bluuebunny/crossref_metadata_2025_split huggingface dataset:
Studies in Absorption of Undigested Proteins in Human Beings
Authors: Walzer Matthew 
Published: December 2022

Summary
A technic for the demonstration of the absorption of undigested protein in human beings is presented in detail. In contradistinction to all previous immunological methods employed in human beings for the same purpose, this test is a direct one, and is performed on the subject himself. It employs the principle of passive local sensitization as its basis. By the intradermal injection of serum, taken from certain fish or egg hypersensitive cases, it is possible to passively locally sensitize an individual to these proteins. Upon the ingestion of such proteins, under proper circumstances, a wheal develops at the sensitized area, which has been proved to indicate the absorption into the circulation of these proteins in an undigested form.
The individual steps in the technic and the factors affecting them have been discussed at length. The advantages and limitations of the procedure have been reviewed.
The fact that the reaction occurs in most individuals when physiological amounts of fish and egg protein are taken under physiological circumstances, indicates that the absorption of these undigested proteins is a normal phenomenon.
Transmission of Protein Hypersensitiveness from Mother to Offspring
Authors: Ratner Bret , Jackson Holmes C. , Gruehl Helen Lee 
Published: December 2022

Abstract
It was first demonstrated by Rosenau and Anderson (2, 3) in 1906, that a state of hypersensitiveness may be transmitted from a mother guinea pig to her offspring. Within the next few years, this discovery was corroborated by Gay and Southard (4), Otto (5), Lewis (6), Schenck (7), and Wells (8). The work of these intestigators has given us the following facts. This state can be transmitted. Hypersensitiveness to horse serum may exist independently of immunity to diphtheria toxin in offspring born of mothers injected with diphtheria toxin-antitoxin. Mother guinea pigs fed oats during gestation can transmit oat sensitization to their offspring, and this transferred state of hypersensitivity is of a passive nature.
Because we have demonstrated in our previous studies (I, II, III) that colostrum and milk are of negligible importance in the transfer of substances from a guinea pig mother to her offspring, and that the placenta in this species is permeable, thus permitting the interchange of heterologous substances, we can regard this passive sensitization as a result of placental transfer.
Transmission of Protein Hypersensitiveness from Mother to Offspring
Authors: Ratner Bret , Jackson Holmes C. , Gruehl Helen Lee 
Published: December 2022

Abstract
It has been our purpose in this series of studies to offer an explanation for the underlying basis that might exist in the allergic cases occurring in infancy as a result of contact with a food for the first time.
In Study I, we have shown that the placenta of the guinea pig may transmit substances from mother to offspring in the same manner as the human placenta, it being permeable to antibodies, heterologous proteins, etc. In Studies II and III, we have offered evidence for the negative rôle that colostrum and milk play in the transmission of these same substances. In Study IV, we have corroborated and amplified previous work and have shown that sensitizing antibodies are transmitted from a mother guinea pig to her offspring with a regularity that is truly remarkable.
Ascoli (2) and Holford (3) have shown definitely a direct passage of antigen from mother to fetus through the placenta.
The Effect of Type-I Pneumococcus Culture Broth on the Phagocytic Action of Type-I Pneumococcus Serum
Authors: Wadsworth Augustus B. , Sickles G. M. 
Published: December 2022

Summary
In normal serum of the horse and rabbit, virulent pneumococci were not phagocyted. In the homologous immune sera, active phagocytosis took place. In the immune sera incubated with the culture broth of virulent pneumococci, centrifugalized or filtered, phagocytosis of virulent pneumococci was inhibited. This inhibitory action was apparently the result of reactions that took place during the incubation of the immune serum with the culture broth. In contrast to previous experiments with diphtheria and other culture broths, the inhibiting action of which was apparently the result of adsorption of the inhibitory substance on the leucocyte, in these later experiments the exposure of the leucocytes to the pneumococcus culture broth failed to give uniform results. Phagocytosis of sensitized S. pyogenes aureus not only varied greatly but, in some instances, was apparently more active than with leucocytes not exposed to the pneumococcus culture broth. Inhibition of phagocytosis of pneumococci was much more pronounced when the serum was exposed with the culture broth before the leucocytes were added, and the degree of inhibition varied with the concentration of the serum.
Inhibition was obtained with eighteen-hour broth cultures and in greater degree with cultures which had been incubated twenty days.
The inhibitory action was not increased by exposure of the culture broth with the serum for more than one hour.
Preliminary exposure at 41° and 44°C. instead of at 37°C. did not appear to increase or decrease the action of the inhibitory substance.
Heating for thirty minutes at 75°C. or for five minutes at boiling did not diminish the inhibitory action of the culture broth.
No inhibition of phagocytosis of virulent pneumococci occurred with eighteen-hour culture broth of an attenuated type-I pneumococcus. Slight inhibition was obtained when a thirteen-day culture broth of the attenuated strain was used.
Sodium-oleate extracts of washed virulent pneumococcus cells had a similar but more marked inhibitory action as compared with the culture broth. Apparently the action of these extracts was, in some degree, type specific: that is, type-I extract with type-I serum inhibited phagocytosis of type-I organisms but not of type-III pneumococci in type-III serum, whereas type-III extract with type-I serum failed to inhibit phagocytosis of type-I cells.
Anti-Ig-mediated proliferation of human B cells in the absence of protein kinase C.
Authors: Francois D T , Katona I M , June C H , Wahl L M , Feuerstein N , Huang K P , Mond J J 
Published: December 2022

Abstract
Cross-linking of surface Ig has been shown to stimulate phosphatidylinositol hydrolysis in murine B cells, leading to increases in [Ca2+]i and activation of protein kinase C (PKC). Preliminary evidence suggests that a similar activation mechanism occurs in human B cells. We wished to examine whether anti-Ig antibody-stimulated human B cell proliferation is as dependent upon the presence of PKC as is anti-Ig-mediated murine B cell proliferation. Using highly purified, small, dense peripheral-blood B lymphocytes from healthy adult donors, we confirmed that PMA, a direct activator of PKC, is a potent mitogen for human B cells that synergizes with anti-mu antibody. Furthermore, we demonstrated that PMA treatment abolishes detectable cellular stores of immunoreactive PKC. However, after such depletion of cellular PKC, anti-mu antibody is still capable of delivering a proliferative signal to human B cells. It is unlikely that this signal occurs solely on the basis of increases in [Ca2+]i, because the calcium ionophore A23187 does not induce a proliferative response in PMA-treated B cells similar in magnitude to that seen with anti-mu. Additionally, the finding that pretreatment of B cells with PMA ablates the ability of anti-Ig antibody to mobilize intracellular and extracellular calcium also suggests that the ability of PMA to enhance anti-Ig mediated stimulation does not depend on elevations of [Ca2+]i induced by anti-Ig. Together, these observations suggest that anti-Ig signaling of human B cells may occur via other pathways in addition to the phosphatidylinositol system of calcium influx and PKC activation.
Inhibition of allergic encephalomyelitis in rats by treatment with sulfated polysaccharides.
Authors: Willenborg D O , Parish C R 
Published: December 2022

Abstract
A number of sulfated polysaccharides were tested for their ability to inhibit passively induced experimental allergic encephalomyelitis (EAE) in rats. Heparin and fucoidan both completely inhibited passive EAE even when treatment was begun 3 days after transfer of cells. Pentosan sulfate was partially inhibitory whereas chondroitin-4-sulfate had no effect. Inhibition was not merely due to killing of the cells since active sensitization 14 days after cell transfer resulted in an early onset of disease indicating the persistence of transferred cells as memory cells. Although all the inhibitory polysaccharides are anticoagulants, it would appear that this function alone is not the reason for inhibition since a heparin preparation devoid of anticoagulant activity also partially inhibited EAE. Actively induced EAE was also significantly delayed by treatment with heparin. The results are discussed in terms of the polysaccharides inhibiting the enzymatic dependent movement of lymphocytes across central nervous system vascular endothelium.
Spontaneous shift of anti-DNA antibody idiotypes in systemic lupus erythematosus.
Authors: Suenaga R , Munoz P A , Bright S W , Abdou N I 
Published: December 2022

Abstract
Spontaneous shift in Id expression of polyclonal anti-DNA antibodies in a patient, BS, with SLE was investigated. BS had active lupus nephritis in 1982 and developed central nervous system lupus in 1986 without evidence of active nephritis. Two rabbit polyclonal anti-Id (BS-82 and BS-86 R-anti-Id) were raised against affinity-purified anti-DNA antibodies prepared from 1982 serum (BS-82) and 1986 serum (BS-86), respectively. In addition, murine monoclonal anti-Id was prepared against BS-82 Id. Direct binding assays showed that all three anti-Id had preferential binding to the immunizing anti-DNA antibodies (the homologous Id) and poor binding to anti-DNA antibodies prepared from the different dated sample of BS. This was confirmed by inhibition assays of binding of anti-Id to the homologous Id by various Id. Moreover, inhibition assays of binding of various Id to DNA by the R-anti-Id showed that the R-anti-Id was the most effective inhibitor for the homologous Id. Testing for Id expression in serial (1982 to 1986) serum samples of BS with the R-anti-Id as probes showed that BS-82 Id declined and was undetectable after October, 1984, whereas BS-86 Id was first detectable in July, 1985, and increased by June, 1986. These results clearly demonstrate spontaneous shifts in Id expression of human anti-DNA antibodies. The phenomenon of Id shift should be considered in any future strategy for the diagnosis and therapy of human autoimmune disease by anti-Id.
Purification and partial biologic characterization of a human lymphocyte-derived peptide with potent neutrophil-stimulating activity.
Authors: Schröder J M , Mrowietz U , Christophers E 
Published: December 2022

Abstract
A novel neutrophil-activating peptide is detected in supernatants from mitogen-stimulated human T lymphocyte preparations. This chemotaxin was purified to apparent homogeneity by sequential Gel G-75 permeation chromatography, wide pore reversed phase (RP-8) HPLC, size exclusion HPLC, and reversed phase (RP-18) HPLC. Additional characterization of this lymphocyte-derived neutrophil-activating peptide (LYNAP) resulted in a single peak upon reversed phase HPLC and size exclusion HPLC. SDS-PAGE under nonreducing conditions revealed a single line at 10 kDa. LYNAP stimulated neutrophil chemotaxis (ED50 of 3 +/- 3 ng/ml), chemokinesis (ED50 of 2 +/- 2 ng/ml), and caused degranulation of cytochalasin B pretreated human neutrophils (ED50 of 20 ng/ml). In purified human monocytes, chemotactic responses to LYNAP at doses up to 100 ng/ml were absent, indicating nonidentity with a lymphocyte-derived monocyte chemotactic factor previously described by other workers. LYNAP shows biochemical and biologic similarities to a recently detected monocyte-derived neutrophil-activating peptide (MONAP). Moreover, desensitization experiments revealed cross-deactivation between LYNAP and MONAP, not, however, between these two chemotactic peptides and other well characterized polymorphonuclear leukocyte chemotaxins, e.g., C5a, FMLP, leukotriene B4, or platelet-activating factor. This finding points toward structure identity or homology of both chemotaxins, MONAP and LYNAP.
Alterations in cell protein phosphorylation in human neutrophils exposed to influenza A virus. A possible mechanism for depressed cellular end-stage functions.
Authors: Caldwell S E , Cassidy L F , Abramson J S 
Published: December 2022

Abstract
When polymorphonuclear leukocytes (PMN) are exposed to most harvests of influenza A virus (depressing virus, DV) for 20 min, chemotactic, secretory, and oxidative functions are depressed upon subsequent exposure to soluble or particulate stimuli. Other harvests of influenza A virus (non-DV) do not alter these activities. The DV-induced changes in multiple functions suggest the virus may interfere with steps involved in PMN activation. Because some of these steps may be regulated by protein phosphorylation, we examined the effect of non-DV and DV on cellular protein phosphorylation. PMN loaded with 32P-labeled inorganic orthophosphate were exposed to non-DV, DV, or buffer for 30 min; cells were then treated with buffer, FMLP (10(-6) M), or PMA (100 ng/ml) for 30 s. Samples were sonicated and centrifuged; cytosolic and particulate fractions were analyzed by SDS-PAGE and autoradiography. Exposure of PMN to either non-DV or DV caused phosphorylation of several cell proteins. However, when DV-treated PMN were then stimulated with FMLP or PMA, further phosphorylation was inhibited compared to non-DV- or buffer-treated cells. This suggests that DV-induced depression of PMN end-stage functions may be due to changes in cell protein phosphorylation. DV could interfere with phosphorylation of PMN proteins by altering protein kinase activity. We therefore examined the influence of non-DV and DV on some parameters that could affect kinase function. PMN intracellular [Ca2+] was monitored by using the fluorescent Ca2+ indicator, Indo 1, and cAMP levels were measured by RIA. PMN treated with DV alone or DV plus FMLP had higher intracellular [CA2+] than PMN similarly treated with non-DV or buffer. Exposure of PMN to non-DV, DV, or buffer caused minimal changes in cAMP levels, and similar increases occurred in cAMP levels upon FMLP stimulation. To determine whether DV interferes with transmembrane signaling, the effect of influenza virus on PMN transmembrane potential was studied by using a fluorescent cyanine dye. Transmembrane potential changes were greater in PMN exposed to DV than to non-DV or buffer; however, subsequent stimulation with FMLP caused equivalent changes in transmembrane potential. Our data show that protein phosphorylation in PMN is induced by DV and non-DV infection; upon subsequent stimulation with FMLP or PMA, there is inhibited cellular phosphorylation only in PMN previously exposed to DV.(ABSTRACT TRUNCATED AT 400 WORDS)
An in vitro model for Toxoplasma infection in man. Interaction between CD4+ monoclonal T cells and macrophages results in killing of trophozoites.
Authors: Canessa A , Pistoia V , Roncella S , Merli A , Melioli G , Terragna A , Ferrarini M 
Published: December 2022

Abstract
The cell interactions that take place between Toxoplasma gondii trophozoites and the human immune system have been investigated by using an in vitro model of infection. PBMC were co-cultured with live, appropriately attenuated, trophozoites. When cells from immune (seropositive) donors were used, a proliferative response was observed. At the same time, the proliferating T cells proved capable of controlling the growth of live trophozoites. By contrast, cells from seronegative donors failed to mount a proliferative response and intracellular overgrowth of trophozoites with subsequent cell injury occurred. Actively proliferating T cells were expanded in continuous cell lines with IL-2 and periodical restimulation with Ag in the presence of autologous irradiated mononuclear cells. From some of the lines obtained, clones were also derived. Ten clones were selected for further studies. They proliferated in response to trophozoites but not to unrelated Ag. Their response required the presence of autologous monocytes-macrophages isolated from peripheral blood on Percoll density gradients. B cells that were obtained from the same donors and immortalized by EBV infection proved inefficient as APC. These data suggest that live trophozoites have to be processed by macrophages in order to be presented to T cells. Upon appropriate antigen stimulation, all of the clones produced IL-2 and IFN-gamma, a finding that was consistent with both their CD4+ surface phenotype and their helper capacity on B cell proliferation and differentiation in vitro. The supernatants of all of the stimulated clones released a factor that activated macrophages to kill intracellular trophozoites as well as an unrelated pathogen, Listeria monocytogenes. This factor was identified as IFN-gamma because it was neutralized by specific anti-IFN-gamma antibodies. The present in vitro model of response to live protozoa may prove suitable to assess the role of both T lymphocytes and macrophages in intracellular parasite infections in man. Furthermore, this experimental system may be applied to detect specific lesions of cell mediated immunity in a number of immunodeficiency syndromes.
Enhancement of a secondary antibody response to vesicular stomatitis virus "G" protein by IFN-gamma treatment at primary immunization.
Authors: Anderson K P , Fennie E H , Yilma T 
Published: December 2022

Abstract
IFN-gamma is a secreted polypeptide product of stimulated T lymphocytes with immunomodulatory properties as well as antiviral activity. We have investigated the effects of IFN-gamma treatment on a neutralizing antibody response to vesicular stomatitis virus (VSV) when administered in conjunction with immunization using purified envelope glycoprotein "G" of VSV. Administration of rIFN-gamma to mice or cattle at the time of primary immunization with VSV G glycoprotein enhanced the magnitude of a secondary virus-neutralizing antibody response after a booster administration of the same Ag without IFN-gamma treatment. Enhancement was statistically significant and occurred at relatively low doses of IFN-gamma in the absence of any additional adjuvants. Furthermore, cattle treated with IFN-gamma at the time of a single primary immunization were more resistant to VSV challenge than those immunized without IFN-gamma treatment. IFN-gamma treatment in conjunction with a single primary immunization may therefore provide a practical means of enhancing protection from a viral challenge without the use of inflammatory adjuvants or booster immunizations.
Genetic engineering of bovine Ig. Construction and characterization of hapten-binding bovine/murine chimeric IgE, IgA, IgG1, IgG2, and IgG3 molecules.
Authors: Knight K L , Suter M , Becker R S 
Published: December 2022

Abstract
A bovine recombinant phage library was constructed and screened with rabbit S mu and human C gamma probes. IgM, IgA, and IgE H chain constant region (CH) genes were isolated with the rabbit S mu probe and three IgG CH genes were isolated with the C gamma probe. The CH genes were individually cloned into an expression vector which contained a murine VDJ gene cloned from a hybridoma producing anti-dansyl hapten antibody. The resulting constructs were transfected into murine hybridoma cells producing L chain of the anti-dansyl antibody and stable transfectomas secreting chimeric bovine-murine IgA, IgE, or IgG subclass anti-dansyl antibodies were obtained. The chimeric antibodies, immunoprecipitated with Ag or with anti-bovine H chain antibodies, were analyzed by SDS-PAGE and were shown to contain H and L chains of expected size. Of the three chimeric antibodies derived from the C gamma genes, one reacted with anti-IgG1 antibody, another reacted with anti-IgG2 antibody and the third did not react with either anti-IgG1 or anti-IgG2. This third IgG appears to represent a "new" subclass of bovine IgG, IgG3. Southern blot analysis indicated that the bovine genome contains a fourth C gamma gene. These experiments demonstrate the usefulness of molecular genetic techniques for the isolation and characterization of Ig which are not readily purified from biologic fluids. These techniques will be useful for isolation and characterization of Ig genes from other outbred mammals.
IL-4-induced lymphokine-activated killer cells. Lytic activity is mediated by phenotypically distinct natural killer-like and T cell-like large granular lymphocytes.
Authors: Peace D J , Kern D E , Schultz K R , Greenberg P D , Cheever M A 
Published: December 2022

Abstract
The purpose of the current study was to characterize lymphokine-activated killer (LAK) activity induced with IL-4/B cell stimulatory factor-1 and to compare IL-4-induced LAK activity with IL-2-induced LAK activity. Culture of murine lymphocytes with high concentrations of IL-4 induced nonspecific lytic activity against a wide variety of tumors. Lytic activity induced by IL-4 increased with increasing concentrations of IL-4 over the range of 1.0 to 25 ng/ml. The kinetics of LAK induction by IL-4 and IL-2 were similar; however, IL-4 was less effective than IL-2 in maintaining lytic activity for longer culture periods and provided lower viable cell yields than did IL-2. Similar to IL-2, IL-4 induced blastogenesis and the generation of large granular lymphocytes, all LAK activity observed was exclusively associated with the large granular lymphocyte fraction, and the cytolytic effector cells were heterogeneous in regards to cell surface phenotype. The majority of IL-4-induced lytic activity was associated with mutually exclusive NK-like (i.e., NK-1.1+ Lyt-2-) and T cell-like (i.e., NK-1.1- Lyt-2+) LAK cells. The precursors for each subset were distinct and expressed the asialo-GM1+ Lyt-2- and the asialo-GM1+ Lyt-2+ phenotypes, respectively. Although IL-4-induced LAK effector cells were morphologically and phenotypically similar to IL-2-induced LAK cells, IL-2 generated equivalent numbers of T cell-like and NK-like LAK cells, whereas IL-4 generated 3.5-fold more T cell-like LAK cells than NK-like LAK cells. It might eventually be possible to exploit the preferential activation of T cell-like LAK by IL-4 for therapeutic advantage.
Target cell expression of MHC antigens is not (always) a turn-off signal to natural killer cells.
Authors: Chervenak R , Wolcott R M 
Published: December 2022

Abstract
Recent evidence has demonstrated that the lytic function of natural killer cells might be regulated by potential target cells through the target cells' expression of cell surface components that are able to inhibit the lytic process. Specifically, it has been shown in many target cell systems that the expression of class I MHC proteins by target cells is inversely proportional to their susceptibility to lysis by NK cells. It has been suggested, therefore, that MHC proteins may act as important negative regulatory elements in the ongoing control of NK cell function. Herein, we examined two closely related murine lymphoma cells (ASL1 and ASL1w), both in terms of their susceptibility to lysis by NK cells as well as their expression of both H-2K and H-2D class I MHC proteins. The results of these studies showed that whereas ASL1 and ASL1w cells differed greatly in their susceptibility to NK cell lysis (ASL1 was much more NK resistant than ASL1w), both expressed high levels of H-2K and D proteins. In contrast to what might have been predicted base on reports from other target cell systems, the more NK susceptible ASL1w cells expressed somewhat higher levels of H-2K Ag than did ASL1 cells. These results indicate that expression of H-2 class I proteins by target cells, in and of itself, is not sufficient to inhibit the lytic activity of murine NK cells.