bluuebunny/crossref_metadata_2025_split huggingface dataset:
A monoclonal antibody detecting a 39,000 m.w. molecule that is present on B lymphocytes and chronic lymphocytic leukemia cells but is rare on acute lymphocytic leukemia blasts.
Authors: Zipf T F , Lauzon G J , Longenecker B M 
Published: December 2022

Abstract
Monoclonal antibody 41H.16 was produced by using the hybridoma methodology in the mouse system with cells from a patient with hairy cell leukemia as the immunogen. This antibody reacts with the majority of Slg+ cells in the peripheral blood and with all B lymphoblastoid cell lines. Reactivity with conventional Ig determinants, Fc or C3 receptors, has been excluded. The antibody reacted with cells from 68 patients with CLL but showed no reactivity with cells in 69 specimens from patients with non-T, non-B ALL. The apparent m.w. of the antigen detected by this antibody is approximately 39,000.
Functional studies on B cell hybridomas with B cell surface antigens. IV. Direct effects of cytochalasin B on differentiation.
Authors: Hamano T , Asofsky R 
Published: December 2022

Abstract
We previously established B cell hybridomas between M12.4.1 B lymphoma of BALB/c mice and normal B cell of C57BL/6 (B6) mice. These hybridomas express Iab, Iad, and IgM molecules on the cell membrane, and can induce the generation of IgM secretion when treated with purified goat anti-mouse-mu antibody (anti-mu) without T cell factors. In this study, TH2.54, a subclone of a B cell hybridoma, was treated with cytochalasin B (CB), a fungal product that disrupts microfilaments, and the direct effect of CB on the proliferation and differentiation of TH2.54 was examined. CB considerably suppressed the spontaneous proliferation of hybrid cells. This product, however, did not inhibit the generation of IgM secretion by TH2.54 treated with anti-mu. Surprisingly, CB could directly induce the development of IgM-secreting cells by TH2.54 at a relatively high frequency. Among cytochalasins, dihydrocytochalasin B (H2CB), cytochalasin C (CC), and cytochalasin D (CD) showed marked effects on the induction of IgM secretion as well as CB. In addition, the differentiative effect of CB was greatly inhibited by N6, O2-dibutyryladenosine 3':5'-cyclic monophosphate (dbc-AMP), but not by N2, O2-dibutyrylguanosine 3':5'-cyclic monophosphate (dbc-GMP). Analysis by flow microfluorometry (FMF), cytotoxicity assays, and quantitative absorption tests demonstrated that CB treatment of TH2.54 resulted in a significant decrease in the expression of Iab, Iad, and IgM molecules on the cell membrane. In contrast, parental M12.4.1 neither generated any IgM secretion nor changed Iad expression on the cell membrane under the same conditions. The present study suggests very strongly that microfilament-microtubule systems are not involved in the differentiative process of TH2.54 induced by anti-mu. The results also indicate that CB can provide the initiative signal for differentiation of TH2.54 into the maturation lineage; this is followed by a significant change in the expression of Ia and IgM molecules on the cell membrane.
Cellular requirements for induction of human primary proliferative responses to trinitrophenyl-modified cells.
Authors: Brown M F , Van M , Abramson S L , Fox E J , Rich R R 
Published: December 2022

Abstract
Cellular requirements for induction of primary proliferative responses by human T cells to trinitrophenylated autologous stimulators have been characterized. Substantial proliferative responses were observed with each of the Ia+ stimulator populations tested. Nevertheless, major differences in the hapten specificity of such responses were observed. Thus purified macrophages/monocytes (M phi) when TNP-modified induced responses that were relatively modest in absolute magnitude, but were highly hapten specific. This reflected the very limited capacity of purified M phi to induce proliferation when unmodified, i.e., an autologous mixed leukocyte response (AMLR). In contrast, unmodified M phi-depleted B plus null cells were potent stimulators of AMLR, but hapten modification did not significantly enhance the responses induced by these cells. Moreover, when M phi were added to B plus null cell stimulators AMLR responses were reduced and, with TNP-modified stimulators, hapten-specific responses were restored. The data thus suggest that M phi may have important roles in induction of primary T cell responses to conventional antigens but function largely as regulators rather than stimulators of AMLR. Finally, we have introduced a novel antigen-presenting cell population, the irradiated Ia+ TNP-specific cloned T cell. The possibility that such cells may utilize autostimulatory positive feedback circuits for activation of naive T cells and in interactions between subpopulations of hapten-reactive T cells is discussed.
Alterations in immunoglobulin synthesis by peripheral blood mononuclear cells from splenectomized patients with and without splenic regrowth.
Authors: Drew P A , Kiroff G K , Ferrante A , Cohen R C 
Published: December 2022

Abstract
Unstimulated and pokeweed mitogen (PWM)-stimulated immunoglobulin (Ig) synthesis by peripheral blood mononuclear cells (PBMC) in vitro, serum Ig concentrations, and the degree of splenic regrowth was studied in 33 patients who had been splenectomized following trauma. The concentration of IgG and IgA was significantly raised in the supernatants of unstimulated cultures of PBMC from the patients. The stimulation of Ig synthesis by PWM, measured as a stimulation index (SI), was significantly less in the culture of PBMC from the patients, compared with the controls. The SI was reduced both in those patients whose unstimulated PBMC secreted normal concentrations of IgG and IgA in culture, as well as in those whose cells secreted elevated concentrations of Ig. The concentration of IgM in the serum of the patients was significantly reduced compared with the controls, the serum IgG was raised, and the serum IgA was not altered. The degree of splenic regrowth (splenosis) was measured in the patients by splenic scanning, by using heat-damaged, radiolabeled autologous erythrocytes. The patients were allocated into four groups, depending on whether they had no (11 patients), minimal (11), moderate (seven), or large (four) splenosis. There was no difference between any of the groups with respect to the synthesis of IgG or IgA in culture or the serum Ig concentrations. These results indicate that Ig synthesis by PBMC in vitro, and serum Ig concentrations in vivo, are abnormal in patients who have been splenectomized for trauma, and that the generation of splenosis tissue does not correct these changes.
Cloned human interferon-gamma, but not interferon-beta or -alpha, induces expression of HLA-DR determinants by fetal monocytes and myeloid leukemic cell lines.
Authors: Kelley V E , Fiers W , Strom T B 
Published: December 2022

Abstract
The antigen presenting function of macrophages and other accessory cells requires the cell surface expression of class II major histocompatibility antigens, e.g., HLA-DR. It has been shown that gamma-interferon (IFN-gamma), a T cell product, can regulate macrophage HLA-DR expression. The effect of absolutely pure or cloned IFN-gamma upon fetal monocytes that do not strongly express DR has not been studied. We have utilized cloned IFN-gamma, IFN-beta, and IFN-alpha preparations to examine the differential effects of these molecules upon the expression of HLA class I (HLA-A,B) and class II determinants by fetal monocytes as well as by myeloid leukemic cell lines. We report that cloned human IFN-gamma induces the expression of HLA-DR and -A,B antigens on cells that normally express low quantities of these molecules, including human fetal monocytes and two (ML-1 and HL-60) but not a third (U-937) myeloid leukemic cell lines. These findings suggest that the acquisition of class II HLA molecules upon fetal tissues and perhaps antigen presenting function is dependent upon IFN-gamma. In contrast, IFN-beta and -alpha induced the expression of HLA-A,B but not HLA-DR antigens by these cells. Thus, these data indicate that the expression of HLA-DR molecules that is vital for monocyte/macrophage and T cell interaction is stimulated by the lymphokine IFN-gamma, and that the effects of IFN-gamma are distinctive from IFN-alpha or -beta.
The role of immune complexes in the activation of the first component of human complement.
Authors: Ziccardi R J 
Published: December 2022

Abstract
Immune complex-induced C1 activation and fluid phase C1 autoactivation have been compared in order to elucidate the immune complex role in the C1 activation process. Kinetic analyses revealed that immune complex-bound C1 activates seven times faster than fluid phase C1 spontaneously activates. The rate of spontaneous C1 activation increased after decreasing the solution ionic strength. In fact at one-half physiologic ionic strength (i.e., 0.08 M), the kinetics of spontaneous C1 activation were indistinguishable from the kinetics of activation of immune complex-bound C1 at physiologic ionic strength. The enhanced fluid phase C1 activation at low ionic strength resulted neither from C1 nor C1q aggregation, nor from selective effects on the C1r2S2 subunit; however, at the reduced ionic strength, the C1 association constant (defined for C1q + C1r2S2 in equilibrium C1qr2S2) did increase to 2.3 X 10(8) M-1, which is equal to that for C1 bound to an immune complex at physiologic ionic strength. Therefore, C1 can spontaneously activate in the fluid phase as rapidly as C1 on an immune complex when the strength of interaction between C1q and C1r2S2 is the same in both systems. In conclusion, under physiologic conditions, C1q and C1r2S2 are two weakly interacting proteins. Immune complexes provide a site for the assembly of a stable C1 complex, in which C1q and C1r2S2 remain associated long enough for C1q to activate C1r2S2. Thus, immune complexes enhance the intrinsic C1 autoactivation process by strengthening the association of C1q with C1r2S2.
Purification of a major sialoglycoprotein (SGP140) on P12/Ichikawa cells and its expression on differentiated HL-60 cells.
Authors: Yamamoto Y , Mitsui H , Nishikawa Y 
Published: December 2022

Abstract
SGP140 glycoprotein, a major cell surface sialoglycoprotein with an apparent m.w. of 140,000, was detected on the human T lymphoblastoid cell line P12/Ichikawa by labeling with periodate-tritiated sodium borohydride, followed by urea-sodium dodecyl sulfate-polyacrylamide gel electrophoresis and fluorography. Then SGP140 was purified from P12/Ichikawa cells for study of its biochemical character and its distribution in various cell lines. The purification was performed by 0.2% Triton X-100 solubilization from crude membranes, DEAE-Sephacel column chromatography, WGA-agarose column chromatography, Blue-Sepharose 6MB column chromatography, and Sephadex G-150 gel filtration. Antiserum raised against SGP140 was then prepared, and immunoprecipitation and membrane immunofluorescence assay were performed on various cell lines. SGP140 was detected on P12/Ichikawa, Raji, P3HR-1, Daudi, Namalva, BALL-1, MOLT-4B, TALL-1, NALL-1, and K562 cells, but was not detected on HL-60 cells. When HL-60 cells were treated with dimethyl sulfoxide, retinoic acid, or 12-O-tetradecanoylphorbol-13-acetate, SGP140 was detected on cell surfaces. We discuss the possibility that SGP140 may be a differentiation antigen.
Molecular mechanisms of lymphocyte extravasation. I. Studies of two selective inhibitors of lymphocyte recirculation.
Authors: Spangrude G J , Braaten B A , Daynes R A 
Published: December 2022

Abstract
Pertussigen, a protein toxin purified from Bordetella pertussis, and fucoidin, a high molecular weight sulfated polysaccharide, were analyzed for their ability to inhibit lymphocyte recirculation in vivo. Pertussigen treatment of lymphocytes resulted in a dosage- and time-dependent loss of their ability to localize in lymph nodes or Peyer's patches. This toxin-induced alteration did not reverse after extended lymphocyte culture in toxin-free media, and had no effect on lymphocyte viability or activation by mitogens. Furthermore, pertussigen-treated lymphocytes retained the ability to specifically adhere to high endothelial cells in an in vitro binding assay. Kinetic studies suggested that the toxin's molecular action on lymphocytes is analogous to that reported for pancreatic islets and hormone-responsive cultured cell lines. Inhibition of lymphocyte recirculation by fucoidin was also observed in vivo. Fucoidin-mediated inhibition of lymphocyte localization to peripheral lymph nodes was reversible with time, and could not be effected by pretreatment of lymphocytes with the polysaccharide. Furthermore, we confirmed the observation that fucoidin blocks lymphocyte adhesion to high endothelial cells in vitro. On the basis of these observations, we propose that the mechanism of lymphocyte extravasation involves a specific receptor-mediated binding event followed by an adenylate cyclase-dependent activation of cell motility. Fucoidin is capable of interfering with the primary adhesion event, whereas pertussigen selectively inhibits the second process to block lymphocyte recirculation in vivo.
A quantitative analysis of C3 binding to O-antigen capsule, lipopolysaccharide, and outer membrane protein of E. coli 0111B4.
Authors: Joiner K A , Goldman R , Schmetz M , Berger M , Hammer C H , Frank M M , Leive L 
Published: December 2022

Abstract
The binding of serum C3 to the O-antigen capsule (OAg Cap), lipopolysaccharide (LPS), and outer membrane proteins (OMP) of Escherichia coli 0111B4 was examined. Bacteria were intrinsically labeled with [3H] or [14C]galactose (*gal) in the OAg Cap and LPS moieties or with [14C]leucine (*leu) to label proteins. Organisms were then incubated in serum containing differentially labeled C3, the above fractions were separated, and the proportion of each binding to a column containing anti-C3 was measured. The OAg Cap fraction bound 72 to 82% of the C3, which bound to E. coli 0111B4 during incubation in absorbed 10% pooled normal human serum (10% PNHS) or absorbed 40% C8-deficient serum (C8D). This distribution did not change when the organism was presensitized with immune IgG before serum incubation. A total of 2.93% +/- 0.48 of OAg Cap and 0.52% +/- 0.16 of LPS *gal bound specifically to Sepharose-containing antibodies to C3 (A:C3-Seph) after incubation in 10% PNHS; these values increased to 10.1% +/- 4.5 and 1.8% +/- 0.3, respectively, when C3 deposition was increased fourfold by incubation in 40% C8D. When encapsulated E. coli 0111B4 was incubated in 10% PNHS containing biotinylated C3, specific attachment of OAg Cap *gal to avidin-Sepharose was demonstrated in 1% sodium dodecyl sulfate (SDS), and complete release of bound *gal but not C3 occurred with 1 M NH2OH. When a mutant of E. coli 0111B4 lacking OAg Cap was incubated in 40% C8D, the outer membrane (OM) bound 85% of C3. Five percent of OM *gal from the unencapsulated organism bound to A:C3-Seph in 0.05% SDS, indicating that the fraction of LPS molecules with bound C3 increased threefold in the absence of OAg Cap. OAg Cap does not contain protein, and no net specific binding of *leu from OAg Cap fractions to A:C3 was detectable; 2.4 to 3.6% of OM *leu bound to A:C3-Seph. Immunoprecipitation of 82.9% of OAg Cap *gal with antisera that were directed to E. coli 0111B4 was associated with co-precipitation of 69.5% of C3 in the capsular fraction. Therefore, the majority of C3 bound to E. coli 0111B4 was covalently attached to OAg Cap and LPS. As corroboration of experiments with whole bacteria, purified OAg Cap and purified LPS consumed C3 when incubated in serum in the fluid phase. These results are the first to evaluate the acceptor site for C3 deposition on a Gram-negative organism incubated in serum, and show that LPS, OAg Cap, and OMP are all major acceptor sites for C3 in nonimmune serum.
Insulin-specific tolerance induction. I. Abrogation of helper T cell activity is controlled by H-2-linked Ir genes.
Authors: Robbins P F , Thomas J W , Jensen P E , Kapp J A 
Published: December 2022

Abstract
Murine antibody responses to heterologous insulins are under H-2-linked immune response (Ir) gene control. We have found that the immune response to insulin in adjuvant can be inhibited by prior i.v. injection of soluble insulin. The effect of i.v. injection of insulin is antigen-specific and dose-dependent and requires the same doses of insulin that are immunogenic if administered with adjuvant. In addition, the inhibitory effect of soluble insulin is dependent upon the route of injection; if soluble insulin is injected i.p., the subsequent response to insulin in adjuvant is augmented rather than inhibited. Unresponsiveness requires at least 4 days after i.v. injection to develop and once induced, it is maintained for 4 wk or more. Unresponsiveness is caused by T cell, but not B cell, tolerance, and we have been unable to demonstrate any role for suppressor T cells in this unresponsiveness. More importantly, analysis of the ability of numerous insulin variants to induce unresponsiveness in several H-2k and H-2b strains of mice has demonstrated that only the variants that were immunogenic in a given strain when administered with adjuvant were able to cause tolerance. This report is, to our knowledge, the first describing that induction of helper T cell tolerance, like the induction of immunity, is controlled by H-2-linked Ir genes.
Identification of stage-specific sporozoite antigens of Toxoplasma gondii by monoclonal antibodies.
Authors: Kasper L H , Bradley M S , Pfefferkorn E R 
Published: December 2022

Abstract
Stage-specific antigens of Toxoplasma gondii have not been reported. We developed a panel of monoclonal antibodies that identified unique surface membrane antigens on the sporozoite and oocyst wall of T. gondii. These monoclonal antibodies failed to react with T. gondii tachyzoite surface membrane antigens in several immunologic assays. A comparison of surface membrane radioiodinated tachyzoites and sporozoites by one- and two-dimensional electrophoresis showed that T. gondii sporozoites have two major membrane proteins of approximate m.w. 67,000 and 25,000, not present in the tachyzoite stage. Two of the stage-specific monoclonal antibodies (2E4 and 5A4) were directed against the sporozoite 67,000 m.w. protein. In addition, T. gondii sporozoites are deficient in the major radioiodinated tachyzoite protein P30, which is identified by both human and mouse convalescent antitoxoplasma antisera. A convalescent antitoxoplasma serum failed to recognize sporozoite antigens by both immunoprecipitation and reaction with nitrocellulose transfer blots.
Prophylactic immunization against experimental leishmaniasis. II. Further characterization of the protective immunity against fatal Leishmania tropica infection induced by irradiated promastigotes.
Authors: Howard J G , Liew F Y , Hale C , Nicklin S 
Published: December 2022

Abstract
The genetic vulnerability of BALB/c mice to Leishmania tropica (L. major) infection renders them incapable of controlling a primary cutaneous lesion that leads to uniformly fatal visceral disease. Potent, long-lasting protection involving both lesion healing and survival can be induced by repeated prophylactic i.v. immunization with gamma-irradiated (150K rad) L. tropica promastigotes. The effect is not dependent on continuing viability or cellular invasiveness of the irradiated parasites because their effective immunogenicity withstands heating at 56 degrees C for 1 hr. Immunity is not stage specific and encompasses both amastigote and promastigote challenges. Similar prophylaxis can be induced by immunization with heterologous irradiated L. donovani promastigotes. Repeated i.v. immunization with irradiated L. tropica promastigotes induces an antibody response in the isotype sequence M leads to G1/G3 leads to G2a/G2b leads to A with substantially higher titres than are found in response to the infection itself. Splenectomy before immunization drastically reduces this antibody response without incurring any impairment of the extent of protection. Passive transfer of large amounts (up to 10 ml) of hyperimmune serum (or isotype fractions thereof) throughout the first 8 wk of infection fails to arrest disease progression during this period. Despite the previously described lack of any detectable cutaneous DTH reactivity, which has hitherto correlated with protective cell-mediated immunity, the results obtained do not support attribution of an alternative causal role to the humoral response.
Recognition of herpes simplex virus antigens on the surface of mouse cells of the H-2b haplotype by virus-specific cytotoxic T lymphocytes.
Authors: Jennings S R , Rice P L , Pan S , Knowles B B , Tevethia S S 
Published: December 2022

Abstract
The recognition by cytotoxic T lymphocytes (CTL) of herpes simplex virus (HSV) glycoprotein(s) in association with the H-2K and the H-2D gene products of the H-2b complex was examined by using cell lines derived from H-2 recombinant mice as target cells, and by using H-2 recombinant mouse strains for the generation of HSV-specific CTL populations. CTL from H-2b HSV-immunized mice were found to lyse HSV-infected B6/WT-3 (KbDb) and K5RSV (KbDd) cells, but not KHTGSV (KdDb) cells. Unlabeled HSV-infected K5RSV cells were as efficient in competing for specific CTL lysis of 51Cr labeled HSV-infected B6/WT-3 cells as unlabeled B6/WT-3 cells themselves, whereas infected KHTGSV cells were ineffective. Furthermore, CTL generated in H-2 recombinant mice containing the H-2Kb allele (KbDd) effectively lysed infected B6/WT-3 cells; no specific lysis was observed with immune lymphocytes from those mice containing the H-2Db (KkDb) allele. Limiting dilution analysis of the interleukin 2 (IL 2)-dependent, antigen-independent, CTL precursor populations showed that CTL precursors giving rise to H-2Kb-restricted progeny were present at a relatively high frequency, whereas H-2Db-restricted progeny were present at low frequency or were undetectable. Target cells carrying mutations in the H-2Kb glycoprotein (H-2Kbm1 and H-2Kbm8) infected with HSV-1 were found to be drastically reduced in their ability to be lysed by anti-HSV-1 CTL. HSV-1-infected H-2Kbm5 cells provided a good target for anti-HSV CTL. We conclude that the HSV-specific glycoprotein(s) are recognized by CTL primarily in association with the H-2Kb gene product.