bluuebunny/crossref_metadata_2025_split huggingface dataset:
Characterization of the accessory cells involved in suppressor T cell induction.
Authors: Noma T , Usui M , Dorf M E 
Published: December 2022

Abstract
The ability of UV-treated splenic adherent cells (SAC) to induce T cell-mediated immunity and suppressor T cells was analyzed in the 4-hydroxy-3-nitrophenyl acetyl (NP) system. UV irradiation of 0.88 KJ/m2 decreased the capacity of NP-coupled SAC to induce delayed-type hypersensitivity (DTH) responses by about 50%. The ability of uncoupled UV-treated SAC to induce allogeneic DTH response was also imparied, indicating that UV-treated SAC are inefficient at inducing DTH in these systems. TS1 induction by UV-treated NP-SAC was evaluated TS1 induction by UV-treated NP-SAC was evaluated by using adherent cells that were subjected to the same dose of UV irradiation that impaired DTH induction. Intravenous administration of 10(3) or 10(4) UV-treated NP-coupled SAC induced TS1 cells with the same efficiency as non-UV-irradiated cells. The TS1 cells induced in this fashion were antigen specific. Furthermore, to establish that the antigen was not reprocessed by the host, I-J-mismatched, UV-treated NP-SAC were unable to induce TS1 cells. The population of antigen-presenting cells responsible for TS1 induction appear to express both I-A and I-J determinants. TS2 induction by UV-treated accessory cells was also analyzed. TSF1 inducer suppressor factor was pulsed onto graded numbers of either normal or UV-treated adherent cells. The same levels of antigen-specific suppression were induced with normal and UV-treated cells. Finally, TS3 induction by UV-treated NP-SAC was analyzed. UV-treated and normal NP-SAC (3 X 10(3] induced antigen-specific suppression of NP DTH responses. I-J-mismatched, UV-treated NP-SAC failed to induce suppression, suggesting that the hapten was not reprocessed by the host under these experimental conditions. The accessory cell population responsible for TS3 induction appears to express both I-A and I-J determinants. Thus, there are at least two functional distinctions between the antigen-presenting cells that induce immunity vs those that induce suppressor cells. First, UV treatment selectively impairs the antigen-presenting cells, which activate the positive limb of the immune response. Second, I-J determinants appear to be specifically associated with the SAC, which induce suppressor T cells. Although these criteria can be used to distinguish the accessory cells involved in suppressor cell pathways from those controlling helper T cell induction, there were no discernible phenotypic differences among the accessory cells that induce the TS1, TS2, and TS3 subsets.
Elimination of terminal complement intermediates from the plasma membrane of nucleated cells: the rate of disappearance differs for cells carrying C5b-7 or C5b-8 or a mixture of C5b-8 with a limited number of C5b-9.
Authors: Carney D F , Koski C L , Shin M L 
Published: December 2022

Abstract
We have previously shown that multiple complement (C) channels are required for lysis of a nucleated cell in contrast to the single channel requirement for erythrocytes. To further investigate this multichannel requirement for nucleated cells, we examined the stability of terminal C complexes in the plasma membrane of Ehrlich ascites tumor cells. Ehrlich cells bearing C5b-7 or C5b-8 with or without C9 were incubated at 37 degrees C or 0 degree C for various time intervals before converting the remaining complexes to lytic C5b-9 channels. C5b-7, C5b-8, and C5b-8 in the presence of a limited number of C5b-9 complexes disappeared functionally from the plasma membrane at 37 degrees C, with initial half-lives of 31, 20, and 10 min, respectively. Disappearance of these complexes did not occur at 0 degree C, nor did disappearance occur at 37 degrees C when formed on sheep erythrocytes. The fate of C5b-8 complexes on the surface of Ehrlich cells was traced with colloidal gold particles bound to C5 determinants on C5b-8 with the use of immunoelectron microscopy. Colloidal gold could be seen on the cell surface after specific binding to cells carrying C5b-8 sites at 0 degree C. After incubating these cells at 37 degrees C, gold particles were internalized into the cell continuously via endocytic vesicles. It is postulated that terminal C complexes may stimulate or accelerate the removal of these complexes from the cell surface.
Effector mechanism of host resistance in murine giardiasis: specific IgG and IgA cell-mediated toxicity.
Authors: Kaplan B S , Uni S , Aikawa M , Mahmoud A A 
Published: December 2022

Abstract
The role of specific serum and milk anti-Giardia muris antibodies in mediation of host-effector responses to this enteric pathogen is unknown. We have investigated antibody-dependent cell-parasite interactions, potentially important as mediators of protection against infection at the mucosal surface. Elicited mouse peritoneal neutrophils and macrophages were incubated with G. muris trophozoites in the presence of either serum or milk antibodies, and their adherence and phagocytosis of the parasites were assessed. The percentage of trophozoites with adherent neutrophils increased significantly in the presence of heat-inactivated immune rabbit serum (93.5% +/- 6.5) and immune mouse milk (54.4% +/- 11.3) and their purified IgG (35.2% +/- 9.7) and secretory IgA fractions (48.0% +/- 12.3) when compared with incubation in RPMI-10% FCS (21.7% +/- 13.9). Similarly, macrophage adherence to trophozoites increased from 49.7% +/- 14.3 in medium alone to respective values of 92.8% +/- 7.1 in immune rabbit serum and 77.3% +/- 11.0 in immune milk. Phagocytosis of parasites by macrophages also was enhanced after incubation in immune rabbit serum (48.0% +/- 4.0) and immune mouse milk (35.0% +/- 5.0) when compared with the percentage of trophozoites ingested when cells and parasites were incubated in RPMI-10% FCS (3.3% +/- 3.0). Transmission electron microscopy showed ingestion of parasites by neutrophils or macrophages after 15 min of incubation. Morphologic evidence of intracellular parasite injury was observed at 6 hr. A decrease in parasite infectivity also resulted when trophozoites were incubated with neutrophils or macrophages and a source of antibodies, and intragastrically fed to weanling mice. These observations show that both antitrophozoite IgG, secretory IgA, and mouse phagocytic cells interact in vitro to promote parasite clearance. Because both the humoral and cellular components of this system are found intraluminally in the small intestine and in milk, they may represent a biologically relevant protective response against giardiasis.
Network regulation of the immune response: modulation of suppressor lymphocytes by alternative signals including contrasuppression.
Authors: Irvine D H , Savageau M A 
Published: December 2022

Abstract
In the preceding paper we demonstrated that comparison of alternative designs for the immune network can be used to examine the functional significance of specified interactions in normal immune responses. In this paper we examine mathematically the functional significance of three interactions affecting the production of suppressor lymphocytes involved in regulation of normal immune responses. The interactions examined in detail are 1) antigenic stimulation of the production of suppressor lymphocytes, 2) idiotypic stimulation of the production of suppressor lymphocytes, and 3) antigenic inhibition of the production of suppressor lymphocytes (i.e., contrasuppression). The results of our analysis suggest that an immune system with only antigenic stimulation of suppressor production is less effective than a system with both antigenic and idiotypic stimulation of suppressor production on the basis of all of the criteria examined in this study. In turn, the latter system is less effective than a system with only idiotypic stimulation of suppressor production. Furthermore, a system with both idiotypic stimulation and antigenic inhibition of suppressor production can be equal or superior to a system with only idiotypic stimulation of suppressor production on the basis of the same criteria. Similar conclusions hold for the comparison of systems in which regulation by the suppressor lymphocytes of interest is exerted upon production of effector molecules rather than upon production of effector lymphocytes, and also for the comparison of systems in which interactions affecting the production of suppressor factors are of interest.
Modulation of cytolytic T cell function by lectins.
Authors: Toribio M L , de la Hera A , Pereira P , de Landázuri M O 
Published: December 2022

Abstract
Human thymocytes cultured for 5 days in interleukin 2 containing supernatants (IL 2 Sup) virtually become a population of mature T cells (T3+, HTA-) that acquires strong cytotoxic activity against NK-sensitive and NK-resistant target cells. The addition of different lectins to the cultures abrogated the expression of the cytotoxic activity and enhanced thymocyte proliferation. The modulation of this cytotoxic activity by lectins has the following properties: a) inhibition of cytotoxicity is related to the concentration of lectins added, but does not correlate with their mitogenic properties, because either strong mitogens such as PHA or weak mitogens such as wheat germ agglutinin (WGA) are both able to strongly decrease cytotoxicity; b) lectin presence is not required at the onset of the culture but is required during the last 24 hr of the 5-day incubation period; c) reversion of inhibition with full expression of cytotoxic activity can be obtained after removal of the lectin and subsequent culture in lectin-free conditions for at least an 18 to 24 hr period; d) lack of cytotoxicity is observed regardless of target cell specificities and cannot be overcome in a lectin-dependent cytotoxicity assay (LDCC); and e) abrogation of cytotoxicity is not restricted to thymocyte cultures because it can also be observed in peripheral lymphocytes. These results cannot be explained by a simple steric blockade, the overgrowth of a distinctive noncytotoxic lymphocyte population, autologous killing, or a failure in the recognition phase of the lytic event. Modulation by lectins of function-associated cell surface structures implicated in cytolysis is discussed as an alternative hypothesis that might account for the observed phenomenon.
Cellular requirements for the generation of primary cell-mediated lympholysis responses to Qa-1 antigens.
Authors: Huston D P , Jenkins R N , Gresens S E , Smith R , Rich R R 
Published: December 2022

Abstract
Mixed leukocyte cultures (MLC) between NZB responder spleen cells and Qa-1-disparate stimulator spleen cells were employed to determine the cellular requirements for the generation of primary anti-Qa-1 cell-mediated lympholysis (CML) responses. Although primary anti-Qa-1 cytotoxic lymphocytes (CTL) were generated during H-2-homologous stimulation, anti-Qa-1 CTL were not detectable from MLC in which the stimulators were H-2 allogeneic. Anti-Qa-1 CTL also were not generated from MLC in which the stimulators were semiallogeneic. Thus, H-2 identity between responder and stimulator cells was not sufficient to permit the generation of primary anti-Qa-1 CTL when H-2 disparity was also present. The capacity for H-2 disparity to prevent anti-Qa-1 CML responses was further demonstrated in MLC containing both H-2-allogeneic and H-2-homologous stimulator cells. Therefore, in subsequent studies we employed NZB responders and H-2-homologous, Qa-1-disparate stimulators. When various subpopulations of stimulator cells were studied for their ability to induce anti-Qa-1 CTL, nylon wool-adherent cells were found to be potent stimulators, but nylon wool-nonadherent cells were not. Furthermore, depletion of macrophages from the stimulator population abrogated the generation of anti-Qa-1 CML responses, despite the presence of responder macrophages in the culture. In contrast, all fractionated subpopulations stimulated anti-H-2 CML responses. When macrophage-enriched cells were used as stimulators, anti-Qa-1 CTL could be generated with approximately 80-fold fewer stimulator cells than when unfractionated splenocytes were used as stimulators. These findings indicated that stimulator macrophages were essential for the generation of primary anti-Qa-1 CTL. Direct evidence for macrophage expression of Qa-1-antigens was obtained by using a Qa-1b-specific CTL clone. These studies provide i) the first evidence for Qa-1 expression on macrophages, ii) a basis for comparison of the cellular interactions necessary to generate CTL against H-2K/D-encoded vs Qa-1-encoded class 1 antigens, and iii) a model for investigating the mechanisms responsible for the immunodominance of H-2K/D alloantigens.
Maturation of B cell subpopulations responding to phosphorylcholine.
Authors: Smyk S , Kohler H 
Published: December 2022

Abstract
In this study, the order of appearance of B cell precursors responding to different phosphorylcholine (PC) antigens was investigated. Cells from neonatal BALB/c mice were transferred to male (CBA/N X BALB/c)F1 immunodeficient mice, and splenic fragment cultures were set up at different times after transfer. Because Xid F1 mice are unable to mount a primary anti-PC response, the time to prepare fragment cultures after cell transfer could be prolonged. This created an expanded maturation effect in which small differences in the response pattern of different precursor subsets are amplified. Splenic fragment cultures containing neonatal precursors were immunized with PG-TGG-HY (TD antigen), PnC (TI-2 antigen), or PC-TGG-LPS (TI-1 antigen), or with combinations of these antigens. The in vitro responses to these antigens were found to be additive, indicating the existence of different subpopulations. The detected precursors were also analyzed with respect to the T15 idiotype, which is the normally dominant idiotype of the response against PC in BALB/c mice. The analysis demonstrated a distinctly different maturation sequence of the three B cell subsets in which the order of appearance is: TI-1, TD, and TI-2 responding precursors. The T15 idiotype is expressed dominantly in all stages except the early stage of the TI-1 precursors.
Pronase treatment of lymphocytes reduces the time required for onset of S phase in response to anti-immunoglobulin.
Authors: Kern M 
Published: December 2022

Abstract
Murine B lymphocytes in the presence of antibody specific for surface membrane immunoglobulin begin to synthesize DNA at about the 36th hr of culture, although the onset of synthesis in response to other B cell-reactive mitogens occurs at approximately 18 hr. In contrast, the onset of DNA synthesis by Pronase-treated cells in response to anti-immunoglobulin required only 18 hr. This earlier onset of S phase was not observed when Pronase treatment was performed in the presence of ovalbumin or the protease inhibitors phenylmethylsulfonyl fluoride or aprotinin. It is unlikely that simple carryover of Pronase from the treatment procedure to the cell culture process was involved, because Pronase treatment for 1 hr at 3 degrees C rather than at 37 degrees C did not result in early onset of DNA synthesis. Cells treated with Pronase and then with mitomycin C to irreversibly inhibit their capacity to synthesize DNA were incapable of inducing early onset of S phase on co-culture with untreated cells, suggesting that Pronase may act directly on B cells rather than indirectly via other cells in the splenocyte population.
Characterization of T cell lines and clones from SJL/J and (BALB/c x SJL/J)F1 mice specific for myelin basic protein.
Authors: Trotter J , Sriram S , Rassenti L , Chou C H , Fritz R B , Steinman L 
Published: December 2022

Abstract
Lines of thymus-derived lymphocytes reactive against bovine myelin basic protein (BP) were established in vitro from SJL/J mice. These lines are stable in long-term culture and mediate inflammatory central nervous system (CNS) lesions and a low incidence of clinical experimental allergic encephalomyelitis (EAE) when injected into recipient SJL/J mice. The line cells proliferate in response to BP of bovine, rat, or mouse origin. Clones were derived from these lines, and the characteristics of these clones were analyzed. The clones express Thy-1, Ly-1, and L3T4 antigens and are negative for Ly-T2. The clones all proliferate in response to bovine BP, with different clones showing varying degrees of cross-reactivity between bovine, rat, and mouse BP. The proliferative response is MHC-restricted; antigen-presenting cells from I-As strains are required. Compatible with their phenotype as helper cells, some of the clones will provide help to primed B cells stimulating antibody production in an in vitro assay. When injected into recipients pretreated with pertussis and irradiation, clones that showed proliferation to mouse BP induced the development of inflammatory lesions in the CNS, with mortality of 28% of the recipients. T cell lines were also established in (BALB/c x SJL/J)F1 mice. In contrast to the homozygous SJL/J lines, these lines were highly encephalitogenic, inducing a high incidence of clinical and histologic EAE when injected in vivo.
Structural and functional characterization of IL 2 receptors on activated human B cells.
Authors: Boyd A W , Fisher D C , Fox D A , Schlossman S F , Nadler L M 
Published: December 2022

Abstract
After activation, B cells express the IL 2 receptor as determined by their reactivity with monoclonal anti-IL 2 receptor antibodies. In this report we show that anti-IL 2 receptor antibodies precipitated comparable 60,000 to 65,000 dalton proteins from highly purified B and T cells. Limited peptide mapping suggested that the receptors on B and T cells were identical. Moreover, activated B cells could be induced to proliferate by IL 2, but not to secrete Ig. Anti-IL 2R antibody blocked the effect of IL 2 but not the proliferative response induced by B cell growth factor (BCGF), suggesting independent growth factor receptors. Investigation of the kinetics of the B cell response to growth factor indicated that BCGF acts within 24 hr, whereas IL 2 was virtually devoid of activity for 48 hr. Nevertheless, after 72 to 96 hr, the effect of IL 2 was equal to or greater than that obtained with BCGF. These studies suggest that the initial stages of B cell proliferation involves a sequential interaction of BCGF and IL 2 with their respective receptors.
Induction of interleukin 2 from a murine B cell tumor by a factor found in immune serum.
Authors: Maino V C , Pace D R 
Published: December 2022

Abstract
The murine B cell tumor line 2 PK-3 secretes T cell growth factor activity after incubation for 6 to 48 hr with a factor present in heterologous immune serum. T cell growth factor derived from 2 PK-3 was compared with IL 2 produced by the Con A-induced T lymphoma cell line EL-4 G12. These studies indicated that T cell growth factor activities derived from both cell lines were similar with respect to m.w., pI values, and the ability to support growth of two IL 2-dependent T cell clones. Three preparations of immune sera were found to be active in the induction of IL 2 activity from 2 PK-3 cells, including rabbit anti-mouse brain, rabbit anti-complete Freund's adjuvant, and goat anti-mouse Ig. None of these preparations, however, induced IL 2 from EL-4 G12 cells. It was also observed that LPS synergized with immune serum to produce enhanced activity. Normal sera prepared from unimmunized animals were not active in the induction of IL 2 activity. Fractionation of immune serum on protein A Sepharose suggested that the IL 2-inducing agent is not IgG.
Opposing effects of glucocorticoids on interferon-gamma-induced murine macrophage Fc receptor and Ia antigen expression.
Authors: Warren M K , Vogel S N 
Published: December 2022

Abstract
Two macrophage markers associated with differentiation are the Fc receptor (FcR) and the Ia antigen. Expression of these markers is increased with IFN-gamma treatment, although some evidence suggests that the induction pathway for Fc receptor and Ia antigen expression may be dissociable. In this study, the effect of glucocorticoids on basal and IFN-induced levels of Fc-mediated phagocytosis and Ia antigen expression was investigated. Macrophages incubated for 2 days with glucocorticoids alone showed no change in basal levels of Fc-mediated phagocytosis. However, incubation with glucocorticoids plus IFN-gamma resulted in increased Fc-mediated phagocytosis and binding to a much greater extent than IFN-gamma treatment alone. This enhancement was specific for IFN-gamma, because the IFN-beta-induced increase in Fc-mediated phagocytosis and binding was not affected by glucocorticoids. In contrast to the expression of Fc receptor capacity, both basal and IFN-gamma-induced levels of Ia antigen expression were inhibited by glucocorticoids. The glucocorticoid effect on these two markers was not observed with other steroid hormones, nor was it altered by inhibitors of the arachidonic acid pathway. The findings of this study provide additional evidence that induction of Fc receptor and Ia antigen by IFN-gamma occurs by different mechanisms.
Expression of 20-alpha-hydroxysteroid dehydrogenase in mouse macrophages, hemopoietic cells, and cell lines and its induction by colony-stimulating factors.
Authors: Hapel A J , Osborne J M , Fung M C , Young I G , Allan W , Hume D A 
Published: December 2022

Abstract
The enzyme 20-alpha-hydroxysteroid dehydrogenase (20 alpha SDH) has been proposed as a T lymphocyte marker that is specifically induced by interleukin 3. We have examined the expression of 20 alpha SDH and its relationship to interleukin 3 responsiveness in other hemopoietic lineages. The enzyme is expressed at high levels in the bone marrow of athymic nu/nu mice, but only at low levels in nu/nu spleen and normal adult bone marrow. 20 alpha SDH is induced in nu/nu spleen and in normal fetal liver cells by granulocyte-macrophage colony-stimulating factor (GM-CSF) as well as by interleukin 3. In longer term cultures of fetal liver and adult marrow, macrophage colony-stimulating factor (M-CSF) also induces the enzyme, which is expressed in proliferating adherent macrophages. The high levels of 20 alpha SDH in purified bone marrow-derived macrophages are maintained by M-CSF, GM-CSF, or interleukin 3. Expression of 20 alpha SDH in these cells is associated with resistance to growth inhibition by progesterone. Additional evidence against the restriction of 20 alpha SDH to T lymphocytes is found in its presence in peritoneal macrophages, myelomonocytic and macrophage-like cell lines, and the L929 fibrosarcoma line. We conclude that 20 alpha SDH is a normal enzyme of proliferating hemopoietic cells irrespective of their lineage or growth factor responsiveness.