bluuebunny/crossref_metadata_2025_split huggingface dataset:
Suppression of human peripheral blood lymphocytes by Fusobacterium nucleatum.
Authors: Shenker B J , DiRienzo J M 
Published: December 2022

Abstract
Fusobacterium nucleatum has been implicated in the pathogenesis of several diseases, including urinary tract infections, bacteremia, pericarditis, otitis media, and disorders of the oral cavity such as pulpal infections, alveolar bone abscesses, and periodontal disease. In this study, we examined sonic extracts of F. nucleatum strain FDC 364 for its ability to alter human lymphocyte function. We found that the soluble cytoplasmic fraction (CF) of the sonic extract was able to cause a dose-dependent inhibition of human lymphocyte responsiveness to Con A, PHA, PWM, and the recall antigen SKSD. Suppression involved altered DNA, RNA, and protein synthesis; there was no effect on cell viability. The suppressive activity is nondialyzable and heat labile. To achieve maximal suppression in 96-hr cell cultures, the CF had to be added to cells during the first 24 hr of incubation. Inhibition was reduced when the CF was added at 48 hr, and no suppression was observed when addition was at 72 or 96 hr (along with [3H]TdR). Furthermore, cells could be protected from the suppressive effects of the CF by washing within 24 hr of exposure. Suppression did not involve nonspecific effects on thymidine utilization. Although the mechanism of action of the F. nucleatum immunosuppressive activity has not yet been determined, we can rule out a requirement for monocytes/macrophages and activation of T suppressor cells. It has been proposed that impaired host defense may play a pivotal role in the pathogenesis of many diseases. The data presented in this paper suggest that local and/or systemic immunosuppression could be initiated by F. nucleatum. This immunosuppression may alter the nature and consequences of host-parasite interactions, thereby enhancing the pathogenicity of F. nucleatum itself or that of some other opportunistic organism.
The immunopathology of experimental allergic encephalomyelitis. I. Quantitative analysis of inflammatory cells in situ.
Authors: Sobel R A , Blanchette B W , Bhan A K , Colvin R B 
Published: December 2022

Abstract
Acute experimental allergic encephalomyelitis (EAE) is a T cell-mediated, neurologic disease that is under immunogenetic control. We systematically analyzed the quantity and distribution of T cells, B cells, and macrophages in the central nervous system (CNS) of susceptible and resistant guinea (GP) with a panel of seven monoclonal antibodies by using the avidin-biotin complex (ABC) immunoperoxidase technique and alpha-naphthyl-butyrate esterase (ANBE) staining. Adult EAE-susceptible strain 13 GP immunized with isogeneic spinal cord homogenate (SC) or with myelin basic protein (MBP) developed clinical signs (paralysis, weight loss, etc.) in 2 to 3 wk. T cells were present in all CNS inflammatory foci and comprised 44% of the perivascular mononuclear cells. T cells diffusely infiltrated the neuropil away from inflammatory cell aggregates. These T cells were judged to be extravascular by the lack of an associated identifiable vessel in counter-stained sections, and by their persistence following exhaustive perfusion of the brains. In routine sections, mononuclear cells could be detected only in perivascular aggregates. IgM+ B cells comprised 9% of the perivascular infiltrates and did not diffusely infiltrate the parenchyma. ANBE+ macrophages comprised the remaining 47% of the identified perivascular cells. SC- and MBP-immunized GP showed equivalent numbers of inflammatory foci, T cells, and macrophages, but SC-immunized GP had more IgM+ cells in the meninges and choroid plexus (p less than 0.001, p less than 0.02, respectively). Virtually all cells in perivascular locations were Ia+. Ia+ mononuclear cells were also present in the neuropil. EAE-resistant strain 2 GP immunized with SC developed no clinical signs. These GP had fewer perivascular foci than strain 13 GP but, when present, the cellular composition, including the density of diffuse parenchymal T cell infiltrates, was indistinguishable. Significantly fewer parenchymal mononuclear cells in the strain 2 GP, however, displayed Ia, both in perivascular and diffuse infiltrates (p less than 0.001). We conclude that T cell migration into the CNS parenchyma is a characteristic feature of acute EAE in the GP, but that T cells can occur in this pattern without clinical signs of disease. The two features that distinguish susceptible and resistant strains were the frequency of perivascular infiltrates and the expression of Ia on parenchymal mononuclear cells, which probably reflects their enhanced immunologic activation in situ.
Modulation of class I HLA antigens on HL-60 promyelocytic leukemia cells by serum-free medium: re-induction by gamma-IFN and 1,25-dihydroxyvitamin D3 (calcitriol).
Authors: Ball E D , Guyre P M , Glynn J M , Rigby W F , Fanger M W 
Published: December 2022

Abstract
During studies on the effect of different nutrient media on the growth and differentiation of the HL-60 promyelocytic leukemia cell line, we found that the density of the class I HLA antigens is profoundly decreased on cells cultured in a serum-free medium. The ability of recombinant DNA-derived interferons (IFN) and a number of myeloid differentiating agents to induce re-expression of class I HLA antigens and beta-2-m was therefore studied. All three classes (alpha, beta, and gamma) of IFN were capable of re-inducing HLA and beta-2-m, although gamma-IFN was more potent. Of a variety of chemical differentiating agents, only 1,25-dihydroxyvitamin D3 (calcitriol) was found to induce HLA class I antigens. These results suggest that HLA and beta-2-m are not necessarily constitutive cell surface proteins, but instead that their expression is highly inducible.
Two-dimensional gel analysis of a second family of class II molecules by polymorphic HLA-DR4,5, and w9 monoclonal antibodies.
Authors: Maeda H , Hirata R , Okuyama M , Thompson A , Tohyama H 
Published: December 2022

Abstract
Human Ia-like, class II molecules were isolated by immunoprecipitation with monoclonal antibodies from various HLA-D/DR homozygous cell lines and were analyzed by two-dimensional gel electrophoresis. The monoclonal antibody PLM12 reacted with B cells carrying DR4, DR5, DRw6.2, and DRw9 phenotypes, and its reactivity perfectly correlated with the previously defined TB21 (MB3-like) specificity. Class II molecules detected by PLM12 were structurally distinct from those precipitated by the anti-DR monoclonal antibody NC1 on all HLA-DR4, DR5, DRw6.2, and DRw9 homozygous cell lines and showed polymorphism in heavy and light chains among these cell lines. The monoclonal antibodies PLM2 and PLM9 only reacted with B cells carrying DR5 and DRw6.2 and also detected a distinct set of class II molecules from those precipitated by NC1 but identical to those of PLM12. Thus, PLM2 and PLM9 serologically detected a new subtypic antigen of the PLM12-reactive class II molecules. Furthermore, the antibody NC1 precipitated two light chains and one heavy chain from HLA-DRw6.2 homozygous cell line EBV-Sh. The result indicated the presence of three sets of class II molecules: two in a DR family and another carrying the polymorphic determinants detected by PLM2, PLM9, and PLM12 in a second family.
Monoclonal antibodies against SSEA-1 antigen: binding properties and inhibition of human natural killer cell activity against target cells bearing SSEA-1 antigen.
Authors: Harris J F , Chin J , Jewett M A , Kennedy M , Gorczynski R M 
Published: December 2022

Abstract
We describe the properties of three monoclonal antibodies (Mab) against stage-specific embryonic antigen-1 (SSEA-1) in terms of their binding activity to HL60, K562, OTF9, and SOTF9 tumor target cells and their functional activity in modulating human natural killer (NK) cytotoxicity assays in vitro against these target cells. Indirect binding, competition, and Western blot analyses indicate that the Mab AEC3A1-9 (3A1), ASSEA-1, and AECAB1-32 (AB1) recognize cell-defined SSEA-1 antigen with activity characteristic of the cell source (HL60 greater than OTF9 greater than K562 much greater than SOTF9). The addition of anti-SSEA-1 Mab to the NK cytotoxicity assay resulted in an inhibition of LU per 1 X 10(6) PBL that correlated closely with the expression of SSEA-1 antigen on the target cell. No significant inhibition was seen for seven other Mab. Inhibition of NK activity (greater than 30%) was observed in the presence of anti-SSEA-1 Mab for 18 of 21 and 6 of 7 human donors examined for HL60 and OTF9 target cells, respectively. The pretreatment of fixed competing cells with anti-SSEA-1 Mab reduced the efficacy of those cells to act as cold competitors in a standard NK cytotoxic assay. Taken together these data suggest that SSEA-1 determinants are important at some stage in the cytolysis produced by NK cells.
Activation of rat serosal mast cells by chymase, an endogenous secretory granule protease.
Authors: Schick B , Austen K F , Schwartz L B 
Published: December 2022

Abstract
Chymase, the major neutral protease of the rat serosal mast cell (RMC) secretory granule, causes RMC to release their secretory granules and to oxidatively metabolize endogenous arachidonic acid to prostaglandin D2 (PGD2). The granule markers, endogenous beta-hexosaminidase and exogenously added [3H]serotonin, were released from 2.5 X 10(5) RMC in 50 microliters in parallel and in dose-response fashion, reaching a maximum net percent release of approximately 50% with 0.5 to 1.0 units chymase (15 U/mg)/ml. With incremental concentrations of chymase, the release of granule markers occurred with a shorter lag period and in a greater maximal net percent, whereas the release of PGD2 was dose-related without a reduction in latency to detectable generation. Inhibition of the esterase activity of chymase with lima bean trypsin inhibitor decreased the subsequent mast cell response, indicating that the active site of chymase was required to initiate granule secretion and PGD2 generation. The monophasic indomethacin-resistant rise in cellular cAMP at 15 to 45 sec coincident with the onset of chymase-induced mediator release and PGD2 secretion is similar to that observed with IgE receptor-initiated coupled activation-secretion. The ability of heparin to block the activation function of chymase without inhibition of esterase activity reveals a possible physiologic regulatory mechanism for limiting the potential action of secreted chymase.
An immunoprotective monoclonal antibody to lipopolysaccharide.
Authors: Kirkland T N , Ziegler E J 
Published: December 2022

Abstract
The ability of antisera against lipopolysaccharide (LPS) raised by immunization with gram-negative bacteria to prevent LPS toxicity and death from gram-negative bacteremia is well established. To demonstrate conclusively that the protective antibody is specific for LPS, we tested an anti-LPS monoclonal antibody (mAb) in three animal models. 7G is an IgG3 mAb directed against an oligosaccharide side chain determinant of LPS from E. coli 0111:B4. This anti-LPS mAb increased the LD50 of 0111:B4 LPS in mice and protected rabbits against the dermal Shwartzman reaction elicited by 0111:B4 LPS. 7G mAb also protected mice against lethal infection with mucin-enhanced E. coli 0111:B4. Pretreatment with 250 micrograms of 7G increased the LD50 by more than 1.5 logs. These studies prove that oligosaccharide side chain-specific antibody to LPS confers protection against LPS toxicity in vivo and against experimental gram-negative infection. In addition, these studies suggest the potential of anti-LPS monoclonal antibody as therapy for gram-negative infection.
Genetic control of the induction of cytolytic T lymphocyte responses to AKR/Gross viral leukemias. II. Negative control by the Fv-1 locus in AKR mice of responder H-2b haplotype.
Authors: Green W R 
Published: December 2022

Abstract
To assess whether the presence of a responder H-2b haplotype would be sufficient to allow mice of nonresponder "high leukemic" phenotype to generate syngeneic anti-AKR/Gross virus cytolytic T lymphocytes (CTL), the AKR.H-2b strain was examined. Although capable of mounting vigorous apparent anti-minor histocompatibility-specific CTL responses, AKR.H-2b mice failed to produce anti-viral CTL after a variety of stimulation protocols. In contrast, the "doubly congenic" AKR.H-2b:Fv-1b strain was able to respond with substantial levels of H-2-restricted anti-AKR/Gross virus CTL activity. These results indicated that Fv-1n alleles could exert negative epistatic control over responder H-2b-encoded gene(s). Because the B6.Fv-1n congenic was also able to generate anti-viral CTL indistinguishable from the prototype B6 strain, however, it was apparent that other genes of AKR background were required for the Fv-1n-mediated inhibition in AKR.H-2b mice. The mechanism by which Fv-1 intereacted with other genes to override positive H-2b control appeared to be related to the expression of the CTL-defined, virus-associated antigens by normal AKR.H-2b cells. Thus, AKR.H-2b spleen cells but not thymus cells were able to stimulate the production of B6 anti-AKR/Gross virus CTL and were recognized as target cells by such anti-viral CTL. In contrast, both spleen cells and thymocytes from AKR.H-2b:Fv-1b mice were negative when tested as stimulator or target cells in these assays. In addition, AKR.H-2b but not AKR.H-2b:Fv-1b spleen cells were shown to display serologically defined gp70 determinants and the Gross cell surface antigen. Taking these data together, it appeared that the inhibition of anti-viral CTL responsiveness might be due to tolerance induced by the cell surface expression of virus-associated antigens by normal AKR.H-2b cells. Widespread display of viral antigens, in turn, may have been due to the permissive effects of Fv-1n on the spread of the early arising N-ecotropic, endogenous AKR leukemia virus controlled by other background genes. In this context, the implications of the multi-gene control of anti-AKR/Gross virus CTL production are discussed with respect to the induction of spontaneous leukemia in the high incidence AKR strain.
Expression and regulation of two idiotype families and subsets within an idiotype family among BALB/c antibodies against p-azophenylarsonate.
Authors: Brown A R 
Published: December 2022

Abstract
The expression and regulation of the two different idiotype (id) families associated with the anti-p-azophenylarsonate (Ar) antibodies of BALB/c mice were examined. Both families ( 5AF6 and 3C6 ) represented cross-reactive idiotypes (CRI) expressed in the anti-Ar of most individual BALB/c mice. In response to keyhole limpet hemocyanin-Ar, an average of about 28% of BALB/c anti-Ar had 5AF6 family idiotopes, while 3C6 family was expressed on about 16% of BALB/c anti-Ar antibodies. Suppression induced by anti-idiotype treatment against one family did not suppress the expression of the other family, suggesting that the two families were regulated independently. However, the relative expression of one family could influence the expression of the other, because depression of the 5AF6 family tended to increase the expression of the 3C6 family of anti-Ar. Analysis of the 5AF6 family showed that a majority of BALB/c mice produced antibodies bearing most or all of the idiotopes associated with the family, but that a subset of about 35% of the antibodies synthesized lacked idiotopes associated with a monoclonal anti-Ar member of this family, 2.4. Treatment of mice with anti-idiotypes prepared against two different monoclonal anti-Ar of the 5AF6 family produced different effects: one enhanced while the other suppressed idiotype expression, suggesting that there are differences in the idiotopes associated with these two regulatory pathways. Additionally, results indicated that subsets of antibodies within the 5AF6 idiotype family could be regulated independently of each other.
B lymphocyte precursors in embryonic and adult W anemic mice.
Authors: Landreth K S , Kincade P W , Lee G , Harrison D E 
Published: December 2022

Abstract
Mice homozygous for mutations at the dominant spotting or W locus on chromosome 5 have been extensively used as models of severe macrocytic anemia caused by defective hemopoietic stem cells. We examined cells of the developing B lineage in adult and embryonic W anemic mice both by phenotypic analyses and by three distinctly different functional assays for B lymphocyte precursors. Adult W/Wv mice had normal numbers of B cells in the spleen and bone marrow, and normal numbers of pre-B cells and cells identified by a monoclonal antibody directed to a B lineage cell surface antigen (14.8) in the bone marrow. Embryonic W/Wv and Wx/Wx mice had hypoplastic liver development at 16 days gestation with a corresponding reduction in absolute numbers of pre-B cells, 14.8+ cells, and clonable granulocyte-macrophage progenitor cells, although their frequencies were normal. As expected, spleen colony-forming units were greatly reduced both in absolute number and frequency. Adult bone marrow cells and fetal liver cells from W anemic mutants generated B cells in vitro as well as did cells from normal littermates, but W anemic cells failed to generate B lymphocytes as well in vivo. These observations likely reflect differences in precursor cells that contribute to B cell formation in these assays, and suggest that early B lineage precursors are reduced or defective in W anemic mice.
Capacity of different cell types to stimulate cytotoxic T lymphocyte precursor cells in the presence of interleukin 2.
Authors: Dröge W , Moyers C , Wehrmaker A , Schmidt H , Panknin S , Männel D , Falk W 
Published: December 2022

Abstract
Plastic-adherent cells enriched for dendritic cells (AC) were found to be among the most potent stimulator cells for the activation of cytotoxic T lymphocytes (CTL) in vitro in the presence of interleukin 2 (IL 2) and a constant second set of allogeneic stimulator cells. Concanavalin A-activated nylon wool-nonadherent spleen cells ( CNWT ), concanavalin A-activated unfractionated spleen cells ( Cspl ), and some variants of the ESb T lymphoma line were equally effective as stimulator cells, however, and provoked a substantial cytotoxic response at concentrations of 10(4) cells per culture or less. In contrast, nonactivated nylon wool-nonadherent spleen cells ( NWT ) or unfractionated spleen cells (Spl) and cells of the P815 mastocytoma, the Meth A fibrosarcoma, and the T cell lymphomas Ly 5178 Eb and ESb did not stimulate cytotoxic responses at these cell concentrations. The strong stimulatory potential of the Cspl preparation was reduced by treatment with anti-Thy-1 antibody plus complement, whereas the stimulatory activity of the AC preparation was resistant to this treatment. All cell types tested expressed class I major histocompatibility antigens. Nonactivated NWT cells, in contrast to the CNWT preparation, showed no detectable staining with anti-I-E or anti-I-A antibodies and also a slightly weaker staining with class I antisera. Experiments with the tumor cell lines revealed, however, that there was no strict correlation between stimulatory potential and density of class I alloantigens or the expression of I-E determinants. Experiments on primary cytotoxic responses in vivo gave similar results. Experiments in cultures with a single set of stimulator cells and I region-compatible responder cells indicated that AC and Cspl or CNWT also have a markedly stronger capacity than NWT to induce IL 2-dependent DNA synthesis.
Tolerance to Mls-disparate cells induces suppressor T cells that act at the helper level to prevent in vivo generation of cytolytic lymphocytes to hapten-altered self.
Authors: Vargo P M , Battisto J R 
Published: December 2022

Abstract
We have been examining the mechanisms that control in vivo development and down regulation of cytolytic T lymphocytes (CTL) to trinitrophenyl (TNP)-altered self antigens. In vivo generation of hapten-specific CTL requires an auxiliary antigenic stimulus, which can be provided by H-2 compatible but Mls-disparate cells. These experiments were designed to study the effect of tolerization with such Mls-disparate cells on CTL development. C3H/HeN (H-2k, Mlsc ) mice sensitized in the footpads with C3H-TNP spleen cells plus CBA/J (H-2k, Mlsd ) spleen cells develop CTL in the draining lymph nodes that will lyse 51Cr-labeled TNP-modified C3H targets. However, we have found that if C3H/HeN mice are given tolerizing doses of CBA/J spleen cells 5 to 7 days before sensitization, a splenic suppressor T cell (Ts) appears. This Ts will suppress CTL development in its tolerant host, and can be transferred adoptively to function in naive mice. Ts and its precursor are cyclophosphamide insensitive and therefore different from the naturally existing suppressor cell present in mice. When triggered by cells with Mlsd , the Ts produces a factor (TsF) that hinders helper factors from functioning in an in vitro CTL assay. Furthermore, TsF acts to prevent utilization of IL 2 by an IL 2-dependent cell line. Thus, evidence has been provided that the in vivo generation of CTL toward hapten-altered self can be down regulated at the level of helper signals by a Ts. The latter is inducible by the Mls-disparate cells that are needed at a different site to trigger the helper factors in this CTL system.
Interleukin 2 enhancement of lymphokine secretion by T lymphocytes: analysis of established clones and primary limiting dilution microcultures.
Authors: Kelso A , MacDonald H R , Smith K A , Cerottini J C , Brunner K T 
Published: December 2022

Abstract
The effect of exogenous interleukin 2 (IL 2) on lymphokine production by T lymphocytes was examined in two systems: the secretion of macrophage-activating factor (MAF) and interferon (IFN) by cloned long-term T cell lines, and a limiting dilution system for estimating the frequency of precursors of MAF-secreting cells in normal spleen. An IL 2-containing, MAF- and IFN-free supernatant from the EL-4 thymoma (EL-4 SN) significantly enhanced release of MAF and IFN by mitogen- or antigen-stimulated, cytolytic or noncytolytic T lymphocyte clones directed against alloantigens or Moloney leukemia virus-associated antigens. Highly purified IL 2 produced equivalent enhancement as EL-4 SN in cultures of alloreactive clones stimulated with concanavalin A. Kinetics experiments showed that EL-4 SN increased both the rate and duration of MAF release by T cell clones. EL-4 SN also increased MAF production when added during restimulation of limiting dilution cultures of positively selected Lyt-2+ and Lyt-2- C57BL/6 splenic T lymphocytes activated against DBA/2 alloantigens. This enhancement resulted in a threefold increase in the apparent precursor frequency of MAF-secreting cells among Lyt-2+ lymphocytes, but did not affect the frequency among Lyt-2- cells. Additional analysis indicated that average MAF production in cultures of Lyt-2-+ cells was sixfold lower than in cultures of Lyt-2- cells, and hence that EL-4 SN allowed detection of a significant proportion of Lyt-2+ cell cultures secreting low levels of MAF. Under these improved conditions, the MAF assay detected the majority of responding Lyt-2+ and Lyt-2- lymphocytes.