal function. Inhibition was not affected when indomethacin (10(-6) M) was included in the assay, which indicated that prostaglandins were not involved in the process. Thus, macrophage tumoricidal responsiveness may be compromised by interaction of biologic substances with macrophage plasma membranes. This process may thereby inactivate an important host defense mechanism against neoplastic cells.
Polyclonal activation of the murine immune system by an antibody to IgD. IV. In vivo activation of B lymphocytes from immune defective CBA/N mice.
Authors: Muul L M , Scher I , Mond J J , Finkelman F D 
Published: December 2022

Abstract
Previous studies with BALB/c mice have established that the injection of a goat antibody to IgD (GaM delta) induces splenic B lymphocytes to undergo T-independent, polyclonal increases in cell surface (s) Ia expression, size, and DNA synthesis 1 day after injection, as well as T-dependent maintenance of this activation and differentiation into sIgG1+ cells and IgG1-secreting cells 6 to 7 days after injection. Because B lymphocytes from mice homozygous or hemizygous for the CBA/N X-linked immune defect fail to proliferate in vitro when cultured with soluble anti-Ig antibodies, yet can make in vivo primary antibody responses to T-dependent antigens, we studied the effects of injecting (CBA/N X DBA/2)F1 male mice (immune defective) and (CBA/N X DBA/2)F1 female mice (phenotypically normal) with 800 to 1600 micrograms of GaM delta. B cells from immune defective mice demonstrated definite but distinctly subnormal increases in B cell size, DNA synthesis, and sIa expression 1 to 5 days after GaM delta injection, but by day 7 showed increases in these parameters as well as in the percentages of splenic sIgG1+ cells and IgM-secreting cells that were similar to those exhibited by the immunologically normal mice. However, IgG1 secretion by the immune defective mice was at this time only one-fourth to one-half as great as that observed with normal mice. Our data raises the possibility that the differentiation of B cells into IgG1-secreting cells may be more dependent upon the GaM delta-induced activation steps that are defective in CBA/N mice than is the differentiation of B cells into IgM-secreting cells or into sIgG1 cells.
Characterization of early B lymphocyte precursors present in long-term bone marrow cultures.
Authors: Dorshkind K , Phillips R A 
Published: December 2022

Abstract
Lymphoid precursor cells are present in long-term bone marrow cultures (LTBMC), but their differentiation into mature lymphocytes is blocked. A quantitative assay for B cell precursors in LTBMC, which gives a linear relationship between the number of grafted LTBMC cells and the frequency of B cell colony forming units (CFU-B) in the spleen and bone marrow of immunodeficient CBA/N mice 19 days after reconstitution, is described. Characterization of the B cell precursor indicates that this assay is detecting a very early precursor and not a B lymphocyte or a late pre-B cell. This conclusion is based on the observations that a) pre-B cells transformable by Abelson murine leukemia virus are not present in LTBMC by 3 days postrecharge and CFU-B are absent by 6 days postrecharge; b) late B cell progenitors capable of rapid repopulation of irradiated CBA/N mice are not present in LTBMC, since a lag in the kinetics of B cell reconstitution in animals grafted with LTBMC cells is observed compared with fresh bone marrow cells; c) the B cell precursors in LTBMC have high proliferative potential, since they can stably repopulate recipient mice for at least 8 wk postreconstitution and through two serial passages in irradiated CBA/N recipients; and d) the B cell precursors are large, rapidly sedimenting cells as determined by velocity sedimentation. The serial transplantation experiment further shows that a split is often observed between lymphoid and myeloid reconstituting ability of LTBMC cells. The LTBMC B cell precursor may be a pluripotent stem cell or a lymphoid stem cell, although its differentiative potential remains to be determined.
In vitro analysis of allogeneic lymphocyte interaction. VIII. Characterization of helper components of allogeneic effect factor (AEF) that activate Lyb5+ and Lyb5- B cells to respond to thymus-dependent and thymus-independent antigens.
Authors: Delovitch T L , Kaufman K , Gorczynski R D , Sinclair G D 
Published: December 2022

Abstract
We analyzed the ability of an allogeneic effect factor (AEF), produced using alloactivated A.SW (H-2s) responder T cells and irradiated A/WySN (H-2a) T cell-depleted stimulator spleen cells, to enhance the responsiveness of Lyb5+ and Lyb5- B cells to thymus-dependent (TD) and thymus-independent type 1 (TI-1) and type 2 (TI-2) antigens. We found that normal adult male CBA/CaHN (Lyb5+ + Lyb5-) B cells are activated by unfractionated AEF in primary in vitro IgM antibody responses to the SRBC (TD), TNP-LPS (TI-1), and TNP-Ficoll (TI-2) antigens. Adult male xid CBA/N (Lyb5-) B cells are activated by unfractionated AEF to respond to TNP-LPS but to neither SRBC nor TNP-Ficoll. Gel filtration of AEF on ACA 54 resolves several helper components. One component, which is I-Ak restricted in its activity and may represent a secreted form of an Ia antigen T cell receptor, interacts with histocompatible and functionally competent CBA/CaHN or CBA/N antigen-presenting cells to activate a primary anti-SRBC response of CBA/CaHN B cells but not of CBA/N B cells. A second antigen-nonspecific and H-2-nonrestricted AEF component, which consists of interleukin 2 and possibly also interleukin 1, activates anti-SRBC and anti-TNP-Ficoll responses of both CBA/CaHN B cells and CBA/N B cells. Such CBA/N B cell responses were potentiated by this AEF component only after its biochemical fractionation and only in the presence of a limiting number of T cells. These data indicate that both Lyb5+ and Lyb5- B cells are responsive to TD, TI-1, and TI-2 antigens in the presence of ancillary antigen-nonspecific help. They are also consistent with the notion that T helper cell activation of Lyb5+ B cells is H-2 nonrestricted and that T helper cell activation of Lyb5- B cells is H-2 restricted.
Murine hybridomas secreting natural monoclonal antibodies reacting with self antigens.
Authors: Dighiero G , Lymberi P , Mazié J C , Rouyre S , Butler-Browne G S , Whalen R G , Avrameas S 
Published: December 2022

Abstract
Spleen cells from nonimmunized BALB/c mice were fused with two nonsecreting myeloma lines. The hybrids were selected in HAT medium and screened for Ig production and for antibody activity against actin, tubulin, myosin, thyroglobulin, myoglobin, spectrin, dsDNA, fetuin, and transferrin. Among 161 hybrids secreting Ig, three were found to react with DNA, one with thyroglobulin, and one mainly with myosin. Two of these hybrids could be propagated and further characterized. On the basis of inhibition experiments, one was found to be directed against dsDNA; the other was directed mainly against myosin but at the same time reacted significantly with actin, tubulin, spectrin, and dsDNA. Reactivity with myosin seemed to be concentrated in the light meromyosin subfragment, known to be rich in alpha-helical structure. These results indicate: 1) There are reactive B cell clones directed against self antigens. 2) The antibody specificities found for these antibodies are very similar to those found for natural antibodies in normal human serum and for human monoclonal Ig. 3) The widespread reactivity found for the clone mainly reacting with myosin raises the possibility that the determinant recognized by this antibody is a conformational structure that possibly is associated with alpha-helical structures.
Interleukin 2 is not sufficient for the continuous growth of cloned NK-like cytotoxic cell lines.
Authors: Olabuenaga S E , Brooks C G , Gillis S , Henney C S 
Published: December 2022

Abstract
Interleukin 2 (IL 2) has been strongly implicated as the agent responsible for the continuous growth of T cell lines in vitro. In the present study we confirmed that IL 2 alone could support the growth of a widely used cytotoxic T cell line. In contrast, we found that IL 2 was not sufficient to support the long-term growth of cloned NK-like cytotoxic lymphocyte cell lines. Whereas such lines would grow indefinitely in concanavalin A-induced mouse spleen cell supernatant, they would only grow for short periods (2 to 3 days) in the IL 2-containing supernatant of phytohemagglutinin-stimulated LBRM-33 tumor cells, or in IL 2 partially purified from spleen cell or LBRM-33 supernatants. The addition of concanavalin-A or interferon (type beta or gamma) to these supernatants did not improve growth. By contrast, the NK-like cells proliferated equally well in a short-term (24-hr) assay, irrespective of the source of IL 2 (spleen or LBRM-33 supernatant, or partially purified IL 2). Furthermore, the NK-like cells readily depleted IL 2 from the medium, either during growth at 37 degrees C or by absorption at 4 degrees C. It is concluded that at least some cytotoxic cell lines require both IL 2 and other, as yet unidentified, spleen cell-derived factors for long-term growth.