bluuebunny/crossref_metadata_2025_split huggingface dataset:
Demonstration of A Rabbit Cell Surface Ig That Bears Light Chain and VH, But Lacks µ-, α-, and γ-Allotypes-Rabbit IgD?
Authors: Wilder Ronald L. , Chew Yuen Catherine , Coyle Sharon A. , Mage Rose G. 
Published: January 2023

Abstract
Based on previous biochemical studies of rabbit sIg, we postulated that if rabbits possessed an IgD-like molecule, its heavy chain might co-electrophorese with the µ-heavy chain on reduced SDS-PAGE. Accordingly, we studied Ig from rabbit spleen cells radiolabeled biosynthetically or by cell surface iodination. Cell lysates were prepared and immunoprecipitation studies were performed by standard techniques. Sequential absorptions in which total removal of µ-allotype (n-locus) was followed by immunoprecipitation with anti-a(VH) or anti-b (kappa) showed residual band(s) with µ-relative mobility on SDS-PAGE under reducing conditions. Similar immunoprecipitations with anti-gamma (γ) or anti-alpha (α) reagents failed to precipitate the residual band with µ-mobility. The residual band was found in both radioiodinated and biosynthetically radiolabeled lysates.
When direct immunoprecipitation was carried out in the absence of proteolytic enzyme inhibitors, the SDS-PAGE pattern of total Ig under reducing conditions frequently showed three peaks, corresponding to µ (MW ∼70,000), light chain (MW ∼23,000), and an unidentified heavy chain (MW ∼65,000). The second heavy chain peak was not immunoprecipitated with µ, γ, or α allotype sera. Thus, we have identified a “new Ig” in the rabbit that bears VH and light chain, and lacks µ, γ and α allotype markers. The molecule appears to be proteolytically labile, but has an undegraded heavy chain that co-electrophoreses with µ-chains on reduced SDS-PAGE. The similarities to published data on human and rat lymphocyte IgD strongly suggest, but do not formally prove, that we have identified the rabbit homologue of IgD.
Bullous Pemphigoid Antigen
Authors: Diaz Luis A. , Patel Harish , Calvanico Nickolas J. 
Published: January 2023

Abstract
This report concerns the isolation of bullous pemphigoid antigen from the nondialyzable urinary components of a patient with the disease. The isolation was accomplished by ion exchange chromatography and gel filtration. Pemphigoid antigen was found to be a basic glycoprotein that on SDS gel electrophoresis showed two major bands, one in the 18,000 m. w. region and the second with a m. w. of 74,000. Between these two bands, two additional bands appeared; one of 35,000 daltons and the other of 68,000 daltons. The 18,000 m. w. band was eluted from the gel and rerun on SDS gels. These gels showed the 18,000 m. w. band and also the appearance of the 35,000 and 74,000 m. w. bands. This finding indicates that urinary pemphigoid antigen may exist both as a single monomeric form and in polymeric aggregates.
Virus Specificity of Human Influenza Virus-Immune Cytotoxic T Cells
Authors: Biddison William E. , Shaw Stephen , Nelson David L. 
Published: January 2023

Abstract
The virus specificity of human in vitro cytotoxic T cell responses to influenza virus was studied with the use of peripheral blood mononuclear leukocytes from normal adult volunteers. Previous natural exposure of these donors to a variety of type A influenza viruses was documented by HI antibody titers. Cells sensitized in vitro with A/HK or A/PR8 were cytotoxic for autologous target cells infected with A/HK, A/PR8, or A/JAP 305 type A influenza viruses, but not for B/HK-infected or uninfected cells. B/HK-sensitized effector cells lysed target cells infected with B/HK but not targets infected with type A viruses. A/HK- and A/PR8-immune effector populations were shown to recognize cross-reactive antigens on A/HK- and A/PR8-infected target cells by cold target competition. Influenza-immune effector cells were cytotoxic for virus-infected autologous targets but much less so for virus-infected allogeneic targets. This self-restriction suggested that the cytotoxicity was largely T cell-mediated and was confirmed by cell separation analysis.
Thus, the human secondary cytotoxic T cell response in vitro to influenza viruses is predominantly directed against cross-reactive determinants on cells infected with serologically distinct type A influenza viruses.
Antigenic Specificities of the Cellular Immune Response of C57BL/6 Mice to the Moloney Leukemia/Sarcoma Virus Complex
Authors: Enjuanes Luis , Lee John C. , Ihle James N. 
Published: January 2023

Abstract
The antigenic specificities of the cellular immune response against MoLV-MSV-induced tumors in C57BL/6 mice were studied by using a variety of purified MoLV virion proteins. Cellular reactivity, as assessed by the ability of purified proteins to induce T cell proliferation, was primarily directed against the virion envelope glycoprotein and to a lesser extent against p12. No blastogenesis was detectable with the viral p10, p15, or p30 proteins. The optimal gp71 and p12 antigen concentrations required for 50% of maximal responses were 0.036 and 0.013 nmoles per 5 × 105 cells per 0.2 ml, respectively. Blastogenesis was dependent upon the presence of T cells, but was apparently independent of the presence of macrophages.
The antigenic specificity of cellular cytotoxicity was assessed by microcytotoxicity assays by using transformed nonproducer and producer cell lines with a various virus serotypes. The results demonstrated that cytotoxicity was immunologically type-specific for MoLV serotype of virus and is dependent upon the expression of the MoLV viral envelope glycoprotein gp71. The requirement for gp71 cytotoxicity was further assessed by antigen-blocking experiments. These results demonstrate that only MoLV gp71 could significantly block cytotoxicity (τ80%), whereas no blocking was seen with RLV gp71, MoLV p30, p15, p12, or p10, suggesting that the major cytotoxic response is directed against MoLV gp71. The temporal relationships of the cellular as well as the humoral immune responses related to tumor development and regression are also described.
Increased photosensitivity to near-ultraviolet light in murine SLE.
Authors: Golan D T , Borel Y 
Published: January 2023

Abstract
We investigated whether there is increased susceptibility to near-UVL in murine SLE. Cultured spleen cells from either strain of mice with lupus disease or conventional strains of mice were exposed to different UVL fractions in vitro. The effect of DNA synthesis, release, and repair was examined. DNA synthesis and release was measured as percent of [3H]thymidine (dT) uptake into either total acid-precipitable radioactive material of cell sediment plus supernatant, or that of the medium alone, whereas hydroxyurea-resistant dT incorporation represented DNA repair. The data indicate that all SLE strains, in contrast to all non-SLE strains, show increased DNA synthesis and release after UV-A exposure. In addition, all murine SLE strains demonstrate increased susceptibility to induction of DNA damage by UV-A. The significance of these observations in relation to the clinical activity of SLE after sunlight exposure is discussed.
Regulation of TCGF production in T cells. II. Early membrane events after anti-Thy-1 binding by the TCGF-producing T lymphoma EL-4 G-12.
Authors: Norcross M A , Smith R T , Shimizu S 
Published: January 2023

Abstract
The T cell lymphoma line EL-4 G-12 produces large quantities of TCGF (IL 2) shortly after exposure to anti-Thy-1 and cross-linking reagents. Early surface events that initiate nonconstitutive synthesis and secretion have been examined by fluorescent microscopy, EM analysis, flow cytometry of anti-Thy-1, and measurements of membrane polarization. The data show that anti-Thy-1 binding leads to immediate and rapid endocytosis and shedding of the antibody molecules, but with no change in membrane potential. Cross-linking of the anti-Thy-1 results in stabilization and accumulation of the antibody on the surface, and rapid hyperpolarization. The data suggest that cross-linking of ligand antibody interactions at the surface is a regulatory event involved in initiation of the signal for TCGF synthesis and secretion.
B cell maturation factor: effects on various cell populations.
Authors: Sidman C L , Marshall J D 
Published: January 2023

Abstract
B cell maturation factor (BMF) is a lymphokine that promotes the maturation of resting murine splenic B lymphocytes, and the analogous B cell tumor line WEHI-279, to the state of active immunoglobulin (Ig) secretion. All subsets of normal B cells examined, including neonatal and adult B cells, B cells from various organs, and B cells from CBA/N mice, are inducible by BMF. Induction of Ig secretion is independent of thymus-derived cells, LPS receptors, and MHC haplotype, because nude, C3H/He, and mice of many strains are equally responsive to BMF. Purified B cells prepared by using a fluorescence-activated cell sorter also respond to BMF, showing that BMF directly interacts with and triggers Ig secretion by B cells. In limiting dilution cultures, most normal resting splenic B cells or WEHI-279 B tumor cells are inducible by BMF. By using the WEHI-279 cells as a model system, specific aspects of the BMF response have been analyzed. In terms of the degree of stimulation observed, the primary mechanism for the induction of Ig secretion by BMF is an enhanced and balanced synthesis of Ig heavy (H) and light (L) chains. A less significant component of the induced Ig secretion is an increase in the ratio of secretory to membrane H chains produced. Kinetically, the shift in the ratio of secretory to membrane H chain forms occurs first, and this is followed by the increased synthesis of both L and H chains. Responding B cells also die during this induction process. Although the changes in the ratio of H chain forms, H and L synthesis, and cell viability take several days to occur, BMF will program significant later responses after only 1 or a few hr of interaction with target B cells.
Fc gamma receptor-mediated suppression of gamma-interferon-induced Ia antigen expression on a murine macrophage-like cell line (P338D1).
Authors: Hanaumi K , Gray P , Suzuki T 
Published: January 2023

Abstract
A variant (HS-1) of a murine macrophage cell line (P388D1) was obtained by cell cluster technique based on the Ia antigen expression induced by lymphokines. Receptors for both IgG2a and IgG2b but no detectable I-Ad are expressed on the surface of the majority of HS-1 cells. Exposure of HS-1 cell to concanavalin A supernatant or recombinant IFN-gamma resulted in the induction of I-Ad antigens on greater than 90% of the cells within 48 hr. The effects of lymphokines were transient and dependent on the synthesis of messenger RNA because the removal of lymphokines or the presence of actinomycin D both blocked Ia expression. The prior or simultaneous binding of monoclonal IgG2a or IgG2b antibodies complexed with sheep erythrocytes to respective cell surface Fc gamma R suppressed the Ia antigen inducing activity of lymphokines. Neither antibody nor antigen alone could suppress the effect of lymphokines. Inhibitors of phospholipase A2 or cyclooxygenase, which have been shown previously to suppress Fc gamma 2bR, but not Fc gamma 2aR, triggered activation of the adenylate cyclase system and reversed Fc gamma 2bR- but not Fc gamma 2aR-mediated suppression of IFN-gamma-induced Ia antigen expression.
Immune response to ferredoxin; nonresponder status is not due to suppression.
Authors: Sikora L K , Levy J G 
Published: January 2023

Abstract
Ferredoxin (Fd), a small protein from Clostridium pasteurianum, has been selected for immunologic studies because of its limited number (two) of antigenic determinants. Functionally (as determined by antibody binding), monodeterminant fragments of Fd can be generated enzymatically, leaving molecules only a few amino acids smaller than the native protein, with unaltered solid phase binding properties. These fragments were used to assess the immune response to each of the two determinants. Clear differences in immunologic properties can be assigned to sequences within Fd: the amino terminal tripeptide is responsible for inducing a proliferative response and limited antibody production, whereas the carboxy terminal dipeptide accounts for most of the antibody activity, yet little, if any, T-proliferative activity. Studies with the enzyme-generated fragments of Fd have unmasked a sequence proximal to the amino terminal that represents a second determinant for T cell proliferation but does not have any demonstrable antibody-inducing activity. This third determinant is shown to induce responsiveness to Fd in nonresponder animals after the removal of the amino terminal tripeptide. The results indicate that nonresponsiveness to this molecule in H-2d mice is not a direct effect of suppression.
A public idiotypic determinant is present on spontaneous cationic IgG antibodies to DNA from mice of unrelated lupus-prone strains.
Authors: Hahn B H , Ebling F M 
Published: January 2023

Abstract
A monoclonal anti-idiotypic antibody (anti-Id) to a public idiotype (Id) present on spontaneous IgG antibodies to DNA from NZB/NZW F1 mice recognized similar determinants on polyclonal and monoclonal IgG anti-DNA antibodies from mice of the unrelated MRL/lpr and BXSB strains. Incubation of the anti-Id with four of five monoclonal Id in solid phase inhibited their ability to bind DNA; however, different Id+ antibodies recognized different epitopes within the DNA molecule. Therefore, the public Id was located close to the antigen-binding regions but did not comprise all of those regions. Analysis of multiple polyclonal and monoclonal antibodies to DNA showed the Id on all subclasses of IgG. However, antibodies bearing the Id carried a neutral or cationic charge (10 of 10 monoclonals with pI greater than 7 were Id+); the presence of the Id on anionic IgG (pI less than or equal to 7) was infrequent (one of 21 serums, one of eight monoclonal antibodies). Therefore, IgG autoantibodies to DNA are constructed from closely related public idiotypes in several mouse strains that spontaneously develop lupus, and that Id is restricted to antibodies with a pI of 7 or greater.
The role of cytoplasmic intermediates in IL 2-induced T cell growth.
Authors: Gutowski J K , Mukherji B , Cohen S 
Published: January 2023

Abstract
In previous studies we showed that PHA-stimulated human peripheral blood lymphocytes contain an extractable cytoplasmic protein that is capable of inducing DNA synthesis in isolated quiescent nuclei. This factor, which we have called ADR (for activator of DNA replication), appears to represent an endogenous intracellular mitogen, or cytoplasmic transducer of extracellular mitogenic signals. In light of the known role of IL 2 in PHA-induced T cell mitogenesis, we continued these studies to investigate whether ADR may be involved in the mechanism of action of IL 2. Results from both dose-response and time-response studies strongly suggest a functional role for ADR in IL 2 mediated T cell growth. Furthermore, the absence of ADR in dexamethasone-treated, PHA-stimulated cells suggests that the induction of ADR is not an early event in T cell activation associated with the expression of IL 2 receptors; rather, the induction of ADR appears to be a later event resulting directly or indirectly from the binding of IL 2 to IL 2-responsive cells. In sum, our findings suggest a pathway for T cell growth in which extracellular exogenous mitogenic signals are transmitted to the nucleus first through an extracellular endogenous growth factor (IL 2) and finally through an intracellular, endogenous molecule (ADR) that acts at the level of the nucleus itself.
Suppressor T cell circuits in contact sensitivity. II. Induction and characterization of an efferent-acting, antigen-specific, H-2-restricted, monoclonal T cell hybrid-derived suppressor factor specific for DNFB contact hypersensitivity.
Authors: Miller S D 
Published: January 2023

Abstract
This report defines a methodology for the production and characterization of an antigen-specific, monoclonal T cell hybrid-derived suppressor T cell factor (TsF) that suppresses the passive transfer of 2,4-dinitrofluorobenzene (DNFB) contact hypersensitivity. Fusion of T cells from BALB/c (H-2d) mice tolerized with syngeneic DNP-spleen cells to BW 5147 thymoma cells resulted in several hybrids that constitutively produce a soluble regulatory molecule. One of these hybrids, 26.10.2, was subsequently cloned, and its soluble factor was characterized with respect to its antigen specificity, biochemical nature, MHC restriction pattern, and identity of its target cell. 26.10.2 TsF suppresses the passive transfer of delayed-type hypersensitivity (DTH) mediated by DNP- but not trinitrochlorobenzene- or oxazalone-primed DTH T cells (TDH) after a 1 hr incubation at 37 degrees C. In contrast, 26.10.2 TsF had no suppressive effect on secondary in vitro DNP-specific T cell proliferative responses. 26.10.2 TsF therefore represents an antigen-specific factor with effector (efferent-acting) function. The monoclonal TsF was shown to consist of a two-chain, disulfide-bonded molecule, and to bear a receptor(s) specific for DNP and determinants encoded by the I region of the H-2 complex. Effector suppressive activity of 26.10.2 TsF was restricted by Class I H-2Dd determinants. One cellular target of this monoclonal factor was shown to be the DNP-specific TDH cell, because DNFB-primed lymph node cells from cyclophosphamide-pretreated donors (lacking Ts-auxiliary (Ts-aux) cells) were efficiently suppressed. The TsF appears to focus on passively bound, TDH receptor-associated, DNP-Class I determinants, as suggested by the observation that freshly prepared, but not overnight cultured, DNP-specific TDH cells were susceptible to suppression.
Enhancement of macrophage immune and nonimmune receptor-mediated phagocytosis by a low molecular weight soluble factor from resident thymocytes.
Authors: Coleman D L , Culver K E , Ryan J L 
Published: January 2023

Abstract
Macrophage phagocytic activity is regulated in part by products of activated T lymphocytes. We previously reported that a heat-stable soluble factor derived from resident (nonactivated) thymocytes increases murine peritoneal macrophage Fc-dependent phagocytosis. In the present study, we further investigate the effect of the thymocyte factor on immune and nonimmune receptor-mediated phagocytosis, Fc receptor expression, and its approximate m.w. After 4 days of incubation, cellfree thymocyte supernatant produced a mean (three experiments) 2.10-, 2.08-, and 1.97-fold increase in macrophage phagocytosis of C3-, IgG-, and tannic acid-treated erythrocytes, respectively. Macrophage IL 1 production was not enhanced by a similar concentration of thymocyte supernatant. The thymocyte factor(s) increased the number of IgG2a Fc receptors (FcRI) from 2.4 x 10(5) to 3.8 x 10(5) receptor sites per macrophage. The number of Fc receptors that bind IgG1 and IgG2b (FcRII) was not altered. The soluble factor(s) that increased Fc-mediated phagocytosis passed through both 6000- to 8000-dalton and 2000-dalton cutoff dialysis membranes and eluted from a Sephadex G-25 Fine column over a m.w. range of 200 to 1000 daltons, with a peak activity at 450 daltons. These data suggest that resident thymocytes enhance macrophage phagocytosis of opsonized and nonopsonized particles through the elaboration of a low m.w. substance(s).
I-A-controlled T cell molecules: protease sensitivity.
Authors: Hullett D A , Klyczek K K , Hayes C E 
Published: January 2023

Abstract
An I-A subregion-controlled structure (I-At) characterizes some helper T cells and augmenting factors. This epitope is associated with a glycoprotein. Extended trypsin digestion removed the determinant; tunicamycin blocked its reexpression. In contrast, limited trypsinization increased the number of I-At-bearing peripheral T cells from 17 to 35%. The I-At molecule density on cells expressing this structure did not change measurably with limited enzyme treatment. Rather, some previously negative T cells (20%) expressed the epitope after mild proteolysis. A third T cell subset (60%) expressed no I-At molecules regardless of enzyme treatment. We conclude that the I-At molecule is shielded by trypsin-labile material on some T cells, whereas on others it is fully exposed. The transition from a shielded to an exposed configuration may correlate with T cell activation. Cycloheximide inhibited the biosynthesis of both the I-At molecule and the shielding substance by T cells. Unlike I-A-controlled T cell structures, B cell I-A-encoded molecules are neither shielded nor trypsin labile. The relationship between I region-controlled T cell and B cell molecules is discussed.
Biochemical and functional evidence that an MT3 supertypic determinant defined by a monoclonal antibody is carried on the DR molecule on HLA-DR7 cell lines.
Authors: Horibe K , Flomenberg N , Pollack M S , Adams T E , Dupont B , Knowles R W 
Published: January 2023

Abstract
A cytotoxic monoclonal antibody, PL3, was produced by immunizing mice with a cell line homozygous for the HLA class II antigenic specificity DR7. The serologic specificity of PL3 was completely concordant with the MT3 supertypic specificity, which is tightly associated with HLA-DR4, -DR7, and -DRw9. This was confirmed by the finding that F(ab')2 fragments of PL3 blocked the cytotoxicity of anti-MT3 alloantisera. Although PL3 bound to each of the MT3-positive cell lines, it showed significantly weaker binding to HLA-DR4 and -DRw9 cells relative to -DR7 cells, both in titration and in quantitative absorption assays. This differential pattern of binding was not found for the polyclonal MT3 alloantisera, suggesting that the PL3 determinant may be one of several closely related determinants that comprise the MT3 allospecificity. To identify which of the subpopulations of class II molecules carry the PL3 determinant, several approaches have been used. F(ab')2 fragments of PL3 which block the anti-MT3 alloantisera were also tested with anti-MB2 and anti-DR7 sera. Binding of the PL3 F(ab')2 fragments to DR7 homozygous target cells had no effect on the anti-MB2 sera, but significantly enhanced the cytotoxic reactivity of some anti-DR7 sera. This finding suggested that the PL3 determinant is distinct from the DR7 determinant, but is carried on the same molecule. PL3 was also used in blocking studies with allocytotoxic T cell clones which only recognize DR7-positive cell lines. Binding of PL3 to the DR7-positive target cells was found to completely inhibit these T cell clones. Complete blocking was also found with a monoclonal antibody, PL8, which recognizes a monomorphic determinant found on the DR subpopulation of class II molecules. This finding suggested that the PL3 determinant is carried on the same molecule that carries these T cell-defined DR7 allodeterminants. In biochemical studies with DR7-positive cell lines, PL3 and PL8 were found to immunoprecipitate the same subpopulation of class II molecules recognized by other DR-specific antibodies, SG157 and TAL-1B5. Two-dimensional gel analysis demonstrated that the pattern of alpha- and beta-chains immunoprecipitated by PL3, PL8, and TAL-1B5 were identical. In sequential immunoprecipitation studies, both PL3 and TAL-1B5 were capable of removing the same DR subpopulation of molecules recognized by PL3, PL8, TAL-1B5, or SG157 while leaving the additional class II molecules (DS) recognized by SG171 on DR7 cells.(ABSTRACT TRUNCATED AT 400 WORDS)