bluuebunny/crossref_metadata_2025_split huggingface dataset:
The terminal membrane C5b-9 complex of human complement. Evidence for the existence of multiple protease-resistant polypeptides that form the trans-membrane complement channel.
Authors: Bhakdi S , Tranum-Jensen J , Klump O 
Published: December 2022

Abstract
C5b-9(m) complexes were incorporated into lecithin liposomes and subjected to proteolysis in the presence of DTT to remove the externally oriented annulus. Liposomes were recovered that selectively carried the membrane-bound, thin-walled cylindrical portion of the C5b-9(m) complex. The presence of DTT during proteolysis enhanced peptide bond cleavage in the C5b-9(m) complex. All C5-C9 components were degraded to lower m.w. fragments. A protease-resistant, but hydrophilic 85 to 86,000-dalton polypeptide derivative of C5, possibly representing the C5 beta-chain, was recovered in the fluid phase. This component is not intimately associated with the target lipid bilayer. Immunochemical analyses yielded evidence for the existence of minor C5-C9 antigenic determinants on the membrane-bound C5b-9(m) residue. SDS polyacrylamide gel electrophoreses of liposomes carrying the C5b-9(m) residues revealed the persistence of at least six major polypeptides of approximately m.w. 50,000, 45,000, 40,000, 38,000, 20,000, and 16,000. The data are interpreted to indicate that multiple protease-resistant polypeptide chains derived from several terminal C components participate in formation of the trans-membrane C channel.
Differential allo-response of murine thymocytes to H- 2 K region different recombinants and to H-2Kb mutants.
Authors: Wu S , Bach F H , Sopori M 
Published: December 2022

Abstract
Thymocytes used as responding cells in a mixed leukocyte culture with x-irradiated splenic stimulating cells generate highly significant proliferative and cytotoxic responses when responding and stimulating cells differ by the entire H-2 complex. On the other hand, when the genetic difference between responding and stimulating cells is only a K region, very little, if any, proliferative response is detectable and no cytotoxic response is found. In contrast, when responding and stimulating cell donors differ by a spontaneous mutation in the K region of the H-2 complex, as found in B6.C-H-2ba, B6-H-2bd and B6.C-H-2bf, highly significant proliferative and cytotoxic responses can be obtained. These results, thus, argue that the H-2 mutants cannot, with regard to their relationship to the parental strain, be readily equated with a K region difference as defined in the recombinant inbred strains.
The T lymphocyte proliferative response to poly-L-Glu-poly-D,L-Ala--poly-L-Lys.
Authors: Solinger A M , Schwartz R H 
Published: December 2022

Abstract
The immune response to several antigens has been shown to be under the control of two complementing major histocompatibility-linked immune response (Ir) genes. In most cases, one gene has been mapped to the I-A subregion and the other to the I-E/C subregion. However, in some cases F1 complementation has been described between two alleles in the I-A subregion, so called beta-beta complementation. In these examples, complementation has been seen at the antibody level but not in a T lymphocyte proliferation assay. In the present work, we studied the T cell proliferative response to poly-L-Glu-poly-D,L-Ala--poly-L-Lys (G-A--L). Peritoneal exudate, T lymphocyte-enriched subpopulations (PETLES) from F1 hybrids between C57BL/10 and B10.A, C57BL/10, and B10.A(4R), or B10.A and B10.A(3R) or (5R) mice responded well to G-A--L. In contrast, PETLES from F1 hybrids between C57BL/10 and B10.A(5R) or B10.A and B10.A(4R) mice, as well as from all inbred strains tested, failed to respond to G-A--L. These results demonstrate for the first time an example of Ir gene complementation at the T cell level in which both genes map to the left of the I-J subregion presumably in I-A. This system should now allow us to determine whether alpha-beta and beta-beta complementation take place through the same biologic mechanism.
Glucocorticoids and lymphocytes. II. Cell cycle-dependent changes in glucocorticoid receptor content.
Authors: Crabtree G R , Munck A , Smith K A 
Published: December 2022

Abstract
To study variations in glucocorticoid receptor levels during the cell cycle, we have separated mitogen-stimulated human peripheral lymphocytes and rat lymph node cells by unit gravity sedimentation and measured glucocorticoid binding in the resultant fractions. By morphologic criteria and thymidine incorporation, the fractions were separated into populations of G0 and G1 phase and S and post-S phase cells. A 2- to 3-fold increase in glucocorticoid receptor sites per cell, for cells in the S and post-S phase over those in G0 and G1, was observed with both nonstimulated rat lymph node cell suspensions and concanavalin A-stimulated human peripheral lymphocytes. These observations together with those from other studies indicate that formation of new glucocorticoid receptors near the S phase may be a general phenomenon in proliferating cells. We propose that this increase in glucocorticoid receptors during the cell cycle may explain the increase in glucocorticoid receptors in mitogen-stimulated lymphocytes.
In vitro growth of murine T cells. V. The isolation and growth of lymphoid cells infiltrating syngeneic solid tumors.
Authors: Yron I , Wood T A , Spiess P J , Rosenberg S A 
Published: December 2022

Abstract
A method has been developed for isolating and growing lymphoid cells infiltrating murine solid tumors. When tumor cell suspensions are placed in T cell growth factor (TCGF) lymphoid cells and not tumor cells proliferate. By 7 to 9 days lymphoid cells free of tumor can be harvested and grown continuously in TCGF. The growth of these cells is dependent on the presence of TCGF but not on the presence of concanavalin-A. Tumor cell suspensions that have been freed of T lymphoid cells by treatment with anti-Thy-1.2 serum and complement or by fractionation on Ficoll gradients exhibit no cell out-growth in TCGF. The lymphoid cells growing in TCGF exhibit significant cytotoxicity for syngeneic tumor cells and normal fibroblasts grown in culture but do no lyse normal lymphoid cells.
The first component of complement. I. Purification and properties of native C1.
Authors: Medicus R G , Chapuis R M 
Published: December 2022

Abstract
The first component of complement has been purified by using affinity chromatography on Sepharose-bound IgG. Unlike earlier procedures that yield the activated form of C1, in this method C1 is maintained in the native form by the protease inhibitor p-nitrophenyl, p'-guanidinobenzoate (NPGB). The procedure requires only two steps and yields pure C1 as judged both by SDS-PAGE analysis and by effective molecule calculations. The yields have varied from 30 to 50% in over 50 preparations. The functional properties of the purified native C1 correspond to those of C1 in serum. The dose-response activity profile is nonlinear, but becomes linear when C1 IS ALLOWED TO SELF-ACTIVATE. From SDS-PAGE analysis of the self-activated C1, all the C1r and C1s subcomponents are converted to the activated split products, indicating that all C1 molecules are biologically active. The recovery of C1 activity is dependent on the use of a heterologous source for the IgG on the affinity absorbant. The conditions of binding and elution from the Sepharose-IgG column are critical, indicating that immunoglobulin-bound C1 is rapidly inactivated under physiologic conditions by serum inactivators. The activation of the purified C1 in fluid phase has been explored both in the presence and absence of C1-inhibitor.
Inhibitory factor(s) of lymphoproliferation produced by synovial fluid mononuclear cells from rheumatoid arthritis patients: the role of monocytes in suppression.
Authors: Zembala M , Lemmel E M 
Published: December 2022

Abstract
Synovial fluid (SF) and synovial fluid mononuclear cells (SFM) were obtained from patients with rheumatoid arthritis (R.A.). The SF stimulated normal blood monocytes for nitroblue tetrazolium (NBT) reduction and inhibited normal lymphocyte response to PHA. Similar activities were found in supernatants from the cultures of SFM cells. Molecular weight of the lymphocytes inhibitory factor(s) produced by SFM was in range 50,000 to 100,000. The factor exerted its inhibitory activity via monocytes and had no direct toxic or blocking effect on lymphocytes. Monocytes played an active role in suppression presumably via production of a second-step inhibitory signal(s). It is suggested that the monocytes activated by the SFM-produced factor(s) are in turn triggered on for suppression of lymphoproliferation. These studies implicate that the state of monocyte activation is important in the regulation of lymphocyte responsiveness. This model of suppression may provide some explanation for SF lymphocyte hyporeactivity to mitogens in R.A.
T cell synergy in the rat: serologic characterization of T cell subsets.
Authors: Loop S M , Bernstein I D , Wright P W 
Published: December 2022

Abstract
The W3/25+ T cell subset in rats, defined by a xenogeneic monoclonal antibody and separated by using the FACS, was demonstrated to be the proliferating cell type in the in vitro MLC and to provide an amplifier function for the W3/25- T cell subset in the generation of cytotoxic effector cells to alloantigenic targets.
Regulation of the immune response. II. Characterization of the cell population(s) involved in the Fc fragment-induced adjuvant effect.
Authors: Morgan E L , Thoman M L , Walker S M , Weigle W O 
Published: December 2022

Abstract
Fc fragments derived from human and murine Ig have been shown to possess adjuvant properties. The spleen cell population(s) affected by the Fc fragments is the T lymphocyte. That Fc fragments do not act directly on the B lymphocyte was shown by the fact that in a system where T cell help was substituted for by TRF and using TI antigens, no adjuvant effect was observed. The adjuvant signal provided by the Fc fragments is needed early in the culture period, because it was reduced by approximately 50% when delayed by 24 hr. When the addition of Fc was delayed by 72 hr, the antibody response was not significantly increased over the culture that received antigen only.
Suppression of spontaneous reticulum cell sarcoma development and of syngeneic stimulator cell by anti-mu treatment of SJL/J mice.
Authors: Katz I R , Asofsky R , Thorbecke G J 
Published: December 2022

Abstract
The cellular origin of reticulum cell sarcoma (RCS) in SJL/J mice was studied by comparing the incidence of spontaneous RCS in control mice and in mice suppressed with goat anti-mu Ig from birth on. At 10 months of age anti-mu suppressed mice had 0% RCS as opposed to 60% in control mice. Growth of two i.v. injected transplantable RCS lines in anti-mu suppressed mice was approximately 60% as compared with growth in normal SJL/J mice. Proliferative responses of thymus and lymph node cells from anti-mu suppressed mice to RCS, mitomycin-treated syngeneic spleen cells (M. Spl.) Con A, and PHA were entirely normal. However, M. Spl. from anti-mu suppressed mice caused minimal or no stimulation of T cells from normal or anti-mu suppressed responders. The results suggest that the normal syngeneic stimulator cell is of B cell origin, either representing a direct precursor of RCS or indirectly influencing RCS appearance. A B cell origin of RCS is, furthermore, in agreement with some of its characteristics, such as surface markers (Ia antigens, Ly b) and in vivo localization properties.
Functional characteristics of TG and TnonG cells in a three party MLR.
Authors: Gebel H M , Radaj P A , Holmes D , Schwartz B D , Rodey G E 
Published: December 2022

Abstract
Human peripheral blood T lymphocytes were separated into highly purified Fc gamma receptor-positive (TG) and negative (TnonG) populations. These subgroups were compared with unseparated T cells for their ability to proliferate in response to concanavalin A or allogeneic cells, and to suppress a mixed leukocyte culture reaction (MLR). TG cells fail to vigorously proliferate in response to Con A or irradiated allogeneic cells. Moreover, the response of TnonG populations to Con A and allogeneic cells is enhanced compared with unseparated T cells, suggesting active suppression by TG cells. The suppressive effects of TG cells was confirmed in a 3-party MLR. In contrast, TnonG cells failed to suppress the MLR. However, Con A-activated TnonG cells did suppress the MLR and were as effective as TG cells.
Cell-surface immunoglobulin and insulin receptor expression in an EBV-negative lymphoma cell line and its EBV-converted sublines.
Authors: Spira G , Aman P , Koide N , Lundin G , Klein G , Hall K 
Published: December 2022

Abstract
Membrane Ig and insulin receptors were assayed in the EBV-negative Ramos lymphoma line and its EBV-converted sublines by surface fluorescence. 125I-protein A-binding assay, immunoprecipitation, and insulin receptor assay. The original Ramos line expressed surface IgM but not IgD and had a low concentration of insulin receptors. Ten of 10 converted lines expressed IgD and a variable but usually high insulin-binding capacity. Molecular weight analysis of immunoprecipitated Ig showed the presence of 2 mu-chains and 2 delta-chains. One of each heavy chain type could be characterized as membrane Ig, whereas the other was cytoplasmic. Antisera against the lambda-chain precipitated mu and delta heavy chains as well, indicating that the delta-chain expressed on the membrane of the EBV-converted Ramos lines is bound to the lambda light chain. The results show that the differentiation of a Burkitt lymphoma line is not completely "frozen" and can be induced to change in a more "activated" direction by EBV conversion.
Idiotypic analysis of anti-GAT antibodies. VIII. Comparison of interstrain and allotype-associated idiotypic specificities.
Authors: Ju S T , Pierres M , Germain R , Benacerraf B , Dorf M E 
Published: December 2022

Abstract
A guinea pig anti-idiotypic antiserum made against pooled specifically purified A/J anti-GAT antibodies was characterized. This antiserum contains anti-idiotypic antibodies specific to interspecies, interstrain, and allotype-linked idiotypic determinants. These idiotypic determinants are associated with the combining sites of idiotypic antibodies that are induced by GT-related but not GA-related antigenic moieties. Genetic and strain distribution studies indicated that the shared allotype-linked idiotypic determinants are controlled by Igh-1e- or Igh-1b-linked genes. The interrelationships of the allotype-linked and interstrain CGAT idiotypic specificities are described using monoclonal anti-GAT hybridoma antibodies. Four of 7 hybridoma anti-GAT antibodies of C57BL/6 origin expressed a major fraction of the idiotypic specificities of A/J anti-GAT antibodies. These 4 hybridoma antibodies also carried the common interstrain idiotype, termed CGAT, but not all CGAT-bearing anti-GAT hybridoma antibodies expressed the allotype-linked idiotypic specificities. The Ig-1b-positive, F17-167.1 hybridoma anti-GAT antibody was used as a ligand to selectively identify the major allotype-linked idiotypic specificities, which were designated Gte idiotype.
Idiotypic analysis of anti-GAT antibodies. IX. Genetic mapping of the Gte idiotypic marker within the Igh-V locus.
Authors: Ju S T , Dorf M E 
Published: December 2022

Abstract
The gene controlling the expression of the murine Gte idiotype marker was mapped within the Igh-V gene complex. This idiotypic marker was identified in B6, C.B-20 and A/J and C.AL-20 anti-GAT antisera, but either was not detectable or was present in very low quantities in the anti-GAT antisera obtained from BALB/c, BAB-14, SM/J, NZW, and NZB mice. The data are consistent with the interpretation that the latter 5 strains do not process Igh-Gte genes and the Igh haplotypes of these strains represent examples of crossing over within the Igh complex. Furthermore, the expression of the Gte idiotype(s) is not influenced by the Lyt-3 linked genes that control the kappa light chain polymorphism. Segregation analysis with 52 recombinant inbred strains confirmed the close linkage of Igh-Gte idiotype with Igh-1b locus. The recombination frequency between these loci was calculated to be 1 +/- 0.7 percent. Furthermore, by using B X D recombinant inbred strains, the Igh-Gte gene was mapped within the Igh-V region gene closely linked to the Igh-Np, Igh-Nbp, and Igh-BgI genes.
Distinct phenotypic expression of immunogenicity and immunosensitivity in sublines of a tumor.
Authors: Greenberg P D , Cheever M A , Fefer A 
Published: December 2022

Abstract
Continuous in vitro or in vivo passage of a BALB/c leukemia has resulted in generation of 2 immunologically distinct sublines. The subline maintained by in vitro passage failed to stimulate an allogeneic response but was susceptible to lysis by alloreactive cytotoxic cells. Conversely, the subline maintained by in vivo passage induced an allogeneic response but was resistant to lysis by cytotoxic T lymphocytes (CTL) reactive to H-2d antigens. Resistance to lysis occurred despite expression of H-2d antigens in a form recognizable by differentiated alloreactive CTL, as determined by cold-target inhibition experiments. Moreover, resistance was immunologically specific, in that the subline was susceptible to immune lysis mediated through recognition of other determinants. The results imply that the display and/or orientation of antigen in the cell membrane of these sublines that is required for a lytic event is distinct from the antigen expression necessary for immunologic recognition.
Macrophages in resistance to rickettsial infections: characterization of lymphokines that induce rickettsiacidal activity in macrophages.
Authors: Nacy C A , Leonard E J , Meltzer M S 
Published: December 2022

Abstract
Lymphokine-rich culture supernatants of antigen- or mitogen-stimulated spleen cells were fractionated by Sephadex G-200 column chromatography; fractions were assayed for capacity to induce tumoricidal and rickettsiacidal activities in mouse macrophages. Lymphokine activity that activated macrophages for tumor cytotoxicity eluted as a single peak in the 45,000 m.w. region. In contrast, activity for intracellular killing of rickettsiae eluted in 3 distinct regions: 115 to 125,000, 35 to 45,000, and less than 10,000 daltons. This elution pattern was observed with both antigen and mitogen-induced lymphokines. Activity of each of the 3 lymphokine species for induction of rickettsiacidal activity was destroyed by heating at 56 degrees C for 1 hr. Tumor cytotoxicity and rickettsiacidal activity, both effector functions of activated macrophages, were dissociated on the basis of lymphokines regulating these activities.
Immune response to acute virus infection in the Syrian hamster. II. Studies on the identity of virus-induced cytotoxic effector cells.
Authors: Nelles M J , Duncan W R , Streilein J W 
Published: December 2022

Abstract
The identity of the effector cell(s) mediating vaccinia virus-induced cytotoxic activity in Syrian hamsters undergoing acute virus infection has been investigated. Two different approaches have been utilized in this regard. Although T cells do not mediate vaccinia virus-induced cytotoxic activity directly, studies employing adult thymectomized, x-irradiated, bone-marrow-reconstituted hamsters lacking discernible T cell reactivity demonstrated that the presence of an intact thymus and/or functional T cells were required for the in vivo development of a significant portion of vaccinia virus-induced cytotoxic activity. In addition, incorporation of aggregated gamma-globulins as well as anti-immunoglobulin reagents into the in vitro 51Cr release assay inhibited a significant proportion of the cytotoxic activity mediated by spleen cells obtained from acutely infected hamsters possessing an intact thymus. Both approaches have yielded information consistent with the idea that a sizable portion of vaccinia virus-induced cytotoxic activity in the Syrian hamster is effected by K cells mediating antibody-dependent cell-mediated cytotoxicity (ADCC). The significance of this observation is discussed with regard to hamster viral immunity in general.
Antigen-binding diversity and idiotypic cross-reactions among hybridoma autoantibodies to DNA.
Authors: Andrzejewski C , Rauch J , Lafer E , Stollar B D , Schwartz R S 
Published: December 2022

Abstract
Hybridoma anti-DNA antibodies produced by clones derived from fusions of spleen cells from unimmunized MRL/l mice with BALB/c plasmacytomas were examined for their binding to nucleic acid antigens and for their reactivities with anti-idiotype antibodies. All the antibodies bound to a variety of nucleic acids and polynucleotides. This finding suggests that epitopes shared by nucleic acid antigens can account for some of the serologic diversity in lupus serum. Each hybridoma autoantibody had a unique pattern of reactivity with nuclei acid antigens, yet cross-reactions among some of them were found by analyses with anti-idiotype antibodies. These cross-reactions were due to similarities in the antigen-binding regions of the autoantibodies because anti-idiotype Ig blocked the binding of the hybridoma antibody DNA; moreover, polynucleotides inhibited the idiotype anti-idiotype reaction. Cross-reactive idiotypes were found not only among hybridoma anti-DNA antibodies produced by clones derived from the same MRL/l mice but also among antibodies produced by clones derived from different MRL/l mice. The latter finding suggests that families of germ line genes may encode some autoantibodies against DNA.
Isolation of C4-binding protein from guinea pig plasma and demonstration of its function as a control protein of the classical complement pathway C3 convertase.
Authors: Burge J , Nicholson-Weller A , Austen K F 
Published: December 2022

Abstract
A decay-accelerating factor of the classical complement pathway C3 convertase, C4b,2a, has been purified to homogeneity from guinea pig plasma by a 5-step procedure that includes 5% polyethyleneglycol-4000 (PEG-4000) precipitation, Sepharose 6B gel filtration, heparin-Sepharose chromatography, DE-52 anion exchange chromatography, and Sepharose-C4gp affinity chromatography. The protein elicited a monospecific antiserum in a rabbit and was found with the Mancini technique in both normal and C4-deficient guinea pig plasma at a concentration of 60 microgram/ml. The purified protein gave a single stained band of 550,000 m.w. on SDS-PAGE under nonreducing conditions and a single band of 72,000 m.w. with reduction and alkylation. On the basis of its m.w. and subunit structure, ability to bind to a C4 affinity column, and ability to regulate the classical C system by accelerating the decay of the classical C3 convertase this protein represents the guinea pig analog of the human C4-binding protein.