bluuebunny/crossref_metadata_2025_split huggingface dataset:
On the Interaction of Rabbit C1q with Sheep and Rabbit Immune Complexes
Authors: Liberti Paul A. , Baillie Richard D. , Milligan Kathleen F. , Bausch Dulcie M. 
Published: December 2022

Abstract
The reversibility of interaction between rabbit C1q and a calcium dependent antigen-antibody system [GAT-anti-GAT-Ca+2], as well as reaction parameters thereof, have been carefully examined. By utilizing the reversibility of the GAT-anti-GAT-Ca+2 reaction by the addition of EDTA, it has been found that 1) C1q-IgG interaction is totally reversed by the disruption of the immune complex, independent of antigen-antibody ratios, 2) the amount of C1q bound to immune complexes mirrors antibody precipitated in the precipitin reaction, 3) the amount of C1q bound to “pre-formed” immune complexes is almost identical to that amount bound when immune complexes are formed in the presence of C1q, i.e., “dynamic complexes,” 4) C1q specifically bound to immune complexes can rebind as many as three times without loss of binding activity, and 5) C1q multiply reacted with immune complexes suffers no loss of hemolytic activity. Items 4 and 5 provide strong evidence that C1q remains native upon binding and that the labile nature of C1q is probably not related to its triggering actions in the complement phenomenon. From quantitative binding studies of C1q with pre-formed immune complexes formed at antibody excess, equivalence and antigen excess, the shapes of the binding curves and Scatchard plots are not suggestive of co-operative interactions between C1q and IgG. Association constants obtained with sheep or rabbit pre-formed immune complexes were significantly greater in antibody excess than at equivalence, as were amounts of C1q bound. For dynamic immune complexes formed in the presence of C1q, more C1q is bound at equivalence. Since more C1q was found to bind to these immune complexes at equivalence than in antibody excess, i.e., similar to an in vivo situation, it appears that quantities of C1q bound, rather than the energy of interaction, may be more related to the degree of complement fixation.
The Cellular Mechanism of Leukocyte Adherence Inhibition
Authors: Koppi Thelma A. , Maluish Annette E. , Halliday William J. 
Published: December 2022

Abstract
Human blood leukocytes from three subjects who had been contact sensitized to dinitrochlorobenzene were used in direct and indirect leukocyte-adherence-inhibition (LAI) reactions in an attempt to elucidate the cellular mechanism of reactivity. The leukocytes were separated and purified by standard procedures. In direct LAI, only T cells or populations containing T cells gave positive reactions (significantly reduced adherence) with the antigen. Supernatants from suitable leukocyte-antigen mixtures contained a soluble leukocyte-adherence-inhibition-factor (LAIF) that reduced the adherence of normal leukocytes. Only T cells or populations containing T cells were active in LAIF production; B cells, granulocytes, and monocytes were inactive. The cellular requirement for the action of preformed LAIF was not restricted: all major types of blood leukocytes were susceptible to its effect.
Response of a Continuous Macrophage-Like Cell Line to Mif
Authors: Newman Walter , Diamond Betty , Flomenberg Phyllis , Scharff Matthew D. , Bloom Barry R. 
Published: December 2022

Abstract
A cloned murine macrophage-like cell line, FC-1, which arose during fusion of a drug-marked myeloma cell line with primary splenic cells was shown to migrate well from capillary tubes both in medium containing 10% horse serum or in serum-free medium containing 0.5% BSA. This cell line was responsive to MIF produced by mouse spleen cells stimulated with either insolubilized Con A or with alloantigens.
Bio Gel fractionation of MIF supernatants showed the same samples to contain inhibitory material for both FC-1 cells and for primary macrophages and that this product had a m.w. of 25,000 to 50,000.
Because the migration of FC-1 was inhibited by MIF prepared and tested in serum-free medium or in plasminogen-depleted serum, migration inhibition must result from the direct interaction of MIF with macrophages rather than indirectly through an activation of serum enzymes. This was confirmed when primary macrophages that require serum were shown both to migrate well and to respond to MIF in plasminogen-depleted serum.
Because of the homogeneity of the cloned FC-1 cell line and its ability to migrate and respond to MIF in serumfree medium, this macrophage-like cell line offers unique advantages for studying the regulation of macrophage functions by products of activated lymphocytes.
Inhibition of Specific Immune Responses by Feeding Protein Antigens
Authors: Miller Stephen D. , Hanson Donald G. 
Published: December 2022

Abstract
We studied the effect of a single intragastric administration of ovalbumin (OVA) on the subsequent development of OVA-specific cell-mediated immune (CMI) responses in BDF1 mice. In animals fed OVA 7 days before subcutaneous sensitization with OVA-CFA, we observed a concomitant dose-dependent decrease in both the humoral and CMI responses specific for OVA. The CMI tolerance was found to be antigen-specific when assayed in vivo by ear swelling or in vitro by an antigen-induced T cell proliferation assay because OVA-fed mice responded normally to sensitization with horse γ-globulin. It was also shown that either spleen or lymph node cells, but not serum, from OVA-fed donors transferred suppression to normal recipients. The transfer was mediated by antigen-specific suppressor T cells (Ts) that appeared to inhibit the induction phase (afferent limb) of the CMI response, since the Ts were only effective when transferred before or shortly after the onset of sensitization.
Biosynthesis of a Single Chain PRO-C5 by Normal Mouse Liver mRNA: Analysis of the Molecular Basis of C5 Deficiency in AKR/J Mice
Authors: Patel Feisal , Minta Joe O. 
Published: December 2022

Abstract
An in vivo labeling technique has been used to probe the molecular lesions precipitating in C5 deficiency in the AKR/J mouse. 14C-labeled amino acids were administered i.p. into normal and C5-deficient mice, and the plasma was harvested 4 hr later. By using monospecific anti-C5, newly synthesized 14C-C5 was immunoprecipitated from the plasma and postmitochondrial supernatants (PMS) of a liver homogenate. By SDS-PAGE analysis it was demonstrated that normal mouse plasma (apparent m.w. 205,000) was composed of two dissimilar subunits, an α-chain (115,000 daltons) and a β-chain (82,000). However, nonsecreted C5 immunoprecipitated from the PMS was resolved into two nonreducible polypeptide chains of m.w. 200,000 and 170,000, respectively. By comparison to plasma C5, the 170,000 dalton peak polypeptide chain probably represents incompletely synthesized, partially degraded, or unglycosylated pro-C5. 14C-C5 immunoprecipitates from the plasma, and the PMS of AKR/J C5-deficient mice contained insignificant radioactivity and on SDS gels did not resolve into any distinct peaks, suggesting that C5 is not synthesized in this strain.
14C-C3 immunoprecipitated from the plasma of normal and AKR/J mice in each case was composed of covalently-linked α- and β-chains (m.w. 130,000 and 85,000, respectively), 14C-C3 immunoprecipitated from the PMS of normal and C5-deficient liver homogenates in each case migrated on SDS gels as a single polypeptide chain, pro-C3 (m.w. 200,000).
Confirmation of these findings have been achieved by cell-free translation studies. Poly(A)-mRNA isolated from normal mouse liver stimulated the incorporation of 3H-leucine into protein in a time-dependent fashion in a reticulocyte lysate system under optimal conditions. 3H-C5 immunoprecipitated from the translation reaction mixture behaved as a single nonreducible polypeptide chain (m.w. 170,000). Poly A-mRNA from the liver of the AKR/J mouse displayed similar kinetics and dose-response stimulation of protein synthesis upon translation in the cell-free system, but failed to direct the synthesis of C5 or C5 immunoreactive peptides, although C3 was synthesized normally as pro-C3. Since the intact machinery for carbohydrate synthesis is not present in the reticulocyte cell-free system, it is envisaged that the 170,000-dalton C5 polypeptide chain is possibly unglycosylated pro-C5. Thus, C5 is synthesized as a single-chain pro-C5 and post-translationally converted to a two-subunit C5 molecule by limited proteolysis. In the AKR/J C5-deficient mouse C5 is not synthesized at all, suggesting the lack of a functional mRNA for C5 in this strain.
Activation of Murine Complement by Cobra Venom Factor in the Presence of EDTA
Authors: Goldman John N. , Bangalore Shrikar , Goldman Margaret B. 
Published: December 2022

Abstract
The anticomplementary factor of cobra venom (CoVF) was found to activate the terminal complement (C) components (C5 through C9) in mouse or rat serum or plasma in the presence of EDTA. The same concentrations of EDTA would block C activation by EA, zymosan, and inulin and would block C activation in human and guinea pig serum by all of these activators, including CoVF. Murine serum was found to contain two factors that allowed CoVF-induced C activation and bystander hemolysis in the presence of EDTA. The first was factor B or a related component of the alternative pathway, which allowed formation of a functionally active complex of CoVF and factor B in the presence of EDTA. The second was murine C5, which led to augmented hemolysis of unsensitized bystander erythrocytes and activation of the other terminal components. Preformed complexes of CoVF and rat factor B were active in leading to C5 and C6 consumption in human or guinea pig serum that had been fortified with rat C5. In contrast to native CoVF, these complexes did not lead to electrophoretic conversion of C3 in the human or guinea pig serum. It was further shown that in the presence of rat C5, purified CoVF led to moderate activation of the terminal components in human serum-EDTA in the absence of electrophoretic conversion of C3, indicating that in these situations, CoVF activated C5 and the other terminal components with little or no utilization of C3.
A Monoclonal Antibody to Viral Glycoprotein Blocks Virus-Immune Effector T Cells Operating at H-2Dd but Not at H-2Kd
Authors: Frankel Mark E. , Effros Rita B. , Doherty Peter C. , Gerhard Walter U. 
Published: December 2022

Summary
A particular monoclonal antibody that binds to the influenza virus HA molecule inhibits HA-specific thymus-derived lymphocytes mediating cytotoxicity in the context of H-2Dd but not of H-2Kd. Another monoclonal antibody blocks both sets of HA-specific effector T cells. This observation, together with related findings from other laboratories, is considered to support the idea that T cell recognition is directed against some association of viral and H-2 glycoproteins, as proposed in the original formulation of the “altered self” concept.
Ecto-5′-Nucleotidase Activity in T and B Lymphocytes from Normal Subjects and Patients with Congenital X-Linked Agammaglobulinemia
Authors: Thompson Linda F. , Boss Gerry R. , Spiegelberg Hans L. , Jansen Inga V. , O'Connor Richard D. , Waldmann Thomas A. , Hamburger Robert N. , Seegmiller J. Edwin 
Published: December 2022

Abstract
Ecto-5′-nucleotidase activity was measured in lymphocyte subpopulations isolated from normal subjects and patients with congenital X-linked agammaglobulinemia. B lymphocytes from normal subjects have at least three times more ecto-5′-nucleotidase activity than T lymphocytes. Patients with X-linked agammaglobulinemia have 56% of normal activity in their T cells, and lack a lymphocyte subpopulation high in nucleotidase activity. High activity of ecto-5′-nucleotidase may be a biochemical marker for mature surface immunoglobulin-bearing B cells.
Demonstration in vitro of Cytotoxic T Cells with Apparent Specificity Toward Tumor-Specific Transplantation Antigens on Chemically Induced Tumors
Authors: Chauvenet Paula H. , McArthur Carole P. , Smith Richard T. 
Published: December 2022

Abstract
Chemically induced tumors of mice exhibit apparently unique antigenicity upon syngeneic transplantation into appropriately immunized hosts. An in vitro counterpart of this pattern in terms of specificity has not been reported. Data are presented that demonstrate that immune peritoneal exudates contain cells cytotoxic for the specific immunogen tumor but with rare exceptions, not toward other syngeneic methylcholanthrene-induced fibrosarcomas. Only tumors highly immunogenic by transplantation criteria induce cytotoxic PEC regularly; nonimmunogenic tumors consistently fail to do so. The effector cell responsible is eliminated by pretreatment with anti-Thy.1 but not anti-Ig plus complement. In concomitant experiments, PEC populations cytotoxic in vitro also conveyed adoptive protection against the specific tumor in syngeneic hosts. This in vitro assay appears to provide a tool for studying T cell-mediated cytotoxicity toward a set of unique surface antigens present on chemically induced tumors.
Serum Opsonic Activity in Rodent Malaria: Functional and Immunochemical Characteristics in Vitro
Authors: Hunter Kenneth W. , Winkelstein Jerry A. , Simpson Thomas W. 
Published: December 2022

Abstract
The functional and immunochemical characteristics of serum opsonic activity in rodent malaria were examined in the present study. Schizont- and late trophozoite-enriched populations of Plasmodium berghei-infected red blood cells (IRBC) were isolated on a Ficoll density-gradient and used in an in vitro phagocytosis system composed of serum and monolayer cultures of rat peritoneal macrophages. Hyperimmune serum augmented the phagocytosis of IRBC to a greater degree than did nonimmune serum. When either IRBC or macrophages were pre-incubated with serum, the phagocytosis-promoting factors acted on the IRBC rather than on the macrophages in a manner characteristic of serum opsonins. The opsonic activity was specific for IRBC since noninfected red blood cells were rarely phagocytized and were unable to absorb opsonic activity from serum. The opsonic activity of both hyperimmune and nonimmune sera was heat stable, and unaffected by agents known to inactivate or inhibit complement (cobra venom factor and ethylenediaminetetraacetic acid). Finally, the opsonic activity was identified in preparations of purified IgG isolated from both hyperimmune and nonimmune sera.
Active Suppression of B Lymphocyte Maturation by Two Different Newborn T Lymphocyte Subsets
Authors: Durandy Anne , Fischer Alain , Griscelli Claude 
Published: December 2022

Abstract
Leukocytes from newborns and pregnant women were shown to be unable to mature into plasma cells in cultures stimulated by pokeweed mitogen (PWM). This is in contrast with the generation of IgM, IgG, and IgA-containing cells constantly observed in adult leukocytes. This defective B cell maturation was due to an active suppression mediated by T lymphocytes. T lymphocytes bearing receptors for IgG (Tγ) and Tγ-depleted populations were both able to exert this effect. Tγ lymphocytes inhibited B cell maturation without significantly affecting T and B cell proliferation, and their effect persisted after an incubation of 18 hr at 37°C. Tγ-depleted lymphocytes suppressed lymphocyte proliferation and, subsequently, B cell maturation into plasma cells. The suppressor activity of this second cell type was markedly diminished after incubation. Co-culture experiments showed that PWM-induced newborn suppressor T lymphocytes suppressed maturation of adult B cells only when T lymphocytes were present, suggesting that suppressor cells acted upon a target T cell population rather than directly upon B cells. Indirect inhibition of B cell maturation resulted in a lack of appearance of membrane IgG and IgA expression, although proliferation and loss of membrane IgD were observed. Although similar suppressor effects can be induced in vitro in adult leukocytes by fixation of immune complexes on Tγ populations or after concanavalin A activation of Tγ-depleted populations, the peculiarity of the perinatal period appears to be the spontaneous activation of the two types of T suppressor lymphocytes.
Immune Suppression in Vivo with Antigen-Modified Syngeneic Cells
Authors: Sherr David H. , Heghinian Krikor M. , Benacerraf Baruj , Dorf Martin E. 
Published: December 2022

Abstract
Intravenous administration of syngeneic spleen cells coupled with the palmitoyl derivative of fowl γ-globulin (p-FγG) results in a profound state of FγG carrier-specific tolerance in C57BL/6 mice. This nonresponsiveness can be attributed to two independent mechanisms, i.e., T cell tolerance and T cell suppression. The two phenomena could be distinguished on the basis of kinetics of induction, inducer cell dose requirements, and cyclophosphamide sensitivity. Thus, a 3-day period is required for the induction of T cell tolerance, and 7 days are required to induce immune suppression. Furthermore, at least 106 p-FγG-coupled cells must be administered to induce tolerance, whereas suppression could be induced with as few as 103 cells. In addition, the T cell tolerance was not sensitive to cyclophosphamide pretreatment, whereas the T cell suppression was cyclophosphamide sensitive. In contrast to T cell tolerance, suppressor T cells exerted their effects nonspecifically in the effector phase once they were stimulated with the inducing antigen.
In addition, a state of split responsiveness was demonstrated in animals given a subcutaneous (s.c.) injection of antigen-coupled cells. The s.c. route of induction resulted in a strong state of PFC nonresponsiveness while simultaneously priming for delayed type hypersensitivity (DTH) responses as assayed by footpad swelling. Thus, p-FγG-coupled syngeneic spleen cells are capable of inducing: 1) T cell tolerance, 2) immune suppression, and 3) priming of DTH-reactive cells, depending on the conditions employed.
Ly Phenotypes and MHC Recognition: The Allohelper That Recognizes K or D Is a Mature Ly123 Cell
Authors: Swain Susan L. , Bakke Anthony , English Michele , Dutton Richard W. 
Published: December 2022

Abstract
This paper describes the further characterization of the T cell activity that is induced by allogeneic MHC gene products and provides help to mouse spleen B cells in a primary in vitro response to sheep erythrocytes.
We have previously shown that the helper activity induced by antigens controlled by the K or D regions was dependent on the presence of an Ly123 cell and that a single cell, present in high frequency, was required. In the present paper we show that activity induced by a difference at H-2K is unaffected by adult thymectomy but is diminished by prior injection of anti thymocyte serum. The spleen cell population positively selected for Ly2 (Ly2 and Ly123 cells) and hence depleted of Ly1 cells retained full helper activity. Ly1 cells were inactive. In contrast, helper activity induced by differences at the whole haplotype or at Mls were present in the Ly1 population and reduced or missing from the Ly2 and Ly123 populations. We concluded that the helper activity induced by allogeneic K or D is the function of a long lived recirculating Ly123 cell present in high frequency. We were unable to find any evidence that the Ly123 matured into an Ly1 cell before performing its effector function. The Ly phenotype of the effector cell is thus more closely linked to the MHC subregion that is recognized than the T cell function performed. Possible interpretations of the findings are discussed.
Spontaneous and Induced in Vitro F1 Anti-Parental Cytotoxic T Lymphocyte Responses: Target Specificities of Cytotoxic Effectors
Authors: Ishikawa Hiromichi , Dutton Richard W. 
Published: December 2022

Abstract
In vitro cultures of spleen cells from about 5-week-old (AKR/J♀ × BALB/c) or (BALB/c♀ × AKR/J)F1 mice spontaneously generate CTL that lyse targets from AKR/J, BALB/c, and their F1 but not allogeneic strains. These spontaneous CTL are not generated in cultures of parental spleen cells and are only detectable in spleen cell cultures from F1 mice that were heterozygous at both the MHC and background loci.
The same F1 mice older than 20 weeks of age can respond to parental BALB/c stimulators in an in vitro culture system and generate cytotoxic T lymphocytes (CTL) that lyse BALB/c targets. This response is significantly higher than that seen in unstimulated cultures. The target antigen of these induced F1 anti-BALB/c CTL maps to H-2Dd but not to H-2Kd, and the CTL lyse not only parental targets but also heterozygous F1 targets syngeneic to the responder mice. In contrast, anti-H-2Kk CTL induced in the same adult F1 mice by stimulation with parental AKR/J cells lyse only homozygous H-2Kk targets.
Target antigen mapping as well as cold target competition analyses showed that the target specificities for these spontaneous CTL of the young F1 mice are indistinguishable from those seen for the induced responses of older mice; i.e., one target maps to Kk, and only homozygous Kk targets are lysed; the other maps to Dd, and homozygous Dd and the F1 targets are not distinguished.
Role of Nominal Antigen and Ia Antigen in the Binding of Antigen-Specific T Lymphocytes to Macrophages
Authors: Werdelin Ole , Shevach Ethan M. 
Published: December 2022

Abstract
We have previously demonstrated that when primed T lymphocytes were repeatedly incubated on monolayers of antigen-pulsed macrophages (Mø), the cells that failed to adhere to the monolayer demonstrated a marked depletion of their proliferative response that was specific both for the antigen used for pulsing the Mø and for Ia determinants on the Mø. In order to further analyze the contribution of the nominal antigen and Ia antigens to the physical binding of T lymphocytes to Mø, we have attempted to block the absorption of T lymphocytes to Mø with a large excess of soluble antigen and with anti-Ia sera. Our results demonstrate that anti-Ia sera inhibit but that soluble antigen augments the binding of specific T lymphocytes to Mø. The implications of these findings for “dual recognition” and “linked recognition” models of T lymphocyte receptors are discussed.
Structural Studies on the Murine Ia Alloantigens
Authors: Cook Richard G. , Capra J. Donald , Bednarczyk John L. , Uhr Jonathan W. , Vitetta Ellen S. 
Published: December 2022

Abstract
The α and β subunits of the murine I-A alloantigens from several H-2 haplotypes were examined by comparative tryptic peptide mapping by using double label (3H and 14C) techniques. Significant structural variation between alleles was detected in both subunits. Tryptic digests of the α polypeptides from s, b, and d showed only 65% co-elution with k; β-chains from s, b, d, and r were about 50% similar to the k β subunit. Peptide analysis of the Ak subunits from intra-H-2 recombinant strains indicated that both the α and β polypeptides are encoded within the I-A subregion.