bluuebunny/crossref_metadata_2025_split huggingface dataset:
Genetic control of C6 polymorphism and C6 deficiency in rabbits.
Authors: Goldman M B , Cohen C , Stronski K , Bangalore S , Goldman J N 
Published: December 2022

Abstract
The genetic control of the sixth component of complement (C6) in rabbits has been studied by quantitation of C6 functional and antigenic levels and identification of polymorphism by isoelectric focusing (IEF) in gels. Patterns of inheritance of C6 variants in families carrying a silent gene for C6 were examined, and it was found that 3 common plasma phenotypic variants, C6 A, C6 B, and C6 QO were under the genetic control of allelic genes, C6*A, C6*B, and C6*QO. In IEF patterns, C6 A could be identified by its isoelectric point that was slightly more acidic than that of C6 B. C6 QO was undetectable because it lacked functional and antigenic activity. The C6*A/C6*B genotype displayed a mixed IEF pattern with bands characteristic of both C6 A and C6 B. Functional and antigenic levels of C6 that were found in heterozygous C6*A/C6*QO and C6*B/C6*QO rabbits were approximately one-half of the C6 levels found in the corresponding homozygous animals. The phenotypic variation closely resembles that previously observed in humans and rhesus monkeys, as well as preliminary data in rabbits. The patterns of inheritance indicated that the two common C6 structural genes and the deficiency gene were allelic variants at the same genetic locus.
A cross-reactive idiotype, QUPC52 IdX, present on most but not all anti-alpha (1 replaced by 6) dextran-specific IgM and IgA hybridoma antibodies with combining sites of different sizes.
Authors: Sharon J , D'Hoostelaere L , Potter M , Kabat E A , Morrison S L 
Published: December 2022

Abstract
Seven BALB/c IgM, 4 BALB/c IgA, and 1 C57BL/6 IgA anti-alpha (1 replaced by 6) dextran hybridoma antibodies were characterized idiotypically. Five of the 7 IgM and all 4 BALB/c IgA proteins bear a cross-reactive idiotype present on the anti-alpha (1 replaced by 6) dextran BALB/c myeloma protein QUPC52 and on a majority of anti-alpha (1 replaced by 6) dextran antibodies in BALB/c mice. Of these 9 monoclonal antibodies, some have combining sites as large as 6 glucose residues, and some have combining sites as large as 7 glucose residues. Individual idiotypes present on QUPC52 are differentially expressed on the 9 hybridoma proteins that bear the cross-reactive idiotype. One BALB/c IgM hybridoma protein and the C57BL/6 IgA hybridoma protein did not react with anti-QUPC52 idiotypic antibodies; another BALB/c IgM hybridoma antibody showed only marginal reactivity.
Role of I-region gene products in T cell activation. I. Stimulation of T lymphocyte proliferative responses by subcellular membrane preparations containing Ia alloantigens.
Authors: Germain R N , Mayer S V , Mescher M F 
Published: December 2022

Abstract
A model system has been developed for exploring the requirements for activation of T cells by subcellular forms of Ia alloantigen. Lymph node cells from mice recently primed subcutaneously with viable allogeneic cells show strong proliferative responses in vitro to membrane preparations derived from cells bearing the appropriate I-region-encoded glycoproteins. This stimulation shows kinetics characteristic of a secondary response, with a peak at 24 to 48 hr. Primary responses to alloantigen-bearing membranes are weak or absent under these conditions. The predominant cell type involved in the secondary response is the Lyt-1+ T lymphocyte, and the major antigenic stimulus is the I-A subregion-encoded Ia glycoprotein. Syngeneic Ia+ accessory cells do not appear necessary for activation to occur. Detergent solubilized reconstituted membrane vesicles also will stimulate primed T lymphocytes to respond by proliferation. The applications of this approach to the study of T cell recognition of antigen and the role of nonspecific lymphokines in T cell triggering are discussed.
Idiotypic analysis of hybridoma antibodies to branched synthetic polymer (Tyr, Glu)-Ala-Lys: idiotypic relationship with antibodies to linear random polymer (Glu60, Ala30, Tyr10).
Authors: Ju S T , Pincus S H , Stocks C J , Pierres M , Dorf M E 
Published: December 2022

Abstract
The expression of three anti-GAT idiotypes, CGAT, Gte, and GA-1, on 17 C57BL/10 and four C3H.SW hybridoma anti-(T,G)-A--L antibodies was analyzed. These hybridoma anti-(T,G)-A--L antibodies exhibited two patterns of fine antigen binding specificity. The majority of the hybridoma antibodies bound the (T,G)-A--L, GT, and GAT polymers but not the GA polymer, and were designated as GT-reactive hybridoma antibodies. A minor population of hybridoma anti(T,G)-A--L antibodies bound to (T,G)-A--L but not to GT, GAT, or GA, i.e., (T,G)-A--L-specific. A complete correlation between fine antigen binding pattern and the expression of CGAT idiotype was demonstrated. None of the 21 hybridoma anti-(T,G)-A--L antibodies expressed the GA-1 idiotype. All of the GT-reactive and none of the GT-nonreactive hybridoma anti-(%,G)-A--L antibodies expressed the CGAT idiotype. Furthermore, the Gte idiotype was found on the majority of CGAT+-bearing C57BL/10 hybridoma anti-(T,G)-A--L antibodies. These results indicate that C57BL/10 anti-(T,G)-A--L antibody repertoire can be grouped into a minimum of three families; i.e., CGAT+ Gte+, CGAT+ Gte-, and CGAT- Gte- families, with the CGAT+ Gte+ family as the major compartment. This is confirmed by the high percentage idiotype binding of serum anti-(T,G)-A--L antibodies with anti-CGAT idiotypic antisera. Finally, anti-idiotypic antisera made against CGAT+ hybridoma anti-GAT or anti-(T,G)-A--L antibodies crossreact extensively with other CGAT+ hybridoma anti-GAT and anti-(T,G)-A--L antibodies. However, additional experiments demonstrated that CGAT+ hybridoma anti-(T,G)-A--L antibodies also possess private idiotypes.
Anti-DNA autoantibodies in (NZB X NZW)F1 mice are clonally heterogeneous, but the majority share a common idiotype.
Authors: Marion T N , Lawton A R , Kearney J F , Briles D E 
Published: December 2022

Abstract
Monoclonal anti-DNA antibodies from 13 cloned hybridoma cell lines have been used to analyze the clonal heterogeneity of autoimmune anti-DNA antibodies. The hybridomas were obtained by fusing spleen cells from a single, autoimmune (NZB X NZW)F1 mouse. With the use of the criteria of isotype, isoelectric focusing patterns, fine specificity for various nucleic acids, and idiotype, the monoclonal anti-DNA antibodies were found to be heterogeneous in that 12 different clonotypes were identified among the 13 monoclonal antibodies studied. However, eight out of the 13 monoclonal antibodies have similar antigen specificity and share a common idiotype. This suggests that although autoimmune anti-DNA antibodies within a single (NZB X NZW)F1 mouse are the products of a large number of different antibody-producing clones, many of the clones produce antibodies with similar antigen-binding regions. Furthermore, in the majority of (NZB X NZW)F1 mouse sera the appearance of detectable levels of the common idiotype coincides with the appearance of anti-DNA autoantibody.
Genetic control of eosinophilia in mice: gene(s) expressed in bone marrow-derived cells control high responsiveness.
Authors: Vadas M A 
Published: December 2022

Abstract
A heterogeneity in the capacity of strains of mice to mount eosinophilia is described. BALB/c and C3H are eosinophil high responder strains (EO-HR) and CBA and A/J are eosinophil low responder strains (EO-LR), judged by the response of blood eosinophils to Ascaris suum, and the response of blood, bone marrow, and spleen eosinophils to keyhole limpet hemocyanin given 2 days after 150 mg/kg cyclophosphamide. Some of the gene(s) for high responsiveness appear to be dominant because (EO-HR X EO-LR)F1 mice were intermediate to high responders. This gene is expressed in bone marrow-derived cells because radiation chimeras of the type EO-HR leads to F1 were high responders and EO-LR leads to F1 were low responders. This description of a genetic control of eosinophilia in mice may be useful in understanding the role of this cell in parasite immunity and allergy.
Immunoglobulin production in human mixed lymphocyte cultures: implications for co-cultures of cells from patients and healthy donors.
Authors: Rümke H C , Terpstra F G , Huis B , Out T A , Zeijlemaker W P 
Published: December 2022

Abstract
When human peripheral blood lymphocytes (PBL) are cultured in the presence of irradiated allogeneic lymphocytes, the resulting mixed lymphocyte reaction (MLR) leads to the secretion into the supernatant of substantial amounts of IgM and IgG, derived from nonirradiated responder B lymphocytes. Our data indicate that stimulation to Ig production by responder B cells may result from different types of interactions. First, B cells and monocytes among the irradiated stimulator cells activate T cells in the responder population, which in turn trigger responder B cells to produce Ig; second, "responder" B cells activate irradiated "stimulator" T cells, leading to a "helper" signal, back to the responder B cells and leading to Ig production. The latter system is radiosensitive, because allogeneic T cells, irradiated at a dose of 4000 rad or more, failed to induce Ig production by responder B cells. In some combinations of human allogeneic lymphocytes, the co-culture of the cells leads to inhibition of Ig production, both in the presence and in the absence of PWM. Thus, co-culture of allogeneic cells may cause "positive" as well as "negative" allogeneic effects. The implications of these findings for the interpretation of co-cultures that are aimed at establishing defects in lymphocytes from patients with, for example, immunodeficiencies, who fail to produce Ig in the presence of PWM are discussed.
Antigen-specific suppression of type II collagen-induced arthritis by collagen-coupled spleen cells.
Authors: Schoen R T , Greene M I , Trentham D E 
Published: December 2022

Abstract
The induction of arthritis in Wistar-Lewis rats was suppressed by i.v. injections of spleen cells coupled to native type II collagen, beginning 14 days before intradermal injection of native type II collagen in incomplete Freund's adjuvant and continuing at 7-day intervals for the next 3 weeks. Cells coupled to native type I collagen or to denatured type II collagen were ineffectual, suggesting antigen-relevant cells were required for suppression. The phenomenon appeared to be mediated by a humoral effector mechanism; IgG antibody titers but not hemagglutinating antibody titers or delayed-type hypersensitivity to collagen were decreased by the injection of type II collagen-coupled cells. These data demonstrate the potential of antigen-specific immunotherapy for autoimmune disease.
Interaction of specific and innate factors of immunity: IgA enhances the antimicrobial effect of the lactoperoxidase system against Streptococcus mutans.
Authors: Tenovuo J , Moldoveanu Z , Mestecky J , Pruitt K M , Rahemtulla B M 
Published: December 2022

Abstract
The antimicrobial effect of the lactoperoxidase (LPO) system (enzyme with the thiocyanate ion and hydrogen peroxide) on Streptococcus mutans NCTC 10449 (serotype c) was significantly enhanced when the system was combined with secretory IgA. Similar enhancement was observed with LPO-myeloma IgA1 or IgA2 combinations. This enhancement of the antimicrobial efficiency was not dependent on the presence of specific antibodies to S. mutans in the IgA preparation, but seemed to require binding between LPO and immunoglobulin. However, neither human polyclonal nor myeloma IgG or IgM nor rabbit IgG enhanced the antibacterial activity of the LPO system. None of the immunoglobulins, when added alone, produced antimicrobial effects. LPO was shown to bind to colostral secretory IgA, myeloma IgA1, IgA2, and to a lesser degree to monoclonal and polyclonal IgG and monoclonal IgM. This binding had a stabilizing effect on the enzyme activity. Our results suggest that IgA significantly enhances the antibacterial efficiency of one of the innate immune factors--the LPO system.
Specific thymus-derived (T) cell recognition of papova virus-transformed cells.
Authors: Greene M I , Perry L L , Kinney-Thomas E , Benjamin T L 
Published: December 2022

Abstract
As a first step toward identifying papova virus-specific transplantation antigens and characterizing the immune response to these antigens, a series of congenic B10 mouse lines transformed by polyoma virus and SV40 has been obtained. B10.D2 (H-2d) mice immunized with x-irradiated polyoma-transformed B10.D2 cells (PyB10.D2) contained within their spleens a population of T cells that upon restimulation in vitro preferentially lyse 51Cr-labeled PyB10.D2 compared with other allogeneic polyoma-transformed target cells or SV40-transformed B10.D2 cells. Twenty hours after acute infection with polyoma virus, SV10.D2 cells express cell surface structures recognizable by polyoma-specific CTL. This CTL activity is therefore both polyoma specific and H-2 restricted, indicating associative recognition of H-2 molecules along with the virus-specific antigen.
Functional heterogeneity of helper T cells: two distinct helper T cells are required for the production of T cell growth factor.
Authors: Larsson E L 
Published: December 2022

Abstract
A rat monoclonal antibody, obtained after immunization with cells from a cytolytic, TCGF-dependent T cell clone, was found to react with 10 to 20% of murine splenic and lymph node cells and with 65 to 70% of thymocytes. Addition of this antibody to normal spleen cell cultures, or cytotoxic elimination of the cells recognized by the antibody before culture, resulted in the abolishment or profound inhibition of the Con A-induced proliferative responses. The antibody did not react with or inhibit the proliferating, TCGF-reactive T cells, but it inhibited lectin-dependent TCGF production. An analysis of this inhibition, using purified cell populations and the macrophage-derived factor LAF, demonstrated that the cell removed by antibody cytotoxicity was neither the macrophage nor the TCGF-producing T cell, indicating that this antibody eliminates a second helper T cell required for lectin-dependent production of LAF by the accessory cells. These results extend previous observations on the T cell dependence of Con A-induced LAF production and identify a fourth cell type involved in the collaborative processes leading to TCGF-dependent T cell proliferation.
T cell-specific suppressor factor(s) with regulatory influence on interleukin 2 production and function.
Authors: Kramer M , Koszinowski U 
Published: December 2022

Abstract
In this study we report that alloantigen-activated spleen cells produce both amplifying and suppressive factors under the same conditions. Both types of soluble mediators--as detected in different assay systems--were present in the supernatants of in vivo sensitized and in vitro restimulated spleen cell populations and were separable by gel filtration. As shown by others, the amplifying factor (IL 2) was eluted in the size range of 30,000 m.w. The suppressive factor(s) (SF) was eluted in the size range of 10,000 m.w. SF was shown to inhibit the proliferative response of T cells to alloantigen, as well as the generation of regulatory T cells and cytotoxic T cells from their precursors when added at the beginning of the in vitro culture. Furthermore, SF inhibited the release of IL 2 from producer T cells but had no detectable effect on the interaction of IL 2 with receptive T cells. In addition it was shown that SF does not affect the generation of PFC from their precursors after activation by T cell-independent antigens. The results indicate that SF selectively acts on T cells and that it is involved in the regulation of the immune response by modulating early events in T cell activation.
Detection of at least two distinct mouse I-E antigen molecules by the use of a monoclonal antibody.
Authors: Ozato K , Sachs D H 
Published: December 2022

Abstract
In an attempt to determine whether the expression of more than a single Ia antigen is determined by the I-E subregion of the mouse major histocompatibility complex (MHC), sequential immunoprecipitation analyses were performed by using a monoclonal antibody and alloantisera reactive with I-E subregion products. 3H-leucine-labeled glycoprotein preparations obtained from H-2d spleen cells were precleared with the monoclonal antibody 14-4-4S and then examined for residual Ia activity precipitable by an alloantiserum detected by SDS-polyacrylamide gel electrophoresis. Residual Ia activity was observed for all three strains of the H-2d haplotype tested. The residual Ia activity could be detected by sera absorbed with B10.A spleen cells, indicating that products of the I-E subregion rather than of the I-C subregion were responsible for this activity. No separable I-Ek molecules were detected in products of B10.A cells with the use of combinations of two monoclonal antibodies (including 14-4-4S) and several appropriate alloantisera. These findings indicate the presence of at least two similar but distinct I-E antigens encoded by the H-2d haplotype.
Characterization and functional properties of tumor cell lines in accessory cell replacement assays.
Authors: Walker E B , Lanier L L , Warner N L 
Published: December 2022

Abstract
This study reports the initial phenotypic and functional characterization of a series of cloned, murine, myelomonocytic tumors and their parent cell line WEHI-3, and a group of murine B lymphoma tumors. The tumor cell lines of the myelomonocytic lineage demonstrated the ability to reconstitute a macrophage-depleted, primary in vitro anti-SRBC PFC response, but only marginally enhanced an accessory cell-depleted, ova-primed, lymphocyte proliferation in vitro response. The B lymphoma tumors displayed exactly the reverse functional profile, being highly efficient in reconstitution of the proliferation response, but not supporting the SRBC PFC response. Detailed analysis of the cell surface phenotype of the various B lymphoma tumors used in this study show they display cell surface markers characteristic of normal B lymphocytes but are heterogeneous in their various stages of differential arrest. Future work will concentrate on the orchestration of Ia-mediated and soluble factor-mediated (IL 1) modalities of antigen-triggering of lymphocytes by these B lymphoma and myelomonocytic tumor cell lines.
The use of conglutinin in a quantitative assay for the presence of cell-bound C3bi and evidence that a single molecule of C3bi is capable of binding conglutinin.
Authors: Brown E J , Gaither T A , Hammer C H , Hosea S W , Frank M M 
Published: December 2022

Abstract
We have developed a quantitative assay for cell surface C3bi using 125I-labeled conglutinin. Conglutinin was purified to homogeneity from bovine serum and radiolabeled with 125I Bolton Hunter reagent. Conditions of time, temperature, ionic strength, and cell concentration that optimized the binding of conglutinin to erythrocytes bearing C3bi were then determined. The interaction between conglutinin and C3bi under these conditions was highly specific, since EAC4b3b, EAC4b3d, EAC4b3b-beta IH, and EAC4b treated with serum did not bind radioconglutinin significance better with EA or EAC4b. Using this assay, was examined the kinetics of inactivation of both human and guinea pig C3b bound to erythrocytes and showed that, for both, maximum conglutinin binding occurred after EAC4b3b had been incubated with a source of beta 1H and C3INA for 10 to 20 min at 37 degrees C.l We showed a linear relationship between the number of molecules of C3bi per erythrocyte and the amount of conglutinin bound for both guinea pig and human C3bi. The affinity of conglutinin for cell-bound C3bi was shown to be independent of C3bi density on the erythrocyte surface, and the Kd for conglutinin binding to erythrocytes bearing human C3bi was determined to be 1.3 X 10(-8) M. The number of conglutinin binding sites per erythrocyte as calculated from Scatchard plots was equal to the number of C3bi molecules on the cell surface as determined by direct assay using 125I-labeled C3. Moreover, for both human and guinea pig C3bi, the plot of log (cell surface C3bi) vs log (conglutinin bound) had a slope of 1. These findings imply that a single molecule of C3bi is capable of binding a molecule of conglutinin under the conditions of our assay.
Feedback regulation of immune responses by immune complexes; possible involvement of a suppressive lymphokine by FcR gamma-bearing B cell.
Authors: Miyama-Inaba M , Suzuki T , Paku Y H , Masuda T 
Published: December 2022

Abstract
Inoculations of antigen-antibody complexes (immune complexes) with the intact Fc portion generates suppressor cells in vivo by binding to FcR gamma on B cells via Fc portions. The cell type responsible for the suppression appears to be B cells bearing FcR gamma. Neither T cells nor macrophages participate in both the inductive and effective phases of this type of regulation. The suppression caused by splenic B cells, previously stimulated with immune complexes in vivo, is mediated by humoral factor(s) released from them. The suppressive factor(s) have H-2 gene product(s) coded by the right-hand side of the H-2 gene complex, but not for FcR gamma themselves or immunoglobulins. It has shared component(s) with suppressive B cell factor (SBF) released from FcR gamma + B cells stimulated with immune complexes in vitro, and it resembles SBF in its mode of action. These findings indicate that immune complexes, the final products of antibody responses, control the immune responses by stimulating surface FcR gamma on B cells. It is of interest that this type of regulation functions in vivo.
Abnormal anti-Epstein Barr virus antibodies in carriers of the X-linked lymphoproliferative syndrome and in females at risk.
Authors: Sakamoto K , Seeley J K , Lindsten T , Sexton J , Yetz J , Ballow M , Purtilo D T 
Published: December 2022

Abstract
The asymptomatic hemizygous female carriers of the X-linked lymphoproliferative syndrome (XLP) have abnormal antibody responses to EBV. This suggests partial expression of the defect that leads to EBV-provoked life-threatening diseases in their affected sons. EBV specific antibodies were measured in 65 serum samples of 12 obligate carrier females and seven of their daughters (females at risk) during periods ranging from 1 to 5 yr. Abnormal qualitative antiviral capsid antigen (VCA) IgG titers were nearly fourfold higher than normal controls, two carriers had persistent IgM anti-VCA antibody, two-thirds had persistent IgA anti-VCA antibody, and half of the women had titers to early antigen (EA). Five of seven females exhibited a similar persistent pattern. In contrast, none of the unaffected family members nor 23 normal controls expressed IgA or IgM titers to VCA even with high exposure to the virus, and anti-EA was detected in only one control. Therefore, these findings may prove useful for detecting carriers of the syndrome. Abnormal anti-EBV titers similar to the carrier pattern have been reported in patients and other immunosuppressed individuals, and are indicative of active viral infection.