bluuebunny/crossref_metadata_2025_split huggingface dataset:
Immunological Studies in Human Parasitic Infestation
Authors: Brunner Matthew 
Published: December 2022

Summary
Intradermal tests with saline extracts of Ascaris and Dibothriocephalus were made upon 277 individuals of from one to sixty-five years of age, and with extracts of Taenia solium upon 20 persons. Reactions similar to those elicited in conditions of atopic hypersensitiveness (hay fever and asthma) were obtained. Of 110 moderate and slight reactions 6 (or about 6 per cent) showed infestation in the excreta, as corroborated by findings. Of 53 individuals presenting marked reactions, 21 (or 40 per cent) revealed positive findings in the stools. Of 309 cases giving negative reactions 1 was found to harbor Dibothriocephalus. The absence of a positive reaction is not an absolute criterion of the absence of infestation with Dibothriocephalus, for one person infested with Dibothriocephalus remained negative to repeated tests. Among those reacting to the Ascaris antigen were some individuals that were infested not with Ascaris lumbricoides, but with other members of the nematode family,—namely Uncinaria (hookworm), Trichiuris trichiuria, Oxyuris vermicularis, and Trichinella spiralis. This indicates a group reaction. Testing with the extract of Ascaris lumbricoides is sufficient therefore for the diagnosis of any nematode infestation. The specificity of Dibothriocephalus latus and Taenia solium reactions was demonstrated. In every case which gave a marked positive reaction, where the transfer of sensitivity passively to the normal human skin was undertaken, the transfer was successful even in individuals in whom active infestation could not be demonstrated, suggesting similarity to the same phenomenon observed in some atopic cases. Constitutional reactions elicited in 3 asthmatic individuals as the result of intradermal tests with the Ascaris extract, indicates that extreme caution is necessary for routine testing, especially in atopic persons, with this type of extract. A marked reaction was interpreted to indicate either the presence of parasites or recent infestation.
On the Anti-Hemolytic Action of Hemolytic Immune Sera
Authors: Yanagihashi Mototoshi 
Published: December 2022

Abstract
I. Introduction. Since Ehrlich (1) in 1898 discovered the inhibition of the hemolytic action of tetanus-toxin by normal horse serum, many investigations of anti-hemolytic action have been made.
Kraus and Clairmont (2) and Eisler (3) found that normal horse serum could inhibit the hemolytic action not only of tetanus toxin, but of staphylococci, streptococci, vibrios, and putrefactive bacilli.
Ranson (4) examining the hemolytic action of saponin against dog's blood corpuscles, discovered that the addition of dog's serum to saponin would inhibit its hemolytic action.
Human serum also has an anti-hemolytic action. But it was due to the discovery of Neisser and Doering (5), Neisser and Friedemann (6), and Senator (7) that the fact that such action of serum was possible only when it was inactivated by being heated to 56°C. became known.
Much (8) reported that the serum of subjects of psychosis has the power of inhibiting the hemolytic action of cobra toxin against human blood corpuscles.
Effect of Serological Systems on Paramecium
Authors: Rakieten Morris L. 
Published: December 2022

Abstract
Within the past two decades a number of investigators have studied the behavior of paramecia in artificially created environments, and many important biological phenomena have been disclosed. Most of these studies are not pertinent to the question here under consideration, but certain of them, notably those of Balbiani (1898), Ledoux-Lebard (1902), and Hamilton (1904), have a direct application, since they involve the reaction of paramecia to antibody-containing sera of various types. Balbiani and Ledoux-Lebard studied the toxic effects of various sera on paramecia, and Hamilton, working specifically with the sera of scarlet fever and pneumonia patients, demonstrated that such sera are definitely more toxic than are normal sera. Certainly the most extensive studies on the behavior of paramecia are those of Jennings (1904) and Woodruff, the first of these authors being concerned with the relation of movement, and the responses of the action system under a variety of stimuli.
Alternatively spliced pp52 mRNA in nonlymphoid stromal cells.
Authors: Gimble J M , Dorheim M A , Youkhana K , Hudson J , Nead M , Gilly M , Wood W J , Hermanson G G , Kuehl M , Wall R 
Published: December 2022

Abstract
The 52-kDa phosphoprotein, also reported as lymphocyte-specific gene 1 and WP34, is transcribed as a 1.6-kb mRNA in B lymphocytes, B cell lines, and untransformed T cells. This gene encodes a cytoplasmic and plasma membrane-associated protein that is phosphorylated at a casein kinase II site and reportedly binds calcium. Based on these properties, it has been hypothesized that lymphoid form of the 52-kDa phosphoprotein protein may play a role in lymphocyte signal transduction. We show that alternatively spliced mRNA are expressed from this gene in nonlymphoid cell lines (myocytes, stromal cells, fibroblasts). These cell lines do not express the 1.6-kb lymphoid cell-specific transcript. Instead, mRNA of 2.0 and 2.8 kb are detected in varying abundance. A full-length 2.0-kb cDNA has been cloned and sequenced from the BMS2 stromal cell line by conventional screening and polymerase chain reaction-based methods. This cDNA clone, designated S37, has a single open reading frame encoding a 328 amino acid peptide. The nucleotide sequence of the S37 stromal cell cDNA is identical to that of the lymphocyte derived pp52 cDNA from the 3' poly(A) tail to the codon encoding the amino acid at residue 24. This region of the S37 cDNA clone encodes a protein that is identical to that encoded by the lymphoid pp52 cDNA and includes a casein kinase II phosphorylation site. However, the two clones differ in their 5' nucleotide sequence and their NH3 terminal amino acid sequence. This organization is consistent with alternative exon utilization. These results suggest that tissue-specific control mechanisms are used to generate different forms of lymphoid form of the 52-kDa phosphoprotein mRNA in lymphoid cells versus mesoderm-derived, nonlymphoid cell lineages.
Identification of 5'-flanking regions affecting the expression of the human decay accelerating factor gene and their role in tissue-specific expression.
Authors: Thomas D J , Lublin D M 
Published: December 2022

Abstract
Decay accelerating factor (DAF) is a complement regulatory protein that protects host tissue from complement-mediated damage by preventing the assembly and/or promoting the dissociation of C3 and C5 convertases. To identify and analyze the DNA sequence elements responsible for controlling DAF expression, the 5'-flanking region of the human DAF gene was cloned. Sequencing of 880 nucleotides upstream from the ATG codon revealed the absence of classic TATA or CAAT boxes. RNase protection and primer extension assays revealed a series of transcription start sites in a 10 nucleotide region located 86 nucleotides upstream from the ATG (the first of these start sites is numbered +1). Using HeLa, K562, EBV, and Molt 4 cells, DAF mRNA and protein were analyzed by Northern and Western blot. The DAF mRNA and protein levels roughly correlated, suggesting transcriptional control of gene expression. K562 and HeLa expressed high levels, EBV expressed intermediate levels, and Molt 4 expressed essentially no detectible DAF mRNA or protein. Regions of DAF 5'-flanking DNA were subcloned into plasmids containing the chloramphenicol acetyltransferase reporter gene and tested in transient transfection assays. The construct extending from -206 to +84 (-206/+84) had transcriptional activity in the DAF-positive HeLa, K562, and EBV lines, but no activity in the DAF-negative Molt 4 line. In the three DAF-positive lines, major enhancer activity was demonstrated between -206 and -77, and between -77 and -54 (containing cAMP responsive element and AP-1 binding site). Additional deletion of the region between -54 and -34 (containing an Sp1 binding site) reduces chloramphenicol acetyltransferase activity further but the low numerical values preclude statistical significance. The identification of transcription start sites and enhancer regions in the DAF gene will be important for studies of the mechanisms whereby cytokines and other factors may modulate DAF expression.
Intratumor gene expression after adoptive immunotherapy in a murine tumor model. Regulation of messenger RNA levels associated with the differential expansion of tumor-infiltrating lymphocytes.
Authors: Evans R , Kamdar S J , Duffy T , Edison L 
Published: December 2022

Abstract
The aim of this paper was to show that the adoptive immunotherapy (AIT) of established tumors resulted in the activation of defined lymphocyte-associated genes at the site of rejection. C57BL/6J mice bearing the moderately immunogenic syngeneic MCA/76-9 sarcoma received combination therapy 10 days after tumor cell implantation. This consisted of a single i.p. injection of cyclophosphamide (CY) followed by the i.v. injection of tumor-sensitized T cells (CY/AIT). The previously observed in situ differential expansion of tumor-infiltrating lymphocytes (TIL) was associated with a parallel modulation of CD4 (L3T4) and CD8 Ag expression. Flow cytometric analysis indicated that the CD8+ TIL appeared to contain two subpopulations during the reported proliferative phase, but by day 8 after CY/AIT the cells were composed of a single bright population. The CD4+ TIL similarly appeared to show two subpopulations, but in contrast to the CD8+ TIL there was a shift to a predominantly less bright single population by day 8. The expression of lymphocyte genes (Ly-2 and Ly-4 encoding the CD8 and CD4 Ag, respectively, IL-2, IL-2R, IFN-gamma, and IL-6) was analyzed by Northern hybridization using RNA extracted from whole tumor tissue. Progressing tumors expressed only low and relatively constant levels of mRNA for all of the genes except Ly-2 over a 19-day period. In contrast, there were considerable temporal fluctuations in mRNA levels depending on whether the mice had received CY or CY/AIT, but it was apparent that CY/AIT induced the more dramatic changes as far as Ly-2, Ly-4, IL-2, and IFN-gamma mRNA levels were concerned. A preliminary survey of cytokine bioactivity released by tumor-associated cells isolated 9 days after CY/AIT indicated that both IFN-gamma and IL-6 activities were released by the cells, but not IL-2, despite the relatively high levels of IL-2 mRNA. These data provide evidence that the differential expansion of TIL after CY/AIT is accompanied by well defined changes in the levels of mRNA-encoding TIL membrane Ag and lymphokine genes and are concordant with the view that amplified anti-tumor immune responses occur after AIT.
Type 1 plasminogen activator inhibitor is not an acute phase reactant in rats. Lack of IL-6- and hepatocyte-dependent synthesis.
Authors: Podor T J , Hirsh J , Gelehrter T D , Zeheb R , Torry D , Guigoz Y , Sierra F , Gauldie J 
Published: December 2022

Abstract
The contributing role of hepatocytes and IL-6 in the acute phase-like elevation of plasma type 1 plasminogen activator inhibitor (PAI-1) in vivo is not known. We addressed this question by comparing the effects of two inflammatory stimuli known to increase plasma concentrations of IL-6 on the plasma concentrations and site of synthesis of PAI-1 and cysteine proteinase inhibitor (CPI) in rats. Subcutaneous injection of turpentine results in a sustained increase in plasma IL-6 and CPI Ag levels over a 24-h period. In contrast, plasma PAI-1 activity was not altered by turpentine treatment. Northern blot analysis of poly(A)+ mRNA extracted from freshly isolated hepatocytes of saline- or turpentine-treated animals demonstrated induction of CPI mRNA expression but failed to detect basal or induced PAI-1 or IL-6 mRNA expression. However, PAI-1 mRNA was detected in rat hepatocytes in primary culture for 24 h and was induced by dexamethasone. Intravenous infusion of bacterial LPS (4 mg/kg) induced a sustained increase in plasma CPI Ag and transient increases in plasma IL-6 and PAI-1. Northern blot analysis of freshly isolated, fractionated liver cells indicated that LPS treatment (3 h) induced PAI-1 mRNA expression most significantly in the endothelial and Kupffer cell fractions. IL-6 mRNA expression was induced in Kupffer cells and CPI mRNA was induced in hepatocytes. Immunocytochemical analysis revealed LPS-induced accumulation of PAI-1 Ag associated with the vascular endothelium, subendothelial matrix, and sinusoidal lining cells. Our results indicate that PAI-1 mRNA is not significantly expressed by rat hepatocytes in vivo and that plasma PAI-1 levels are not influenced by increased IL-6 expression in Kupffer cells or in plasma.
Selective transformation of host lymphocytes in vivo by retrovirus-producing macrophages.
Authors: Bosco M C , Musso T , Gusella G L , Giovarelli M , Forni M , Soleti A , Masuelli L , Modesti A , Forni G , Varesio L 
Published: December 2022

Abstract
Macrophage-mediated retroviral transformation of host cells was studied in vivo utilizing the cloned murine macrophage-line GG2EE, generated by in vitro infection of bone marrow cells from C3H/HeJ mice (H-2k) with the acute transforming retrovirus J2 bearing the v-myc and v-raf oncogenes. Because GG2EE macrophages produce the J2 retrovirus, the development of secondary, J2 virus-induced tumors after the injection of the cell line into several strains of mice was evaluated. GG2EE cells proliferated and gave rise to histiocytic tumors in syngeneic mice and in allogeneic athymic Swiss mice. The inoculum of GG2EE cells in allogeneic DBA/2 mice (H-2d) and, to a lesser extent, in BALB/c (H-2d) and BALB/k (H-2k) mice gave rise to a small, solid mass at the injection site. Although the initial tumor was slowly rejected, secondary lymphomas belonging to the B or T cell lineage developed, leading to mouse death. Extensive phenotypic, functional, and chromosomal analyses proved that lymphomas were derived from host T and B cell transformation. Southern and Northern blot studies showed that J2 virus was integrated and expressed in lymphoma cells, demonstrating that the virus was transmitted to the host lymphocytes and suggesting that it was causal in lymphoma development. The existence of close and protracted interactions between GG2EE macrophages and allogeneic host lymphocytes and the presence of viral particles in the area of macrophage-lymphocyte contact were demonstrated by histologic and ultrastructural analysis. Rejection of J2 virus-infected lymphocytes in allogeneic mice suggested that host lymphocyte transformation was dependent upon the macrophage cell type. These results demonstrate that macrophage-derived J2 retrovirus transforms host lymphocytes in vivo in allogeneic mice and that a condition of host alloreactivity is critical for such event.
Differential expression of IL-4 receptors in human T and B lymphocytes.
Authors: Mozo L , Rivas D , Zamorano J , Gutierrez C 
Published: December 2022

Abstract
IL-4R have been described in unstimulated human T and B lymphocytes. However, a precise comparative study on the expression and regulation of IL-4R in isolated human T and B cell populations has not yet been fully assessed. We examined the mRNA levels and the cell membrane expression of IL-4R in freshly isolated T and B lymphocytes as well as in in vivo- and in vitro-stimulated cells. IL-4R protein expression and transcript levels were higher in tonsillar unstimulated B cells than in T cells. Splenic and peripheral blood B lymphocytes also expressed higher surface IL-4R in their membranes than T cells did. Large B lymphocytes from tonsils (in vivo-activated cells) obtained by Percoll gradient centrifugation displayed higher IL-4R levels than resting cells. On activation in vitro of T lymphocytes with IL-2 or PHA, slight increments on the IL-4R mRNA and protein levels were achieved. However, maximal levels of IL-4R expression were obtained on T cell incubation with IL-4 at a concentration of 100 U/ml. Similarly, the same concentration of this lymphokine up-regulated the surface IL-4R molecules and the IL-4R mRNA levels in purified B lymphocytes. Cross-linkage of surface Ig by insolubilized anti-IgM potentiated the effect of IL-4 in up-regulating IL-4R expression in B cells, probably by inducing outgrowth of IL-4R positive subpopulations. The B cell mitogen, Staphylococcus Aureus Cowan I, although inducing cell proliferation, was ineffective in promoting new receptor synthesis. Cell proliferation was not required for IL-4-dependent IL-4R up-regulation on both T and B lymphocytes.
Selective up-regulation of the 75-kDa tumor necrosis factor (TNF) receptor and its mRNA by TNF and IL-1.
Authors: Winzen R , Wallach D , Kemper O , Resch K , Holtmann H 
Published: December 2022

Abstract
In cells of the fibroblastoid line SV-80, rapid down-modulation of TNF binding in response to TNF itself, or to IL-1, was followed by a gradual recovery of binding, which occurred even in the continuous presence of the cytokines. Untreated cells carried mainly the 55-kDa receptor species. In cells treated with TNF or IL-1, the 55-kDa TNF-R, although increasing after initial down-modulation, remained lower than before treatment. Expression of the 75-kDa TNF-R species upon treatment with either cytokine was markedly increased. Both TNF and IL-1 also induced a strong increase of the mRNA for the 75-kDa receptors, whereas the amount of mRNA for the 55-kDa receptors decreased. The effects of TNF on cell surface expression of the TNF-R could not be blocked with antibodies to IL-1, nor could the effects of IL-1 be blocked with antibodies to TNF, indicating that each cytokine affects the cell surface expression of the receptors independently of the other. Applying both cytokines together resulted in much stronger increase in expression of the 75-kDa TNF-R than applying each alone. Similar changes in cell surface expression and mRNA levels of the two TNF-R as observed in SV-80 cells were also found in TNF and IL-1-treated human foreskin fibroblasts. It is suggested that these sustained changes in the pattern of receptor expression contribute to the adjustment of the cellular response to TNF when formation of TNF and IL-1 takes place over a prolonged period.
Rat class III Fc gamma receptor isoforms differ in IgG subclass-binding specificity and fail to associate productively with rat CD3 zeta.
Authors: Farber D L , Giorda R , Nettleton M Y , Trucco M , Kochan J P , Sears D W 
Published: December 2022

Abstract
Several new rat class III Fc gamma R isoforms are described here, extending the genetic complexity of this receptor family and further distinguishing rat CD16 from mouse CD16, represented by only one receptor isoform, and human CD16, represented by only two isoforms. RNase protection assays reveal that three rat tumor cell lines--RBL-1 basophilic leukemia cells, RM-SV1 macrophages, and CRNK-16 NK cells--all coordinately express multiple and probably identical rtFc gamma RIII-related transcripts in similar relative proportions but at significantly different levels. These results indicate that no single isoform predominates in these cell types but that the overall level of rtFc gamma RIII-related transcripts is differentially regulated. Two of the rtFc gamma RIII isoforms found to have extensive amino acid sequence differences in their second extracellular (EC2) domains are shown to bind rat and mouse IgG subclasses differently. This result suggests that the receptor isoform diversity in this species may function as a mechanism for extending the IgG-binding capacity of rat leukocytes. Cloned cDNA for the rat CD3 zeta protein was also isolated in this study and its ability to augment surface expression of class III Fc gamma R was tested by rosetting of cDNA-transfected COS cells. Like the structurally homologous mouse CD3 zeta, rat CD3 zeta fails to promote surface expression of Fc gamma RIII, sharply contrasting the efficient receptor expression produced by human CD3 zeta. Variations in the transmembrane amino acid sequences correlate with the divergent capacities of these CD3 zeta molecules to augment receptor expression. The high levels of CD3 zeta message expressed in rat NK cells may indicate that other unidentified hetero-subunits are required for assembly of rat CD3 zeta into functional CD16 receptors.
Functional importance of the cyclic AMP response element-like decamer motif in the CD8 alpha promoter.
Authors: Gao M H , Kavathas P B 
Published: December 2022

Abstract
Expression of the CD8 gene is highly regulated during lymphocyte differentiation and in a tissue-specific manner. We characterized the human CD8 alpha promoter region to determine whether tissue specificity resides within the promoter and to define important regulatory elements. A set of six fragments 5' of the CD8 alpha gene were linked to a luciferase reporter gene. The luciferase activity was then measured in a transient transfection assay. We found that CD8 alpha promoter activity can be detected from a 146-bp fragment upstream of the translation start site, but not from a 133-bp fragment. The cyclic AMP response element (CRE)-like site within the 10 bp from -143 to -133 is critical for promoter activity. Mutation of the CRE/decamer in the context of a 429-bp fragment causes loss of activity. Tissue specificity does not reside in the 146-bp fragment because this fragment directs expression in both T and non-T cell lines. Fragments longer than 146 bp are generally expressed less well in the cell lines suggesting the potential existence of negative regulatory elements upstream of -146. Using a CRE/decamer-containing oligomer as a probe in an electrophoresis mobility shift assay, three retarded bands formed by proteins binding to the DNA were detected using nuclear extracts from two T cell lines. Two of the three bands contain proteins of the CRE-binding protein (CREB)/activating transcription factor (ATF) family. Because the CRE-binding protein/activating transcription factor proteins play a role in the expression of many other T cell-specific genes, our work strengthens the hypothesis that the CRE motif is important for regulating the expression of T cell-specific genes.