bluuebunny/crossref_metadata_2025_split huggingface dataset:
Altered natural killer cell biology in C57BL/6 mice after leukemogenic split-dose irradiation.
Authors: Parkinson D R , Brightman R P , Waksal S D 
Published: December 2022

Abstract
Natural killer (NK) cell activity was examined in the spleens of C57BL/6 mice given leukemogenic split-dose irradiation. The radiation protocol resulted in severe depression of spontaneous NK cell activity; this activity was not fully restored after treatment with the interferon inducer poly I:C. In vitro mixing studies provided no evidence for active suppression in vivo as a mechanism for this decrease in activity. In addition, spontaneous activity was restored towards control levels after bone marrow transfusion from nonirradiated mice. Despite the low NK cell activity, there was no difference between control and irradiated mice in the numbers of target-binding cells (TBC). The results are most compatible with the radiation-induced loss of a cell with normal NK activity from spleen and bone marrow after the split-dose radiation protocol. In addition, a population of cells able to competitively block normal NK cell lysis of YAC-1 tumor cells is found in the bone marrow, spleen, and thymus of the irradiated mice lacking NK cell activity. These findings are considered from the perspective of their implications regarding NK cell ontogeny, and the possible role of the NK cell in radiation leukemogenesis.
A monoclonal antibody that identifies human peripheral blood monocytes recognizes the accessory- cells required for mitogen-induced T lymphocyte proliferation.
Authors: Rosenberg S A , Ligler F S , Ugolini V , Lipsky P E 
Published: December 2022

Abstract
These studies were carried out to evaluate the functional characteristics of the cells identified by a monoclonal anti-human mononuclear phagocyte (M phi) antibody, 63D3. This antibody reacts specifically with all human peripheral blood M phi and not with normal human peripheral blood T or B cells. By using the fluorescence-activated cell sorter, human peripheral blood mononuclear cells (PBM) were sorted into 63D3-positive and 63D3-negative populations. Cell volume analysis indicated that 63D3-negative cells were identical to the non-adherent cells (NAC) in PBM, whereas 63D3-positive cells had a bimodal size distribution comparable to glass-adherent cells (AC). Neither 63D3-negative cells nor NAC were able to proliferate in response to mitogenic stimulation, whereas co-culture with either mitomycin C-treated AC or 63D3-positive cells restored mitogen responsiveness. Thus, the 63D3-positive population contains the relevant accessory cell required for mitogen-induced human lymphocyte proliferation.
The role of subcellular factors in pulmonary immune function: physicochemical characterization of two distinct species of lymphocyte-activating factor produced by rabbit alveolar macrophages.
Authors: Simon P L , Willoughby W F 
Published: December 2022

Abstract
T cell stimulatory factors produced by rabbit alveolar macrophages were investigated. Physicochemical characterization revealed that alveolar macrophages (harvested by bronchopulmonary lavage and stimulated in tissue culture with bacterial lipopolysaccharide) released 2 predominant species of lymphocyte-activating factor (LAF) with isoelectric points of 4.6 and 7.4, and m.w. of 14,400 and 11,600 daltons, respectively, as calculated by the Svedberg equation. Using C3H/HeJ mouse thymocytes (and in some instances nylon wool-purified nonadherent rabbit spleen or lymph node cells) as target cells, rabbit LAF was found to induce proliferative responses directly, as well as enhance proliferative responses to phytomitogens. Both LAF species were inactivated by heating, treatment with trypsin, or at low (2.3) pH. The pI 7.4 LAF was also unstable at high pH (9.0). The thymocyte stimulatory activity of both LAF species was not inhibited by the anti-proteases alpha-1-anti-trypsin, Traysylol (aprotinin), leupeptin, or pepstatin.
Neutralization of vesicular stomatitis virus (VSV) by human complement requires a natural IgM antibody present in human serum.
Authors: Beebe D P , Cooper N R 
Published: December 2022

Abstract
Neutralization of VSV by human serum ws previously shown to involve C1, C2, C3, and C4 of the classical complement (C) pathway. All normal human sera tested were equivalently active in this regard. However, purified C1, C2, C3, and C4 were unable to mediate VSV neutralization. In the present studies an additional factor required for C-mediated neutralization was isolated from normal human serum and identified as a natural IgM antibody specific for a viral encoded antigen. Purified IgM bound to the virus and formed a complex that activated component C1. Normal serum concentrations of purified IgM, C1, C2, C3, C4 neutralized VSV to the same extent as normal serum. Purified IgM did not neutralize VSV alone or in conjunction with C1, C2, and C4. Inclusion of C3 resulted in full neutralization and C3b binding to the virus was demonstrated. Thus, normal human serum contains a natural antibody of the IgM class that is directed toward a viral antigen. The antibody facilitates neutralization by forming an immune complex that activates C1 and thus efficiently initiates the classical pathway at the viral surface. Neutralization occurs with C3b deposition on the viral envelope and probably results from a blanket of C protein that interferes with viral attachment to susceptible cells.
The third component of complement inhibits human lymphocyte blastogenesis.
Authors: Needleman B W , Weiler J M , Feldbush T L 
Published: December 2022

Abstract
Purified human C3 was studied for its ability to regulate human peripheral blood lymphocyte activation in a serum-free tissue culture system. C3 and its fragments formed by trypsin digestion were not mitogenic. However, C3 inhibited both mitogen- and antigen-induced lymphocyte proliferation in a dose-related manner. The observed inhibition by C3 increased with an increase in the dose of mitogen, with 50% inhibition seen at a C3 dose of 2.5 to 25 microgram/ml. Inhibition was induced even when C3 was added at 69 hr in a 99-hr culture, suggesting an effect on late events in activation. The inhibition was not mediated through generalized cytotoxicity, was not an artifact of kinetic alteration and still occurred in macrophage-depleted cultures. A small m.w. fragment of C3 which contained the inhibitory capacity in our C3 preparation was similar to C3a in size, anaphylatoxin activity, heat and acid stability and inhibition by serum. Our results indicate that cleavage products by C3 may play a negative role in lymphocyte activation.
The involvement of herpes simplex virus type 1 glycoproteins in cell-mediated immunity.
Authors: Carter V C , Schaffer P A , Tevethia S S 
Published: December 2022

Abstract
The participation of herpes simplex virus (HSV) glycoproteins in T cell-mediated lysis of HSV-infected syngeneic target cells was examined by using a temperature sensitive (ts) mutant defective in glycoprotein synthesis at the nonpermissive temperature (39 degrees C), and 2-deoxy-D-glucose and tunicamycin, known inhibitors of both HSV replication and glycoprotein synthesis in HSV-infected cells. Lymphocytes cytotoxic for HSV-infected cells lysed C57BL/6 Wt-3 cells infected with the mutant, ts A1, at 39 degrees C less efficiently than at 33 degrees C. Treatment of HSV-infected C57BL/6 Wt-3 cells with 1% 2-deoxy-D-glucose for 14 hr reduced their susceptibility to T cell-mediated lysis by 73% in the 51Cr release assay. Treatment of HSV-infected C57BL/6 Wt-3 cells with 0.2 microgram/ml tunicamycin for 14 hr reduced their susceptibility to T cell-mediated lysis by 78% in the 51Cr release assay. The reduction in T cell-mediated lysis by 2 deoxy-D-glucose and tunicamycin was found not to be due to the effects of the compounds on the H-2 antigens. We conclude that HSV specific glycoproteins are involved in T cell-mediated lysis of HSV-infected cells.
Membranes of EBV-carrying virus nonproducer cells inhibit leukocyte migration of EBV-seropositive but not seronegative donors.
Authors: Szigeti R , Volsky D J , Luka J , Klein G 
Published: December 2022

Abstract
We have previously shown that the leukocytes of healthy EBV-seropositive (but not seronegative) donors respond with migration inhibition (LMI) when confronted with extracts of EBV-carrying (but not EBV negative) cells. In the present study, we have examined whether this EBV-specific LMI response is capable of detecting a membrane antigen on the surface of EBV-carrying virus nonproducer cells. Crude membranes from EBV-genome carrying and EBV-negative cell lines were used as antigen. Contamination with the EBV-determined nuclear antigen (EBNA) was ruled out. Membranes from EBV-genome carrying nonproducer cells inhibited the migration of leukocytes from healthy seropositive donors, whereas membranes from EBV-negative lines had no such effect. Seronegative donors did not show any LMI. The clear difference between the EBV-negative Ramos line and its EBV-converted sublines was particularly conclusive in showing that the membrane component is determined or induced by the viral genome.
Constitutive production of interleukin 2 activity by a T cell hybridoma.
Authors: Stull D , Gillis S 
Published: December 2022

Abstract
Several laboratories have recently confirmed the importance that interleukin 2 (IL-2, formerly referred to as T cell growth factor) plays not only in the maintenance of cultured functional T cell lines but also as a potent regulator of immune responses. Despite the development of preparative IL-2 purification procedures, as well as identification of IL-2 producer tumor cell lines, simple sources of lectin-free IL-2 containing conditioned medium remain undefined. In hopes of establishing such a source of mitogen-free IL-2, we elected to fuse the high titer IL-2 producer tumor cell line, LBRM-33, with a drugmarked T cell lymphoma. In this communication we report the successful isolation of a T cell hybridoma that constitutively synthesizes and secretes biologically active IL-2. Hybridoma conditioned medium contained approximately 10 to 100 times the amount of IL-2 produced by conventional T cell mitogen-stimulated murine splenocyte preparations. In addition to providing a simple means for producing IL-2 containing conditioned medium without the presence of contaminating lectin, we hope that constitutive IL-2 producer hybrid cell lines will prove interesting as vehicles for dissection of the molecular events involved in IL-2 biosynthesis.
Functional analysis of human T cell subsets defined by monoclonal antibodies. II. Collaborative T-T interactions in the generation of TNP-altered-self-reactive cytotoxic T lymphocytes.
Authors: Friedman S M , Hunter S B , Irigoyen O H , Kung P C , Goldstein G , Chess L 
Published: December 2022

Abstract
In previous reports we have demonstrated that human T cells, responding to soluble and alloantigens, release helper factor(s) that amplify primary in vitro hapten-altered-self-reactive CTL responses. In the present studies, we have employed complement-fixing monoclonal antibodies (OKT4 and OKT8) that recognize functionally distinct human T cell subsets to investigate the role of T-T interaction in the generation of these killer cells. In all experiments, purified OKT4+ responder T cells were deficient in cytotoxic activity, whereas responder populations containing OKT8+ T cells generated substantial cytotoxicity; demonstrating that TNP-altered-self-reactive CTL precursors are contained within the OKT8+ T cell subset. Further, optimal cytotoxic responses were obtained from responder populations containing both OKT4+ and OKT8+ T cells, suggesting that cooperative interaction between these subsets may result in an amplification of killer cell activity. This interpretation was supported by the following observations: (1) the amplifying effect of soluble antigen required the presence of both OKT4+ and OKT8+ responders; (2) during MLC, OKT4+ but not OKT8+ responder T cells generate helper factor(s) that amplify TNP-altered-self-reactive CTL responses; (3) helper factor(s) bypass the requirement for direct OKT4-OKT8 T cell interaction, triggering a CTL response that is proportional to the percentage of OKT8+ T cells present within the responder population. In additional studies, we determined that the TNP-altered-self-reactive effector CTL maintain the OKT3+, OKT4-, OKT8+ surface phenotype displayed by the CTL precursor.
Comparison of pyrimidine and purine nucleoside secretion and nucleoside kinase expression in resident and elicited peritoneal macrophages.
Authors: Stadecker M J 
Published: December 2022

Abstract
Thymidine was found in culture supernatants from both normal peritoneal macrophages and macrophages elicited in vivo with LPS under conditions in which there was no detectable TK activity. Abrogation of thymidine secretion was observed only when elicited macrophages were cultured in the presence of macrophage growth factor (MGF), whereas resident macrophages continued secreting under similar conditions. Similarly, TK activity was induced with MGF only in elicited, but not in resident, macrophages; LPS added in vitro failed to render resident macrophages susceptible to stimulation by MGF. Tests for adenosine and deoxyadenosine in macrophage supernatants proved that these nucleosides were not secreted by these cells. Although AK was consistently expressed in both resident and elicited macrophages, no significant dAK levels could be detected in either cell population. In contrast to TK, both purine nucleoside kinases could not be modulated or induced with MGF. The data indicate different reactivity to MGF by resident and elicited macrophages and a difference in pyrimidine vs purine nucleoside secretion as well as nucleoside kinase expression by these cells.
Mechanisms of contraction induced by partially purified slow reacting substance from human polymorphonuclear leukocytes and leukotriene D in guinea pig ileal smooth muscle.
Authors: Findlay S R , Lichtenstein L M , Siegel H , Triggle D J 
Published: December 2022

Abstract
On the basis of the experiments described here, we suggest that the mechanism of action of SRS in guinea pig ileal longitudinal muscle is very similar to that used by other agonists in this preparation, namely interactions at a specific receptor to activate Ca++ channels leading to Ca++ influx and mechanical response. SRS responses differ in 1 important respect from those produced by other agonists. SRS and leukotriene D cause the generation of a slower contraction, which has a greater resistance to reversal by washing. The basis for this unique and prolonged duration of action is unknown but may represent an exceptionally tight, or even irreversible, association with a membrane component. Current studies on the structure of SRS may be helpful in this regard. Although not definitive, this report clearly indicates that a SRS "receptor" is, in fact, present on smooth muscle and that it utilizes a pool of calcium channels common to all smooth muscle agonists.
T lymphocyte-mediated cytotoxicity against autologous EBV-genome-bearing B cells.
Authors: Tsoukas C D , Fox R I , Slovin S F , Carson D A , Pellegrino M , Fong S , Pasquali J L , Ferrone S , Kung P , Vaughan J H 
Published: December 2022

Abstract
We have stimulated human peripheral blood lymphocytes in vitro with autologous EBV-infected or noninfected B cells. A cytotoxic response was obtained only when virally infected cells were used. The activity of the effector cells was restricted by the major histocompatibility complex and was directed against EBV-genome-bearing targets. The highest cytolytic response was obtained when lymphocytes of individuals previously exposed to the virus (EBV-VCA positive) were used. Lymphocytes of noninfected donors (EBV-VCA negative) gave a low response; the relative frequency of their effector cells was at least 4-fold lower. Lymphocytes of newborns did not respond. The cytotoxic activity was mediated by T lymphocytes of the cytotoxic/suppressor subset, as determined by cytofluorographic analysis and antibody plus complement-mediated lysis, using monoclonal antibodies to human lymphocyte surface antigen.
Cell-mediated cytotoxicity to non-MHC alloantigens on mouse epidermal cells. III. Epidermal cell-specific cytotoxic T lymphocytes.
Authors: Tyler J D , Steinmuller D 
Published: December 2022

Abstract
We have previously shown that murine epidermal cells (EC) from 5 H-2 compatible donor strains induce cytotoxic T lymphocytes (CTL) in C3H hosts that preferentially lyse donor EC as opposed to donor lymphoid cells (LC). This preference has been shown to be dependent on a single alloantigen disparity, designated epidermal alloantigen (Epa). In this report we studied the specificity of the CTL to determine whether Epa-antigens are in fact EC specific. Two populations of CTL could be identified by cross-immunization, cold-target inhibition, antigen-driven suicide, and limiting-dilution analyses. A minor CTL population recognizes alloantigens that are expressed by both EC and LC, but this population is necessary only for lysis of LC targets. The major CTL population is specific for Epa-antigens and reacts only with EC targets. At the induction phase of CTL responses, donor LC stimulators can weakly stimulate Epa-specific CTL, indicating LC populations express Epa-antigens in immunogenic form but at very low levels compared with EC. The preferential lysis of EC targets in these strain combinations can be attributed to the major Epa-specific CTL population, whereas lysis of LC targets is due to CTL specific for other alloantigens that are shared by EC and LC. The identification of CTL-activating, EC-specific alloantigens may help to explain the extreme immunogenicity of MHC compatible skin allografts.
Evidence for IgE-dependent cytotoxicity by rat eosinophils.
Authors: Capron M , Bazin H , Joseph M , Capron A 
Published: December 2022

Abstract
Human and rodent eosinophils have been shown previously to act as effector cells against Schistosoma mansoni schistosomula by ADCC mechanisms involving IgG antibodies. The present work brings novel evidence for the existence in rat schistosomiasis of an IgE-eosinophil dependent cytotoxicity mechanism. The role of IgE antibodies present in the rat serum after 6 weeks of infection was clearly established by immunoadsorption and inhibition experiments, whereas the participation of IgG and complement in this system could be ruled out. Mast cell products, including ECF-A tetrapeptides, appear to play an essential role in significantly increasing eosinophil cytotoxicity. A kinetic study of the IgG-dependent cytotoxicity mechanism previously described and of this IgE-mediated mechanism according to rat schistosomiasis revealed the preeminent role played by IgG antibodies in early infection, whereas IgE predominated after 6 wk of infection. The possible significance of IgE-eosinophil cooperation in ADCC mechanisms in parasite and nonparasite models is discussed.
Complement does not facilitate plasmodial infections.
Authors: Ward P A , Sterzel R B , Lucia H L , Campbell G H , Jack R M 
Published: December 2022

Abstract
The influence of the complement (C) system on Plasmodial infections in vivo (Plasmodium berghei in rats) and in vitro (Plasmodium falciparum) has been determined. In rats C3 depletion by treatment of animals with the C3 inactivator isolated from cobra venom factor results in infection that develops more rapidly, reaches a higher peak of parasitemia and is associated with an increased mortality rate (60%), in contrast to a lower degree of parasitemia and lack of mortality in C3-intact rats. The infection of human red cells by P. falciparum is not affected when serum C is inactivated either by heat treatment or by incubation with preformed immune complexes. Furthermore, human sera genetically deficient in C2, C3, C4, or C5 are as effective in facilitating the infection of red cells as is C-intact serum. These data suggest that, in contrast to Babesia sp., the in vitro or the in vivo infection of red cells by Plasmodium sp is not facilitated by the availability of C.
Characterization of genetic defects in macrophage tumoricidal capacity: identification of murine strains with abnormalities in secretion of cytolytic factors and ability to bind neoplastic targets.
Authors: Adams D O , Marino P A , Meltzer M S 
Published: December 2022

Abstract
Peritoneal macrophages from BCG-infected C3H/HeJ or A/J mice, in contrast to BCG-activated macrophages from C3H/HeN mice, were ineffective at lysing adherent 1023 sarcoma targets, nonadherent P815 mastocytoma targets, or nonadherent EL-4 lymphoma targets. The ability of macrophages from BCG-infected C3H/HeJ mice to secret cytolytic factor (CF) into the supernatant medium was markedly impaired. This secretory deficit, however, did not extend to plasminogen activator, secretion of which was augmented. In contrast, the ability of BCG macrophages from A/J mice to secrete CF was comparable to or even slightly higher than that of macrophages from C3H/HeN mice. The ability of BCG-elicited macrophages from A/J mice to bind either of 2 neoplastic targets (the P815 mastocytoma and the EL-4 lymphoma), however, was greatly reduced. The ability of BCG-elicited macrophages from C3H/HeJ mice to bind these targets was comparable to that of macrophages from C3H/HeN mice. The data suggest that the phenotypically-similar deficits in tumoricidal capacity of BCG-elicited macrophages from C3H/HeJ and A/J mice are mediated by mechanistically different defects in macrophage-tumor cell interactions.
Serum-mediated suppression of nonspecific B cell activation. I. Description of an inhibitory capacity in normal mouse serum and characterization of the inhibitory component.
Authors: Walker S M , Sturtevant J E , Weigle W O 
Published: December 2022

Abstract
Normal mouse serum (NMS) in relatively small amounts was demonstrated to inhibit in vitro splenic B cell activation by several B cell mitogens, polyclonal activators, and T-independent antigens. Proliferative and polyclonal responses elicited by bacterial endotoxin (ET), PPD, or Fc fragment of Ig were suppressed routinely 90% or greater when 0.5% homologous NMS was present in the culture medium. Similar suppression of T-independent antibody responses to TNP-ET and TNP-Ficoll was also observed. In contrast, activation by the T cell mitogen, Con A, and a T-dependent antigen response to SRBC was not inhibited by NMS. Suppression of B cell responses by NMS was not dependent on T cells. Preliminary characterization of NMS-In revealed a m.w. of approximately 200,000, an isoelectric point of 5, and solubility in 40% saturated ammonium sulfate. Both functionally and physically, NMS-In appears to be different from other currently relatively well characterized regulatory substances in serum. NMS-In was found in plasma as well as in serum, suggesting that NMS-In may function naturally in vivo to minimize nonspecific activation of B cells.