bluuebunny/crossref_metadata_2025_split huggingface dataset:
A rapid, large scale purification procedure for gibbon interleukin 2.
Authors: Henderson L E , Hewetson J F , Hopkins R F , Sowder R C , Neubauer R H , Rabin H 
Published: December 2022

Abstract
Interleukin 2 (IL 2) was purified from the conditioned medium of a gibbon T cell line, MLA144, which releases IL 2 constitutively. The IL 2 was obtained free of contaminating proteins by a simple process consisting of an initial batch purification on trimethylsilyl-controlled pore glass followed by reversed phase high pressure liquid chromatography. Overall recovery of IL 2 activity ranged from 70 to 100% of initial activity and yielded 2 X 10(6) or greater units of IL 2 per 15 liters of serum-free MLA144 conditioned medium. The specific activity of purified IL 2 ranged from 0.5 to 1 X 10(8) IL 2 U/mg protein. The purified IL 2 showed four molecular species when analyzed by two-dimensional isoelectric focusing-SDS-polyacrylamide gel electrophoresis. Each of the four molecular forms was active in the bioassay for IL 2 activity. Three molecular forms had apparent m.w. of 16,000 but different isoelectric points of 5.9, 6.3, and 6.7. One molecular form had an apparent m.w. of 15,000 and an isoelectric point of 7.2. The most abundant form of IL 2 had an apparent m.w. of 16,000 and an isoelectric point of 6.3. The purified IL 2 supported the growth of IL 2-dependent lymphocytes to a greater extent than did the same level of crude IL 2-containing MLA144 conditioned medium. The ability to purify large amounts of IL 2 by a rapid and efficient procedure will be of great help in both biochemical and immunologic studies of this lymphokine.
Macrophage-activating factors from different T cell clones induce distinct macrophage functions.
Authors: Gemsa D , Debatin K M , Kramer W , Kubelka C , Deimann W , Kees U , Krammer P H 
Published: December 2022

Abstract
The data reported in this paper are the first demonstration that different T cell clones (PC-AKR-CI 96, clone 96; PK 7.1.2 E8, clone 7.1.2 E8) secrete different macrophage-activating factors (MAF) that induce distinct macrophage activities. Incubation of resident murine macrophages with MAF 7.1.2 E8 increased RNA, protein, and glycoprotein synthesis, hexosemonophosphate shunt (HMPS) activity, release of oxygen metabolites (O-2, H2O2), pinocytosis, phagocytosis, and tumor cytostasis, whereas no effect on prostaglandin E (PGE) release, schistosomula killing, and tumor cytolysis could be observed. In contrast, MAF 96 increased glycoprotein synthesis, HMPS activity, release of oxygen metabolites and PGE, schistosomula killing, and tumor cytostasis and cytolysis, whereas RNA and protein synthesis and pinocytosis were decreased and phagocytosis remained unaffected. Thus, MAF from both T cell clones share some macrophage-activating properties but differ in others. Most importantly, both MAF could be differentiated serologically by a rabbit anti-lymphokine antiserum that selectively inhibited MAF 96 but not MAF 7.1.2 E8 activity. At optimal concentrations, MAF 96 and 7.1.2 E8 were active in the absence of lipopolysaccharide (LPS) whereas LPS enhanced the activity of suboptimal doses of MAF 96 but not of MAF 7.1.2 E8. These data are discussed with respect to the possibility that the functional dichotomy of T cell clones might reflect different activities of normal T cell subpopulations.
Localized elaboration of IgA in normal and neoplastic murine mammary cell cultures: relationship to fibronectin matrix.
Authors: Myrdal S E , Snoddy S , Ashkar S , Nixon D W , Binkley F 
Published: December 2022

Abstract
IgA secretion by the lactating mammary gland culminates a complex sequence of biologic events both within the gland and at distant sites. Because of the many extraglandular influences, it is difficult to investigate IgA secretion at the tissue and cellular levels in the intact animal. In this study, with the use of immunohistofluorescence, we have observed elaboration of IgA by primary monolayer cultures of mammary cells from the glands of mid-pregnant mice and from mammary tumors. In cultures of normal cells, IgA appeared first in vesicular structures on the upper surfaces of the monolayers. Vesicular IgA was maximal at day 5 in culture, and at that time, was observed only over mounds (domelike structures) that were covered with fibrillar fibronectin (FN), and eventually developed a subpopulation of fusiform cells. It appears that the IgA observed was secreted in vitro, that normal mammary epithelial cells must form multicellular FN-bearing structures to secrete IgA in culture, and that by mid-pregnancy the murine mammary gland contains all of the lymphoid cells required for IgA secretion. In contrast, primary cultures of mammary tumors displayed minimal amounts of IgA and FN. The small amount of cell-associated IgA that was detected on tumor cultures was not localized to any multicellular structures nor was it associated with FN, but instead appeared as minute, punctate accumulations on individual cells scattered across the epithelioid areas. This finding is consistent with the loss of specialized functions and the increased autonomy typical of malignant cells. The study in cultured cells of a function as specialized as IgA secretion should permit greater understanding of both the process itself and the despecializations that accompany malignancies of secretory epithelia.
Activation of the fifth and sixth components of the human complement system: C6-dependent cleavage of C5 in acid and the formation of a bimolecular lytic complex, C5b,6a.
Authors: Hammer C H , Hänsch G , Gresham H D , Shin M L 
Published: December 2022

Abstract
Acidification of C5 and C6 or serum to pH 6.4 at 0 degrees C, followed by neutralization, generates a factor-designated C(56)a that causes lysis of nonsensitized erythrocytes in the presence of C7, C8, and C9. C(56)a is functionally similar to alternative pathway-generated C5b,6 in respect to the formation of C5b,6,7 sites on cells, the potentiation of lytic activity by membrane-bound C3b or the membrane-active agent A2C, and the required species compatibilities between target membranes and terminal components for optimal activity. The formation of C(56)a complex from purified components C5 and C6 proceeds independently of the classical or alternative pathway C5 convertases and requires the simultaneous H+ ion treatment of the components. The generation of C(56)a from C5 and C6 and the physicochemical properties of the complex were studied in detail and compared with those of C5b,6. Acid generation of C(56)a is dose-dependent on C5 and C6 and its efficiency is similar to that of the conventional convertase in the production of lytic activity. Sucrose gradient ultracentrifugation of C(56)a containing activated 125I-C5 demonstrated a shift in sedimentation from that of native C5 to 11S, which is consistent with C5,6 complex formation. C(56)a sedimentation was identical to C5b,6, and both migrated coincident with lytic complex activity. These complexes, however, are not identical because unlike C5b,6, C(56)a is unstable at 37 degrees C, demonstrating a nonlinear decay curve. In the presence of C7, both complexes exhibit similar first order decay with a T1/2 of 3 min at 37 degrees C. SDS-PAGE autoradiographic analysis of the C5-subunit structure of 125I-C5 in C(56)a and the Zx-activated C5b,6 complex prepared from purified components showed similar alpha-chain cleavage to several fragments of 109,000, 100,000, and 58,000 daltons. Conversion to lower m.w. peptides by acid treatment was more extensive. Comparison of the 125I-C5 polypeptide chains in the membrane attack complex extracted from guinea pig erythrocyte membranes, prepared by acid activation or classical pathway lysis with whole serum, demonstrated similar C5 alpha-chain cleavage to a predominant subunit of 102,000 daltons. Acid activation also produced a 109,000 dalton C5 alpha'-fragment barely detectable with classical pathway activation. Low pH treatment of C5 alone did not inactivate C5 function, form a lytic complex on the subsequent addition of C6, or cleave the C5 alpha-chain. Thus, it is postulated that local high H+ ion concentration during simultaneous acidification of C5 and C6 allows complex formation with the concomitant C6-dependent cleavage of the C5 alpha-chain and the generation of lytic capacity.
Complement receptor expression by neoplastic and normal human cells.
Authors: Gaither T A , Magrath I T , Berger M , Hammer C H , Novikovs L , Santaella M , Frank M M 
Published: December 2022

Abstract
Complement receptor (CR) expression in cell lines derived from Burkitt's lymphoma (BL), Epstein Barr virus-transformed cord blood lymphocytes (CB), and peripheral lymphocytes from patients with infectious mononucleosis (IM) was examined. Red cell intermediates bearing various densities of C4b, C3b, C3bi, or C3d were tested for rosette formation with the cell lines. In addition, a series of studies was performed under conditions that precluded the cleavage of cellbound C3b by Factor I (C3bINA). These conditions did not alter rosetting by the cells that were tested. RAJI cells rosetted with EAC3bi greater than EAC3d greater than EAC3b, but not with EAC4b. EAC3b/RAJI rosette formation required much greater quantities of C3b bound to red cells than did CB and IM lines, which unlike RAJI, also bound EAC4b. All of the BL lines failed to bind EAC4b even at a C4b density of 50,000 molecules/cell, but several lines did form rosettes with EAC3b, and most formed rosettes with EAC3bi and EAC3d. Fluid phase C3b blocked RAJI/EAC3b rosetting while having little effect on RAJI/EAC3bi rosette activity. Moreover, fluid phase C3b, as well as C4b, blocked RAJI/EAC3b rosettes more effectively than CB/EAC3b rosettes. The results indicate that the RAJI cell line has a receptor for C3b, with characteristics that differ markedly from the C3b receptor of cell lines derived from CB lymphocytes and of lymphoblastoid cell lines derived from patients with IM. This receptor is capable of interacting with soluble but not cellbound C4b. In these studies, rosette formation was examined under various ionic conditions. RAJI/EAC3b rosette formation was severely reduced as ionic strength was increased, whereas RAJI/EAC3bi binding was only moderately decreased at physiologic ionic strength. In striking contrast, EAC3bi binding to monocytes, PMN, and human erythrocytes was markedly reduced as ionic strength increased, but EAC3b binding to these cells was less sensitive to changes in ionic strength. Under conditions of physiologic ionic strength, the C3bi receptor of phagocytic cells may be at a functional disadvantage in the binding of C3bi-coated particles. This may have major physiologic implications.
The biologic activity of mast cell granules. VII. The effect of anti-neutrophil antibody-induced neutropenia on rat cutaneous late phase reactions.
Authors: Lemanske R F , Guthman D A , Kaliner M 
Published: December 2022

Abstract
Mast cell-dependent late phase reactions (LPR) occur in rat skin and are characterized histologically by an early (1- to 8-hr) neutrophil-rich and later (8- to 24-hr) mononuclear cell-rich infiltrate. To extend previous observations on the role of the neutrophil in the sequential histologic development of cutaneous LPR, rats were selectively depleted of circulating neutrophils using rabbit anti-rat neutrophil antibody (anti-neut), and the effects of this treatment on the histologic intensity of LPR were analyzed. In addition, the effects of neutrophil depletion on cutaneous delayed-type hypersensitivity (DTH) reactions produced by immunization with Freund's complete adjuvant followed by intradermal challenge with purified protein derivative (PPD) were assessed. Following anti-neut treatment, cutaneous DTH reactions were unaffected. In contrast, selective neutrophil depletion resulted in significant reductions in the intensity of cutaneous LPR at both 6 to 8 and 24 hr following anti-IgE or rat mast cell granule injection. Further, statistical comparison of circulating neutrophil counts with the capacity of the animal to express LPR revealed a highly significant direct correlation. These data confirm the previous observations that rat LPR are neutrophil-dependent reactions.
Elevated natural killer cell-mediated cytotoxicity, plasma interferon, and tumor cell rejection in mice persistently infected with lymphocytic choriomeningitis virus.
Authors: Bukowski J F , Biron C A , Welsh R M 
Published: December 2022

Abstract
To assess the effects of chronic virus infection on NK cells, the related phenomena of interferon (IFN) production, NK cell activation, and resistance to tumor implants were studied in mice persistently infected with lymphocytic choriomeningitis virus (LCMV). NK cells from these LCMV-carrier mice displayed augmented killing of the NK-sensitive YAC-1 target cell. They did not lyse the more resistant targets L-929 and P815, whereas NK cells from acutely infected mice efficiently lysed all three cell types. The plasma from LCMV-carrier mice contained an antiviral substance identified as IFN type I, based on species specificity, virus nonspecificity, resistance to pH 2, and sensitivity to antibody to type I IFN. IFN titers in plasma from LCMV-carrier mice were 32 to 64 U/ml, about 20-fold less than those in acutely infected mice. Both the IFN and NK cell levels continuously remained elevated in the LCMV carrier mice up to at least 6 months of age. IFN is known to activate NK cells and to induce their blastogenesis in vivo. As determined by centrifugal elutriation, large NK blast-size cells were isolated from the spleens of acutely infected mice, but not from either normal or LCMV-carrier mice, suggesting augmented NK cell-mediated lysis in the absence of enhanced proliferation. Poly inosinic-cytidylic acid induced high levels of NK cell-mediated cytotoxicity and blastogenesis in both control and LCMV-carrier mice, but IFN was induced to lower levels in carriers as compared with controls. Coincidental with augmented NK cell activity, the LCMV-carrier mice rejected intravenously injected 125IUdR-labeled tumor cells more efficiently than did normal mice. Thus, LCMV carrier mice have low levels of type I IFN, moderately augmented NK cell activity lasting for at least 6 months, and increased resistance to tumor cell implants. This indicates that augmented NK cell-mediated cytotoxicity can be maintained in vivo over prolonged periods of time in the presence of chronic low-level IFN stimulation.
Involvement of lipopolysaccharide in the pathogenicity of Treponema hyodysenteriae.
Authors: Nuessen M E , Joens L A , Glock R D 
Published: December 2022

Abstract
Treponema hyodysenteriae, the etiologic agent of swine dysentery, caused gross and microscopic lesions in the large intestines of C3HeB/FeJ mice. No gross lesions were observed in the intestines of the closely related, but lipopolysaccharide-resistant, C3H/HeJ strain of mice, and microscopic lesions were mild, if present at all. In the presence of actinomycin D, 1 mg of T. hyodysenteriae lipopolysaccharide (LPS) was lethal for C3HeB/FeJ but not for C3H/HeJ mice. Also, the treponemal LPS was chemotactic for macrophages from C3H/HeJ mice but not for macrophages from C3HeB/FeJ mice. The difference between the two mouse strains in lesion development may be due to the nondestructive nature of LPS in C3H/HeJ mice, which suggests that the treponemal LPS is involved in the pathogenicity of T. hyodysenteriae. T. hyodysenteriae may prove to be a useful bacterium in the study of LPS-resistant C3H/HeJ mice, because resistance to the treponemal LPS and to the treponeme itself appear to correlate.
Inhibition of proliferation of MIs- and Ia-reactive cloned T cells by a monoclonal antibody against a determinant shared by I-A and I-E.
Authors: Wall K A , Lorber M I , Loken M R , McClatchey S , Fitch F W 
Published: December 2022

Abstract
The interaction between cloned amplifier T cells and stimulating cells has been probed with the use of a monoclonal antibody selected for its ability to inhibit stimulation of Mls- and la-reactive T cells. The antibody recognizes a public determinant on I-A- and I-E-coded molecules of a variety of murine H-2 haplotypes. The antibody inhibits the proliferation of the I-Ab-reactive T cell clone 48.1 and of the Mls-reactive T cell clones L2 and Fa 13. The antibody may be added as late as 3 hr after initiation of culture to cause inhibition of L2 proliferation and release of interleukin 2. A profound inhibition of primary and secondary mixed leukocyte responses also is observed. The results indicate that a large fraction of Mls reactive T cells require interaction with la antigens.
A possible maternal effect in the abnormal hyporesponsiveness to specific alloantigens in offspring born to neonatally tolerant fathers.
Authors: Gorczynski R M , Kennedy M , MacRae S , Ciampi A 
Published: December 2022

Abstract
Newborn CBA mice were inoculated i.p. with 1 X 10(8) adult (CBA X A)F1 lymphoid cells with 5 X 10(7) F1 hybrid lymphoid cells thereafter inoculated i.v. at 14-day intervals. The mice were subsequently grafted with A/J tail skin at 24 days of age. At 8 wk of age, individual tolerant males with intact skin grafts were each mated with similar tolerant skin-grafted females or with 8-wk-old control normal CBA females. Approximately 0.4 ml of peripheral blood from 7-wk-old progeny born to these crosses, along with the blood from age-matched progeny born to normal CBA incrosses, were used for in vitro mixed leukocyte cultures (MLC). All progeny received skin grafts of (CBA X A)F1 tail skin at 7 1/2 wk of age. In this study, we show i) that MLC hyporesponsiveness to histocompatible cells is an acquired phenotype expressed by lymphoid cells of the progeny of tolerant male mice, and ii) that these progeny also show delayed rejection of (CBA X A)F1 skin grafts. The continued breeding of the first generation animals established that a similar transmission of hyporesponsiveness can be observed in the second generation progeny. When putatively normal females, however, which had borne several litters after mating with neonatally tolerant males, were mated with "normal" (nontolerant) males; their offspring also exhibited a specific hyporesponsiveness in MLC to the initial tolerizing allodeterminants. This suggests that there may ultimately be a maternally derived origin for the transmission of characters from tolerant males.
NZB cells actively interfere with the establishment of tolerance to BGG in radiation chimeras.
Authors: Laskin C A , Smathers P A , Lieberman R , Steinberg A D 
Published: December 2022

Abstract
We report experiments designed to determine if the tolerance defect in NZB mice results from i) failure of NZB cells to become tolerant, or ii) the ability of NZB cells to interfere actively with the development of tolerance. The results indicate that NZB cells are primed by the tolerogen itself and actively interfere with the expression of tolerance by DBA/2 cells, which normally can be rendered tolerant.
Antigen presentation by human monocytes: evidence for stimulant processing and requirement for interleukin 1.
Authors: Scala G , Oppenheim J J 
Published: December 2022

Abstract
We studied the role of stimulant processing and presentation and of IL 1 in monocyte-mediated activation of human lymphoproliferative responses. The effects of two lysosomotropic agents, ammonium chloride and chloroquine, on the capacity of human monocytes to activate T lymphocyte responses to the soluble antigen streptolysin O (SLO) and to the polyclonal stimulant S. aureus protein A (SpA) were investigated. These agents inhibited the presentation of SLO and SpA by human monocytes in a dose-dependent manner. The inhibition occurred if monocytes were treated with ammonium chloride and chloroquine for 1.5 hr, starting only 30 min after exposure to the stimulants, whereas only minimal inhibition occurred when monocytes were treated with the two lysosomotropic compounds 2 hr after pulsing with SLO or SpA. In contrast, cell membrane alloantigen presentation by monocytes in the MLR was not affected by ammonium chloride or chloroquine treatment. Thus, these reversible inhibitors of monocyte phagosome-lysosome functions presumably interfere with intracellular processing of the stimulants but do not seem to interfere with alloantigen presentation at the cell surface. Furthermore, we investigated whether gently fixed monocytes were still capable of passively presenting stimulant or whether active metabolic processes as well as IL 1 were required. We observed that only monocytes treated with paraformaldehyde after SLO or SpA pulsing stimulated a proliferative response by T lymphocytes, provided 50 U/ml of partially purified human IL 1 were added back to cultures. In contrast, monocytes fixed before exposure to SLO or SpA were not able to stimulate T lymphocytes even if supplemented by IL 1. Taken together these data suggest that a finite incubation period is required for human monocytes to become able to present SLO or SpA to T lymphocytes. During this time the soluble stimulants presumably undergo some metabolic process in viable macrophages perhaps at the phagosome-lysosome level, to become recognizable by T lymphocytes.
Specific binding sites for vasoactive intestinal polypeptide on nonadherent peripheral blood lymphocytes.
Authors: Danek A , O'Dorisio M S , O'Dorisio T M , George J M 
Published: December 2022

Abstract
Vasoactive intestinal polypeptide (VIP), an octacosapeptide isolated from porcine duodenum and thought to have neuromodulator function in several functional systems (gastrointestinal tract, brain, lung, genital tract, heart), was recently detected in human neutrophils by radioimmunoassay. Subsequent studies demonstrated a VIP-mediated increase in lymphocyte adenylate cyclase. In this paper, VIP binding studies are presented using viable nonadherent human lymphocytes. Binding of 125I-VIP to nylon wool column-purified lymphocytes is specific, time dependent, rapid, and reversible. Bound radioactivity varies linearly with the number of cells used and is displaceable by non-iodinated VIP in a dose-dependent manner with complete displacement between 1 pM and 50 nM. Scatchard analysis of competition experiments demonstrates one class of specific binding sites with a KD of 0.47 +/- 0.23 nM and a Bmax of 24.9 +/- 7.0 pM. This Bmax represents 1700 binding sites/cell. secretin, gastric inhibitory polypeptide, and glucagon did not effectively compete with 125I-VIP for binding sites. This is the first demonstration of VIP receptors in a purified population of human lymphocytes; the data suggest that VIP may modulate lymphocyte function.
Generation of antigen-specific suppressor cells in vitro in man.
Authors: Morimoto C , Reinherz E L , Todd R F , Distaso J A , Schlossman S F 
Published: December 2022

Abstract
The generation of human antigen-specific suppressor cells in vitro was examined in a primary anti-DNP antibody-forming system. It was found that specific T8 suppressor cells could be induced in vitro with high doses of antigen. The suppression obtained was macrophage dependent and carrier specific. KLH-specific T8 suppressor cells suppressed the anti-DNP antibody response induced by DNP-KLH but not by DNP-FGG. Similarly, T8 suppressor cells induced with FGG specifically suppress the anti-DNP response stimulated by DNP-FGG. These T8+ suppressor cells bear Ia molecules arising as a consequence of activation. This in vitro antigen-specific system should be useful for the further dissection of human immunoregulatory circuits.