bluuebunny/crossref_metadata_2025_split huggingface dataset:
Functional analysis of mononuclear cells infiltrating into tumors. II. Differential ability of mononuclear cells obtained from various tissues to produce helper factors that are involved in the generation of cytotoxic cells.
Authors: Uede T , Kohda H , Ibayashi Y , Osawa H , Diamantstein T , Kikuchi K 
Published: December 2022

Abstract
The requirement of CGF in the generation of cytotoxic cells against syngeneic tumor cells (T-9) and in the rejection of transplanted T-9 cells has been investigated. Spleen cells obtained from sensitized rats showed strong cytotoxicity against 51Cr-labeled T-9 cells upon incubation with CGF for 48 hr. Human recombinant IL 2 and rat IFN failed to generate cytotoxic cells from spleen cells of sensitized rats. CGF are produced by spleen cells upon inoculation of T-9 cells into sensitized rats as a host in vivo immune response. Production of CGF preceded the appearance of cytotoxic cells in regional lymph node and tumor tissues. In those rats, inoculated tumor cells were eventually rejected. In contrast, spleen cells failed to produce CGF upon inoculation of T-9 cells in unsensitized rats. Cytotoxic cells were not detected in unsensitized rats, and inoculated tumor grew in those rats. Thus, CGF is likely to be involved in the generation of cytotoxic cells and in the rejection of inoculated syngeneic tumor cells. A Mono Q anion-exchange column with an FPLC system allowed the chromatographic separation of CGF from IL 1, IL 2, IL 3, and CSF.
Expression of polypeptide segments of the human complement component C3 in E. coli: genetic and immunological characterization of cDNA clones specific for the alpha-chain of C3.
Authors: Ma D , Sessler M J , Meyer T F , Schrod L , Hänsch G M , Burger R 
Published: December 2022

Abstract
The third component of complement C3 and its fragments have a central role in a variety of host defense mechanisms. The identification of functionally relevant C3 domains is important because of the marked functional versatility of the C3 molecule. Several human C3 cDNA clones from a human liver cDNA library were isolated and characterized. A bacterial expression vector system was used to express cDNA clones that were identified by an immunological screening procedure. The C3 cDNA clones produced in E. coli the hybrid proteins consisting of cro-beta-galactosidase and polypeptide segments of human C3, as revealed by Western blotting with antisera to human C3. The C3 moiety of the hybrid proteins had a m.w. of up to 46.000. Polyclonal antibodies against the C3 segments expressed by one of the C3 cDNA clones (ReC3-1) have been raised in mice and rabbit, and in addition, a monoclonal antibody was produced. The antisera and the monoclonal antibody reacted in Western blotting analysis selectively with the alpha-chain, but not the beta-chain of human C3. Restriction mapping of the different cDNA clones was performed, and revealed that the different clones were partially overlapping. The ReC3-1 cDNA clone included a 0.7 kb noncoding region at the 3' terminal end of the C3 cDNA. One of the restriction sites (Hind III) identified in the ReC3-1 cDNA clone was not present in the recently published sequence of human C3 cDNA. This difference in nucleotide sequence provides direct evidence for C3 polymorphism at the DNA level. The combination of immunologic procedures with recombinant DNA methodology should facilitate additional analysis of the structure-function relationship of the C3 molecule.
The stimulations of arachidonic acid metabolism by recombinant murine interleukin 1 and tumor promoters or 1-oleoyl-2-acetyl-glycerol are synergistic.
Authors: Levine L , Xiao D M 
Published: December 2022

Abstract
Recombinant murine IL 1 stimulated arachidonic acid metabolism by rat liver cells (the C-9 cell line) and squirrel monkey smooth muscle cells, and in the presence of tumor promoters this stimulation was synergistic. In the rat liver cells that had been prelabeled with [3H]arachidonic acid, the release of 6-keto-PGF1 alpha and arachidonic acid also was stimulated by the IL 1, and this release was synergistic in the presence of TPA. 1-Oleoyl-2-acetyl-glycerol (OAG) stimulated prostaglandin production, and IL 1 synergized the prostaglandin production in the presence of OAG. OAG and TPA mimic the endogenous activator of protein kinase C, 1,2-diacylglycerol, and therefore IL 1 may amplify arachidonic acid metabolism during signal transmission processes.
Phorbol myristate acetate receptors in human polymorphonuclear neutrophils.
Authors: Nishihira J , O'Flaherty J T 
Published: December 2022

Abstract
Resting or phorbol myristate acetate (PMA)-pretreated neutrophils were disrupted by nitrogen cavitation and were fractionated on Percoll density gradients to identify the subcellular location of PMA receptors. Receptors were found in the cytoplasm of resting cells; neither primary nor secondary granules bound [3H]PMA, and the few binding sites located in non-granule membrane fractions appeared to reflect cytosolic contamination. Contrastingly, PMA-pretreated cells lost cytosolic receptors; greater than 80% of PMA-binding sites were associated with non-granule membranes. Protein kinase C activity similarly shifted from cytosol to membranes after PMA treatment. Indeed, protein kinase C and PMA receptors co-sedimented on Percoll gradients, co-eluted from Ultragel AcA 44 columns loaded with neutrophil cytoplasm, and were identically influenced by various phospholipids. Finally, PMA, mezerein, diacylglycerol, and dialkylglycerol activated protein kinase C with potencies that paralleled their respective abilities to stimulate neutrophil aggregation responses and inhibit [3H]PMA binding to whole cells or cytosol. These results fit a model of stimulus-response coupling wherein exogenous PMA or endogenous diacylglycerol solvate in cellular membranes. Cytosolic protein kinase C binds to the intramembranous ligand, forming an active, membrane-associated complex that phosphorylates nearby elements involved in triggering aggregation and other responses.
Selective regulation of chemotactic lymphokine production. I. Selective potentiation of eosinophil chemotactic lymphokine production in alum hydroxy gel- and Bordetella pertussis vaccine-treated guinea pigs.
Authors: Sakata K , Tashiro K , Hirashima M , Hayashi H 
Published: December 2022

Abstract
Delayed tissue eosinophilia in DNP-ovalbumin-induced allergic inflammatory skin lesions of guinea pigs was markedly enhanced by previous treatment with alum hydroxy gel (Alum) or Bordetella pertussis vaccine. This enhancement seemed due to increased production of a lymphocyte-derived eosinophil chemotactic factor (ECF) at the skin site. Treatment of animals with Alum potentiated antigen-induced in vitro ECF production by lymphoid cells from spleen and mesenteric lymph node of sensitized animals. The co-culture supernatants of lymphoid cells from Alum-treated animals also potentiated concanavalin A (Con A)-induced in vitro ECF production. The potentiating effect of Alum on ECF production seemed to be ascribed to the release of soluble factors from macrophages of the Alum-treated animals. The macrophage-derived soluble factor ECF-potentiating factor (ECF-PF) selectively potentiated ECF production but not macrophage chemotactic lymphokine production by Con A-stimulated lymphoid cells from normal animals. ECF-PF activity was associated with two separate m.w. fractions: one was 50,000 to 70,000 and the other was 10,000 to 20,000. The present study provides one of the explanations for enhanced ECF production by adjuvants, such as Alum and Bordetella pertussis vaccine.
Production of IL 2 and IFN-gamma by T cells from malaria patients in response to Plasmodium falciparum or erythrocyte antigens in vitro.
Authors: Troye-Blomberg M , Andersson G , Stoczkowska M , Shabo R , Romero P , Patarroyo M E , Wigzell H , Perlmann P 
Published: December 2022

Abstract
T cells from patients acutely infected with malaria exhibit a disease-related stimulation of DNA synthesis in response to Plasmodium falciparum antigen in vitro. This response is weak and short-lived, suggestive of induction of suppressor mechanisms. Exogenous T cell growth factor (IL 2) that was added to antigen-stimulated T cell cultures enhanced proliferation in antigen-responsive cultures, indicating that the lymphocytes expressed IL 2 receptors. In contrast, the addition of IL 2 to cultures that did not respond to antigen had no effect. Antigen-responsive cultures contained endogenous IL 2 as well, and the antigen-induced lymphocyte proliferation was correlated with IL 2 production. However, the results suggested that IL 2 production by the patients' T cells was insufficient or actively shut off, and that this was responsible for the premature cessation of their DNA synthesis. Supernatants from 60% of the T cell cultures treated with malaria antigen and from 30% treated with RBC ghost antigen contained interferon-gamma (IFN-gamma), as determined by a cytopathic effect inhibition assay combined with acid treatment and antibody neutralization or by an IFN-gamma-specific ELISA. There was no obvious correlation between antigen-induced lymphocyte proliferation and the presence of IFN-gamma in the culture supernatants. A high IFN-gamma activity was also seen in antigen-treated cultures from P. falciparum-immune donors living in highly endemic malaria areas. In contrast, no IFN-gamma was found in supernatants of antigen-treated T cells from healthy donors or patients with Plasmodium vivax malaria. Thus, the IFN-gamma activity of these cultures appears to reflect the presence of antigen-reactive T cells and may be useful as a sensitive indicator of cellular immunity in P. falciparum malaria.
Macrophage activation to kill Leishmania major: activation of macrophages for intracellular destruction of amastigotes can be induced by both recombinant interferon-gamma and non-interferon lymphokines.
Authors: Nacy C A , Fortier A H , Meltzer M S , Buchmeier N A , Schreiber R D 
Published: December 2022

Abstract
Macrophages treated with lymphokine (LK)-rich culture fluids from antigen- or mitogen-stimulated spleen cells or the hybridoma T cell 24/G1, or murine recombinant interferon-gamma (IFN-gamma) from either transfected monkey kidney cells (cos rIFN-gamma) or bacterial (E. coli) DNA (rIFN-gamma) developed the capacity to kill intracellular amastigotes of Leishmania major. Removal of IFN activity from LK by neutralizing fluid phase monoclonal anti-rIFN-gamma antibody, or by solid phase immunoadsorption, left residual macrophage activation factors that induced approximately 50% of the macrophage anti-leishmanial activity of untreated LK. In contrast, rIFN-gamma subjected to the same antibody treatments lost all capacity to induce this macrophage effector function. These results suggest that the intracellular destruction of amastigotes is regulated by several different factors. One of these factors is clearly IFN-gamma, which is pleiotropic in its effects on macrophage functions. The other non-IFN LK factors are immunochemically unrelated to IFN-gamma, and may regulate macrophage microbicidal activities in a more selective manner.
H-2-restricted cytolysis of L cells doubly transformed with a cloned H-2Kb gene and cloned retroviral DNA.
Authors: Abastado J P , Plata F , Morello D , Daniel-Vedele F , Kourilsky P 
Published: December 2022

Abstract
We report the construction of target cells by the double transformation of mouse L cells with a cloned H-2Kb gene and molecular clones of Akv or Gross murine leukemia virus (MuLV) or the cloned gag gene of Akv MuLV. Cytolytic T lymphocytes (CTL) generated in BALB.B mice specific for Gross MuLV (closely related to Akv MuLV) kill these doubly transformed cells. This is a direct indication that a CTL subpopulation recognizes H-2Kb antigen in association with a viral antigen encoded by the gag gene of Gross MuLV.
Influenza viruses as lymphocyte mitogens. II. Role of I-E molecules in B cell mitogenesis by influenza A viruses of the H2 and H6 subtypes.
Authors: Scalzo A A , Anders E M 
Published: December 2022

Abstract
Influenza A viruses of the H2 and H6 subtypes behave as T cell-independent B cell mitogens for lymphocytes from strains of mice that express the class II MHC glycoprotein I-E (Ia.7+ haplotypes). We have examined the role of I-E molecules in mitogenesis by these viruses. Lymphocytes from (Ia.7+ X Ia.7-)F1 hybrid strains that express lower levels of I-E antigen than homozygous Ia.7+ strains showed a level of response to H2 and H6 influenza viruses that was intermediate between the high response of the Ia.7+ parent and the low response of the Ia.7- parent. The mitogenic response of H-2k lymphocytes to these viruses was completely inhibited by low concentrations of anti-I-Ek monoclonal antibody that had no effect on B cell proliferation induced by LPS or by influenza A virus of the H3 subtype. Furthermore, incubation of H-2k spleen cells with high concentrations of H2 (but not H3) influenza viruses substantially inhibited the binding of radio-labeled anti-I-Ek, but not anti-I-Ak, monoclonal antibody. Cell mixing experiments indicated that expression of I-E by the B cells was critical to the mitogenic response, whereas I-E expression by accessory cells may not be necessary. The data support a model in which B cell mitogenesis by these viruses results from direct binding of the viruses to I-E molecules on B lymphocytes.
An innate host response to the neoplastic cell: syngeneic rat tumor cells can elicit a rapid de novo lymphoid procoagulant response.
Authors: Lando P A , Edgington T S 
Published: December 2022

Abstract
To analyze unique molecular differences between normal and neoplastic cells, we have examined host responses to tumor cells. The present study provides the first evidence for an innate rapid recognitive response of the lymphoid system to some syngeneic tumors. The lymphoid procoagulant (PCA) response, a T cell-instructed monocyte response that activates proteases of the coagulation cascade culminating in thrombin formation, is considered a component of classic delayed-type hypersensitivity responses. We have demonstrated that three syngeneic rat mammary carcinomas elicit this cellular response in vitro in lymphoid cells of the unimmunized rat. The response was rapid, reaching maximum within 6 hr. Analysis was compounded by the constitutive PCA activity of some tumors; however, the PCA product produced in the response to tumor challenge in vitro was newly biosynthesized and was of lymphoid cell origin, differing from the PCA of tumor cells. The lymphoid PCA response was prothrombinase-like and did not require vitamin K for biosynthesis, nor were other gamma-carboxylation-dependent extrinsic pathway proteases other than prothrombin required for thrombin generation. Both in vivo and in vitro derived mammary carcinoma cells elicited the response, whereas a fibrosarcoma and nontransformed syngeneic cells did not. Tumor shed substances, which were devoid of PCA and sedimentable only in part at 100,000 X G, induced this cellular response. The same stimuli shed from tumor cells did not directly elicit a PCA response from elicited peritoneal macrophages; however, in the presence of T lymphocytes a PCA response of these macrophages was produced. This study provides novel information to indicate that a T-enriched lymphocyte-dependent monocyte-macrophage response to some tumors, before effective in vivo immunization, may participate in initial local protease generation and fibrin deposition, both thought to play a significant role in the local pathobiology of tumors.
Migration of natural suppressor cells from bone marrow to peritoneal cavity by live BCG.
Authors: Kato K , Yamamoto K , Kimura T 
Published: December 2022

Abstract
Delayed-type hypersensitivity (DTH) responses were suppressed in mice inoculated with bone marrow cells from mice that had been injected with 10(8) colony-forming units (CFU) of live BCG. Upon analysis of this DTH-suppression by the use of a macrophage migration inhibition (MI) assay, the in vitro correlate of DTH, suppressor macrophages in the peritoneal cavity were found to play an important role in DTH suppression. However, neither suppression of DTH nor production of suppressor macrophages was observed in mice inoculated with bone marrow cells from mice that had been injected with methotrexate (MTX), a folic acid antagonist, and 10(8) CFU of live BCG. Moreover, suppressor cells against the MI activity of peritoneal exudate cells from BCG cell wall-immunized mice existed in bone marrow cells from normal mice, natural suppressor (NS) cells, and they were sensitive to MTX. In addition, these NS cells phagocytized carbonyl iron particles, were adherent to Sephadex G-10, and had Fc receptors, but they had no B or T cell markers, suggesting that these cells belonged to a macrophage compartment. From this evidence, we hypothesized that the origin of suppressor macrophages in the peritoneal cavity induced by live BCG injection was MTX-sensitive NS cells in bone marrow, and that these NS cells were stimulated by a small dose of live BCG trapped in bone marrow after i.v. injection of a high dose of live BCG and migrated from bone marrow to the peritoneal cavity.
Immune complex effects on murine macrophages. II. Immune complex effects on activated macrophages cytotoxicity, membrane IL 1, and antigen presentation.
Authors: Virgin H W , Kurt-Jones E A , Wittenberg G F , Unanue E R 
Published: December 2022

Abstract
We investigated the effects of immune complexes on macrophage functions in vitro. Immune complexes inhibit lymphokine induction of both I-Ak expression and cytotoxic activity by fetal calf serum elicited macrophages during long-term (7 days) culture. In addition, induction of antigen presentation was significantly inhibited by immune complexes. Expression of membrane interleukin 1 (IL-1) (a membrane-bound bound form of the T cell mitogen required for antigen presentation by fixed cells) was minimally inhibited by immune complexes. Therefore, inhibition of antigen presentation was primarily due to effects on Ia expression rather than membrane IL 1 expression. The inhibitory effect of immune complexes was not found during short-term culture (4 to 48 hr) when activated macrophages (bearing high levels of Ia) from mice infected with Listeria monocytogenes were examined. Immune complexes maintained or even increased levels of both I-Ak and cytotoxicity in activated macrophages. The implications of these findings for immune complex modulation of the immune response are discussed.
A novel method to bursectomize avian embryos and obtain quail----chick bursal chimeras. I. Immunocytochemical analysis of such chimeras by using species-specific monoclonal antibodies.
Authors: Belo M , Martin C , Corbel C , Le Douarin N M 
Published: December 2022

Abstract
Chick embryos were bursectomized at 5 days of incubation according to a novel surgical technique described in this article. This method yields birds that are able to hatch and are devoid of the physiologic deficiencies resulting from the previously used method, which involved resection of the cloacal and posterior embryonic region. The bursectomized embryos were grafted in situ with a quail bursa of the same age, which thereafter became chimeric through chick host hemopoietic cell invasion. By means of species-specific antibodies, the chimeric condition revealed 1) that the bursal epithelium expresses a unique antigenic determinant (MB1 determinant), until now considered to be an exclusive feature of blood vessel endothelium and hemopoietic cells, and 2) that this determinant appears in bursal epithelium at the time and site of hemopoietic cell invasion. The other point arising from this work concerns the apparent constitutive Ia expression by perifollicular blood capillary endothelial cells in normal and chimeric bursas.
A potential role for adrenocorticotropin in regulating human B lymphocyte functions.
Authors: Alvarez-Mon M , Kehrl J H , Fauci A S 
Published: December 2022

Abstract
Adrenocorticotropin (ACTH) was found to enhance the growth and differentiation of human B lymphocytes. By using highly purified preparations of human tonsillar B cells, the effects of ACTH on the growth and differentiation of in vitro activated B cells were examined. Optimal concentrations of ACTH were found to increase the proliferation of activated B cells by twofold to threefold when ACTH was present in culture with either a B cell growth factor or recombinant interleukin 2 (IL 2). ACTH had essentially no effects when added to cultures of activated B cells in the absence of the growth factor. Additionally, when ACTH was added in conjunction with an optimal concentration of either a B cell differentiation factor or IL 2 to cultures of activated B cells, the combination of ACTH and factor enhanced Ig secretion by twofold compared with the factor alone. In the absence of the differentiative signal, ACTH had minimal effects on Ig production. Only the first 24 amino acid fragments of ACTH were required to enhance B cell growth and differentiation when combined with the appropriate, more classical signals. Thus, ACTH may have a physiologic role in regulating human B cell function.
Autoimmunization in murine graft-vs-host disease. I. Selective production of antibodies to histones and DNA.
Authors: Portanova J P , Claman H N , Kotzin B L 
Published: December 2022

Abstract
A lupus-like disease characterized by a severe immune complex glomerulonephritis and IgG autoantibody production was induced in (C57BL/6 X DBA/2)F1 mice by injection of parental DBA/2 lymphoid cells. The ensuing graft-vs-host (GVH) reaction resulted in a 10- and a 100-fold increase in serum IgG antibody levels to denatured DNA and total histones, respectively, compared with that in F1----F1 control mice. The level of anti-DNA antibodies peaked 2 wk after injection of DBA/2 cells and preceded peak anti-histone levels by approximately 2 wk. Anti-histone antibodies were generated predominantly to histones H1, H2A, and H2B, a profile different from that observed in NZB/NZW and MRL-lpr/lpr mice. The marked increase in IgG antinuclear antibodies did not correlate with increases in total IgG serum levels and was not associated with comparable increases in antibodies to transferrin, hemoglobin, fibrinogen, or thyroglobulin. Selective autoantibody production was also observed in vitro, wherein GVH spleen cells produced high levels of IgG antibodies to total histones and denatured DNA but not to these non-nuclear protein antigens. In contrast, spleen cells stimulated in vitro with lipopolysaccharide produced equivalent amounts of antibodies to all antigens tested. Our results are in agreement with those of other investigators and collectively suggest that IgG autoantibodies in GVH disease, and possibly in spontaneous lupus-like disease, are not secondary to a generalized B cell activation, but may be selectively generated in response to self antigens with unique configurational properties.