bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of Ricinoleated Vaccine of the Hemolytic Streptococcus (Scarlet Fever) on Animals
Authors: Kozlowski Anthony 
Published: December 2022

Abstract
Of the many different substances which have been tried in detoxifying bacterial toxins for the purpose of immunization, sodium ricinoleate has recently been suggested as very suitable (1–6). Thus, it has also been reported that broth toxin from a culture of the hemolytic streptococcus (scarlet fever) when mixed with sodium ricinoleate and injected intramuscularly into man did not induce any severe reaction such as usually follows an administration of the same amount of untreated broth toxin; moreover, after the elapse of a certain time, the intracutaneous test became negative in a large percentage of cases.
To gain some insight into the efficacy of soap-vaccine and into the mechanism of soap action, the following experiments have been carried out on mice.
Method. Sodium ricinoleate was prepared from castor oil saponified by alcoholic potassium hydroxide and purified by cooling, by fractionation of its potassium, sodium, and barium salts by the method described in another paper which will be published later.
The Zonal Action of Antiserum in Pneumococcus Infections
Authors: Sobotka Harry , Friedlander Mae 
Published: December 2022

Summary
The prozone phenomenon in serum treatment of experimental pneumococcus septicemia is described. The fact that excessive amounts of protective antibody in many instances fail to prevent death, is discussed. It is suggested that the presence of an interfering factor is responsible for the prozone. The mechanism of the action of this factor is treated mathematically for characteristic cases and the resulting formulae are applied to actual observations. This factor may interfere with the reaction between antibody and bacteria either by reacting with the antibody or by reacting with the antigen. The action of the antibody may be impaired to a certain extent by precipitation with the injurious factor which, under this assumption, is identical with the soluble specific substance as suggested by Felton and Bailey and by other authors. For instance if there are 100 units of antibody and 10 equivalent units of the interfering substance, then the potency of the antiserum will be reduced to that extent; the relative amount of this reduction will be constant however, in this example a reduction of 10 per cent; but this does not explain the complete inactivation of large doses of antibody as occurs in the prozone phenomenon. The interfering substance may react with the bacteria. In that case it does not decrease the neutralizing power of the antibody proper. Although it might be present only in minute quantities it reacts with the bacteria making some of them less susceptible or entirely resistant to the action of the antibodies. Thus both the limitation of protection to a certain maximal number of bacteria and the prozone can be explained on the same basis. The properties ascribed to the interfering factor sub 3 (b) and its irregular occurrence in antisera and concentrated antibody solutions suggest that it is a modified antibody.
Studies on the Antigenic Properties of the Ultraviruses
Authors: Schultz Edwin W. 
Published: December 2022

Abstract
In a recent critical review of the literature on the antigenic properties of the ultraviruses, the writer (1928) called attention to the fact that these agents of disease, as far as they have been studied, seem to exhibit antigenic properties which suggest placing them in the general group of toxins and ferments rather than with such antigens as bacteria and other more highly organized proteinaceous bodies. Since the various facts which have suggested such a probability have been fully treated in the paper referred to, it will be unnecessary to discuss them at length here. The writer will, therefore, confine himself in this paper to a more general outline of the theoretical and other considerations which have prompted the studies that are to appear under the general title indicated.
According to Zinsser (1915) anl~igens may be classified into two general classes.
Pasteurella Avicida Vaccination by the Oral, Subcutaneous, and Intravenous Methods
Authors: Barnes LaVerne 
Published: December 2022

Abstract
Subcutaneous vaccination is more effective than oral vaccination in stimulating the production of typhoid agglutinins in rabbits (1). It is questionable which method is more effective in stimulating the production of immunity. Besredka believes that agglutinins and other specific antibodies in the blood stream are practically negligible as factors in immunity (2). He believes that immunity is cellular and in order to produce a “solid” immunity, the vaccine must be applied directly to the body ceils. This immunity appears, in certain cases, within twenty-four hours. If Besredka is correct, current conceptions of immunity and methods of immunization will have to be modified.
Calmette (3), and Enlows (4) have reviewed the evidence concerning oral vaccination. Sufficient data regarding the comparative efficiency of oral, subcutaneous, and intravenous methods of vaccination in stimulating the production of immunity are not available.
The experiments described in this paper were designed to compare: (a) The production of agglutinins for Past. avicida in the blood of chickens and rabbits following oral, subcutaneous,and intravenous administrations of vaccine; and, (b) the resistante of the vaccinated animals to intravenous inoculations of Past. avicida.
LP-BM5 murine retrovirus-induced immunodeficiency disease in allogeneic SCID chimeric mice. Inability to recognize a putative viral superantigen does not prevent induction of disease.
Authors: Gilmore G L , Cowing C , Mosier D E 
Published: December 2022

Abstract
T cell recognition of viral superantigens has been postulated to contribute to the pathogenesis of the immunodeficiency disease induced in mice by infection with the LP-BM5 murine leukemia virus complex. A candidate superantigen has been identified in the B cell lymphoma line B6-1710 derived from an LP-BM5-infected C57BL/6 (H-2b) mouse. We have asked whether the stimulatory activity expressed by B6-1710 behaves as a superantigen by assessing the ability of T cells from fully allogeneic H-2b--&gt;H-2d SCID chimeric mice to respond to the line. T cells from allochimeric mice failed to respond to B6-1710, whereas they responded normally to Staphylococcus enterotoxin B, a well characterized superantigen. Despite this finding, allochimeric mice were fully susceptible to the immune deficiency disease induced by LP-BM5 virus infection. These findings show that the role of superantigen expression in retrovirus-induced immune deficiency disease remains to be defined.
T cell receptor antagonism mediated by interaction between T cell receptor junctional residues and peptide antigen analogues.
Authors: Ostrov D , Krieger J , Sidney J , Sette A , Concannon P 
Published: December 2022

Abstract
A major objective of new rational immunosuppressive therapies is to be able to inhibit deleterious T cell responses in an Ag-specific manner. Recently, a novel approach to inducing Ag-specific nonresponsiveness in T cells, termed receptor or TCR antagonism, has been described. Several analogues of the influenza hemagglutinin (H3) peptide HA307-319 were shown to block recognition of the native HA307-319 peptide by a DR1-restricted T cell clone at concentrations 1,000- to 10,000-fold less than required to competitively inhibit HA307-319 binding to DR1. These Ag analogues that inhibited T cell recognition differed from the stimulatory antigenic peptide only at single positions. How such limited changes affect the ternary complex interactions of TCR, peptide, and DR remains unclear. In the present study, we have utilized two different DR5-restricted T cell clones that exhibit mutually exclusive specificities for HA peptides with or without substitutions at position 313 to investigate the molecular requirements for receptor antagonism. In this reciprocal model system, we show that a single peptide/DR complex can antagonize one T cell clone while stimulating another. A comparison of nucleotide sequences derived from the TCR of the T cell clones that were either antagonized or stimulated by the peptide analogue/DR5 complex indicated that the different responses of these T cells result from minor differences in the amino acid residues in junctional regions that most likely interact directly with position 313 of the peptide analogues. Our results suggest that TCR antagonism is an Ag-specific phenomenon in which T cells are inhibited by interactions involving TCR residues required for the recognition of conventional Ag and the altered residues in peptide analogues.
HB4 antibody recognizes a carbohydrate structure on lymphocyte surface proteins related to HB6, CDw75, and CD76 antigens.
Authors: De Lau W B , Kuipers J , Voshol H , Clevers H , Bast B J 
Published: December 2022

Abstract
Cells regulate the specificity of the carbohydrate chains on their membrane-bound glycoconjugates by differential expression of glycosyltransferases. In lymphocytes, beta-galactoside alpha 2,6-sialyltransferase is reportedly involved in the generation of epitopes recognized by HB6, CDw75, and CD76 mAb. The HB4 mAb binds to an Ag present on subpopulations of B and NK cells. We now show that this Ag represents another member of a set of neuraminidase-sensitive, alpha 2,6-sialyltransferase-generated sugar Ag. Transient expression of a cDNA encoding this enzyme in COS cells generated a minor population of HB4+ cells that was completely contained within the HB6+ COS cell population. Using various proteinases and an inhibitor of N-linked carbohydrate processing, we show both epitopes to represent components of N-glycosylated membrane proteins. Remarkably, porcine thyroglobulin, an alpha 2,6-NeuAc+ glycoprotein, is specifically recognized by both mAb. These data underline a close relationship between HB4 and HB6 epitopes and imply further that both mAb react with oligosaccharide chains irrespective of the carrier molecule nature. Thus, the terminal sugar residue sialic acid plays a pivotal role in at least four distinct epitopes that are expressed differentially in immune cells. This may point at an important role for these epitopes in biologic recognition.
Genomic structure and chromosomal mapping of the human CD22 gene.
Authors: Wilson G L , Najfeld V , Kozlow E , Menniger J , Ward D , Kehrl J H 
Published: December 2022

Abstract
The human CD22 gene is expressed specifically in B lymphocytes and likely has an important function in cell-cell interactions. A nearly full length human CD22 cDNA clone was used to isolate genomic clones that span the CD22 gene. The CD22 gene is spread over 22 kb of DNA and is composed of 15 exons. The first exon contains the major transcriptional start sites. The translation initiation codon is located in exon 3, which also encodes a portion of the signal peptide. Exons 4 to 10 encode the seven Ig domains of CD22, exon 11 encodes the transmembrane domain, exons 12 to 15 encode the intracytoplasmic domain of CD22, and exon 15 also contains the 3' untranslated region. A minor form of CD22 mRNA likely results from splicing of exon 5 to exon 8, skipping exons 6 and 7. A 4.6-kb XbaI fragment of the CD22 gene was used to map the chromosomal location of CD22 by fluorescence in situ hybridization. The hybridization locus was identified by combining fluorescent images of the probe with the chromosomal banding pattern generated by an Alu probe. The results demonstrate that CD22 is located within the band region q13.1 of chromosome 19. Two closely clustered major transcription start sites and several minor start sites were mapped by primer extension. Similarly to many other lymphoid-specific genes, the CD22 promoter lacks an obvious TATA box. Approximately 4 kb of DNA 5' of the transcription start sites were sequenced and found to contain multiple Alu elements. Potential binding sites for the transcriptional factors NF-kappa B, AP-1, and Oct-2 are located within 300 bp 5' of the major transcription start sites. A 400-bp fragment (bp -339 through +71) of the CD22 promoter region was subcloned into a pGEM-chloramphenicol acetyltransferase vector and after transfection into B and T cells was found to be active in both B and T cells. Further studies of the CD22 gene should lead to a greater understanding of the expression of CD22 during B cell development and differentiation.
Microvascular effects of complement blockade with soluble recombinant CR1 on ischemia/reperfusion injury of skeletal muscle.
Authors: Pemberton M , Anderson G , Vĕtvicka V , Justus D E , Ross G D 
Published: December 2022

Abstract
Reperfusion of ischemic tissue is associated with tissue injury greater than that resulting from ischemia alone. C activation has been hypothesized to mediate the so-called ischemia/reperfusion injury through both membrane attack and C5a-dependent recruitment of neutrophils to sites of C3 fixation on the endothelium via C3 receptors. Adherence of neutrophils is preconditional to expression of their deleterious effects, which are central to the pathophysiology of ischemia/reperfusion injury. This study was designed to evaluate the effect of inhibition of C activation on ischemia/reperfusion injury using a soluble and truncated recombinant human CR1 (sCR1) molecule, a "tail-less" form of the membrane C3b/C4b receptor (CD35) that functions as a regulator of C activation. Capillary perfusion and leukocyte adherence to venular endothelium were measured after reperfusion in a mouse cremaster muscle model that allowed microscopic video observation of microcirculatory changes. Infusion i.v. with sCR1 before a 4-h period of ischemia and during a 3-h subsequent period of reperfusion prevented the increase in leukocyte adherence to venular endothelium seen in controls, and enhanced the number of reperfusing capillaries by 55%. Trypan blue staining showed an increase in muscle cell viability from 11 to 50% in mice receiving sCR1 as compared to controls. Tests of blood samples from mice infused with sCR1 demonstrated nearly complete inhibition of the mouse alternative pathway of C activation, but no detectable loss of the mouse classical pathway of C activation. It was concluded that C activation in this model of skeletal muscle injury is likely to be due to the alternative pathway, and that inhibition of C activation during reperfusion inhibits leukocyte adherence to blood vessel walls and protects the capillary microcirculation.
Cloning and expression of immunologically active recombinant Amb a V allergen of short ragweed (Ambrosia artemisiifolia) pollen.
Authors: Ghosh B , Perry M P , Rafnar T , Marsh D G 
Published: December 2022

Abstract
We have cloned and sequenced Amb a V, an Ambrosia artemisiifolia (short ragweed) pollen allergen that has proved to be particularly useful in the genetic analysis of human immune responsiveness. The amino acid sequence deduced from the cloned cDNA sequence corresponds to the published sequence of the protein, except that the cDNA sequence encodes an extra 10 amino acids at the C-terminus. The expressed 55-residue protein is then presumably cleaved enzymatically at the C-terminal lysine found in the 45-residue protein isolated from the pollen. The cloning and sequencing of Amb a V genomic DNA confirmed the cDNA sequence and showed that the Amb a V gene has no introns. Recombinant Amb a V allergen, expressed in Escherichia coli, bound to IgG and IgE antibodies in all Amb a V-allergic individuals tested and inhibition studies demonstrated that the recombinant protein contains a subset of the antigenic epitopes found on native Amb a V. In addition, recombinant Amb a V released histamine efficiently from basophils from Amb a V-allergic patients. The recombinant Amb a V allergen and mutants of Amb a V should, therefore, be useful in studies of allergen epitopes in humans, as well as providing a diagnostic tool.
Anergized T cell clones retain their cytolytic ability.
Authors: Go C , Lancki D W , Fitch F W , Miller J 
Published: December 2022

Abstract
CD4+ T cells have been described to have both helper and lytic function. The helper function of Th1 cells in particular can be inactivated by inducing the T cell into a state of nonresponsiveness in which the T cell is no longer capable of producing IL-2 or proliferating in an autocrine way to a conventional antigenic stimulus. To determine whether the lytic ability of Th1 cells can also be rendered nonfunctional upon anergy induction, we induced Th1 clones into a nonresponsive state and tested their ability to lyse target cells in an Ag-specific and MHC class II-restricted manner. We show that cells newly induced into an anergic state were able to lyse target cells nonspecifically. This effect was short-lived and after resting in culture media, the cells regained their ability to lyse target cells in an Ag/MHC-specific manner, and this ability was comparable to normal resting T cells. In contrast, the helper function of these cells remained nonresponsive, and the cells were unable to proliferate or to secrete IL-2 in response to the same antigenic stimulus used for lysis. Therefore, the lytic pathway appears to be regulated separately from the proliferative/lymphokine pathway(s) and is not affected long-term by an anergic stimulus.
IL-2-independent activity of IL-7 in the generation of secondary antigen-specific cytotoxic T cell responses in vitro.
Authors: Kos F J , Müllbacher A 
Published: December 2022

Abstract
Purified CD8+ splenocytes from influenza virus strain A/WSN/33 (H1N1)-immune BALB/c (H-2d) mice responded to a synthetic peptide, synthetic influenza nucleoprotein peptide 147-158 R-, with a sequence (147-158 R156-) derived from influenza A virus nucleoprotein with high affinity for Kd class I MHC molecules, with the generation of effector cytotoxic T (Tc) cells specific for influenza A virus-infected target cells in vitro. The process of the conversion of synthetic influenza nucleoprotein peptide 147-158R- -Kd-responding memory Tc into effector Tc cells requires Ag in the form of peptide associated with Kd class I MHC molecules and the presence of endogenously produced IL-2 by CD8+ T cells. Under blockade of utilization of endogenous IL-2 by mAb to IL-2 or IL-2R, no effector Tc cells were generated, but the addition of IL-7 restored the process of the conversion of CD8+ memory into effector Tc cells and significantly enhanced the specific cytolytic activity of Tc cells above those of controls. IL-7-reactive cells were found in both IL-2Rhigh- and IL-2Rlow-expressing responder CD8+ T cells. We conclude that the requirement for endogenous IL-2 in Ag-induced conversion of CD8+ memory Tc cells into effector Tc cells can be replaced by exogenous IL-7. This demonstrates that IL-7 is a potent regulatory cytokine with similar activity to IL-2 and may act independently of IL-2 in the Ag-specific activation of memory CD8+ Tc cells.
Pertussis toxin-sensitive factor differentially regulates lipopolysaccharide-induced tumor necrosis factor-alpha and nitric oxide production in mouse peritoneal macrophages.
Authors: Zhang X , Morrison D C 
Published: December 2022

Abstract
It has been established that LPS, the major constituent of the outer membrane of gram negative bacteria, stimulates macrophages to produce numerous inflammatory mediators, including TNF-alpha and nitric oxide (NO). Both TNF-alpha and NO are important in the macrophage-mediated cytotoxicity against invading microorganisms and tumor cells. Although many LPS-dependent immune responses have been well characterized phenomenologically, the precise signal transduction pathways in LPS-induced macrophage activation are not clear. We reported that 1) pretreatment of C3HeB/FeJ mouse peritoneal macrophages with pertussis toxin (PT) markedly enhanced LPS-induced TNF-alpha production but inhibited LPS-dependent NO production under the same conditions; 2) kinetics of the PT effects on these LPS-responses were correlated with PT-mediated ADP-ribosylation of a 41-kDa protein(s); and 3) PT pretreatment did not correct the refractory states of C3H/HeJ macrophages to wild type smooth-LPS. These results suggest that LPS stimulates TNF-alpha and NO production in mouse peritoneal macrophages through different biochemical pathways, and that the signal transduction for both pathways is regulated by a PT-sensitive factor. It is possible that this factor is a guanine nucleotide-binding regulatory protein(s). Finally our data indicate that it is unlikely that the defect of the C3H/HeJ macrophages in response to LPS is at the level of this PT-sensitive factor.
T cell-induced suppression of IgG2ab expression in vivo leads to a large reduction of C gamma 2ab mRNA levels.
Authors: Bénaroch P , Georgatsou E , Bordenave G 
Published: December 2022

Abstract
In the T cell-induced suppression of IgG2ab expression, the level at which B cells are blocked in their development to IgG2ab-producing plasma cells was investigated. Although IgG2ab+ lymphocytes were barely detected in normal and IgG2ab-suppressed mice, intracellular IgG2ab was only detected in crude cell extracts from normal mice. B lymphocytes producing IgG2ab were revealed in T cell-depleted splenocytes from normal mice (86 +/- 15/10(6) cells), whereas corresponding cell preparations from IgG2ab-suppressed mice were completely free of such lymphocytes. However, in vitro stimulation of cell preparations from both normal and IgG2ab-suppressed mice with LPS plus rIFN-gamma resulted in IgG2ab production. Accounting for differences in spleen size between the two types of mice, these stimuli induced comparable cell proliferation and numbers of IgG2ab-producing lymphocytes. In addition, the level of IgG2ab production per cell was similar in the two types of stimulated cells. This demonstrates that normal and IgG2ab-suppressed mice have the same potential to generate IgG2ab-producing cells. By using a sensitive and specific RNase protection assay, C gamma 2ab transcripts were detected in total RNA preparations from IgG2ab-suppressed mice. The levels of C gamma 2ab gene expression in spleen were much lower (between 150 and 400 times less) in IgG2ab-suppressed mice than in normal mice. Taken together, our data suggest that B lymphocytes committed to IgG2ab production represent the target of CD8+ T cells, which we have previously shown to be required for suppression. The target B cells are very efficiently and rapidly silenced, as demonstrated by the absence of detectable serum IgG2ab and corresponding low levels of C gamma 2ab mRNA.
B lymphocyte development and activation independent of MHC class II expression.
Authors: Markowitz J S , Rogers P R , Grusby M J , Parker D C , Glimcher L H 
Published: December 2022

Abstract
A murine model of MHC class II deficiency created by targeted gene disruption was used to investigate whether class II expression influences B cell maturation and function. There appeared to be fewer total B cell precursors, a higher proportion of which were in a very early stage of maturation, in class II-deficient vs control bone marrow; however, the differences did not reach statistical significance. Mature B cells were unaffected; IgM, IgD, B220, and CD5 surface expression were similar in class II-deficient and control animals. Serum Ig determinations revealed that the class II-deficient animals had elevated IgM but decreased IgG1 (and, variably, IgE) compared to control. The antibody response against thymic-independent Ag was intact in class II-animals, as was the in vitro response of small resting B cells from class II deficient animals to stimulation with polyclonal B cell activators. Preactivated T cells were able to induce differentiation and proliferation of class II-deficient, small resting B cells. Together, these data indicate that B cell development, T cell-independent, and T cell-dependent B-cell activation, can occur independently of class II MHC expression.