bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differential requirements for the production by a T helper clone of the lymphokines involved in the induction of polyclonal proliferation and differentiation of unstimulated B lymphocytes.
Authors: Gougeon M L , Leclercq L , Bismuth G , Thèze J 
Published: December 2022

Abstract
Antigen-activated T helper (TH) cells secrete into their supernatant various lymphokines that are able to drive B cells to proliferate and to differentiate into Ig-secreting cells. In this report, we compared the production of these two types of activities by a TH clone. We found that B cell proliferating activity was released by TH cells under conditions in which T cell proliferation and the release of the B cell differentiating activity were totally blocked by anti-L3T4 monoclonal antibody GK1.5. The release of these two activities also dissociated during the reversion of T cells to the resting state after activation with antigen. Two weeks after activation, the T cell clone still secreted B cell proliferating activity, but did not secrete B cell differentiating activity. Three to four weeks after activation, neither activity was produced. The data suggest that the genes coding for these two activities are independently regulated in activated T cells. The implications of these observations concerning B lymphocyte development are discussed.
Lipopolysaccharide receptors on lymphocytes. I. Lack of immunologic recognition of a putative LPS receptor on LPS-responder lymphocytes by LPS-nonresponder mice.
Authors: Goodman S A , Morrison D C 
Published: December 2022

Abstract
We have examined the potential immunogenicity of viable lymphocytes from C3HeB/FeJ responder mice adoptively transferred into congenic nonirradiated C3H/HeJ nonresponder mice. Immunologic rejection or acceptance of donor cells was employed as indirect evidence for the presence or absence of an antigenically distinct "LPS receptor" present on donor lymphocytes. Immunogenicity was evaluated by in vitro assessment of the subsequent proliferative response of recipient splenocytes to protein-free LPS after multiple i.p. injections of responder lymphocytes. Control experiments have made use of syngeneic donor lymphocytes differing immunologically by the presence of the H-Y minor histocompatibility antigen. The results of these experiments provide evidence for the concept that if the phenotypic difference between LPS responder and nonresponder mice is also expressed antigenically in the form of an LPS receptor, that antigenic difference is significantly less immunogenic than a minor histocompatibility antigen.
Carbohydrate determinants associated with carcinoembryonic antigen (CEA).
Authors: Nichols E J , Kannagi R , Hakomori S I , Krantz M J , Fuks A 
Published: December 2022

Abstract
The reactivities of eight purified preparations of carcinoembryonic antigen with monoclonal antibodies directed to tumor-associated carbohydrate determinants have been studied. All eight preparations showed strong reactivities with AH6, which defines Y structure (Fuc alpha 1----2Gal beta 1----4[Fuc alpha 1----3] GlcNAc beta 1----R), whereas only a few preparations showed reactivity with FH4-defining dimeric X determinants, (Gal beta 1----4 [Fuc alpha 1----3]GlcNAc beta 1----3Gal beta 1----4 [Fuc alpha 1----3]GlcNA beta 1----3Gal beta 1----R). No other antibodies tested showed any reactivity with these preparations. These carbohydrate markers associated with carcinoembryonic antigen will be useful to enhance the diagnostic value of the antigen.
Analysis of idiotope variability as a function of distance from the binding site for anti-streptococcal group A carbohydrate antibodies.
Authors: Greenspan N S , Davie J M 
Published: December 2022

Abstract
We have extended our analysis of rat monoclonal anti-idiotopes (anti-Id) specific for previously mapped binding site-associated (distal) and less-or nonbinding site-associated (proximal) idiotopes on a murine monoclonal anti-streptococcal group A carbohydrate (GAC) antibody. By utilizing other monoclonal anti-GAC antibodies and anti-idiotypic antibodies as radiolabeled probands in both competitive and direct radioimmunoassays, we have detected previously unsuspected reactivities of some of the anti-Id. Although the anti-Id recognizing the most proximal idiotopes manifest relatively narrow ranges of binding strengths for anti-GAC antibodies, the anti-Id recognizing the most distal idiotopes display broader, more continuous distributions of binding strengths. These results suggest that mimicry of antigen structure by anti-Id might best be understood from a quantitative perspective, and that idiotopes intimately associated with binding sites display a broader range of variants than those not associated with binding sites. In addition, for one monoclonal anti-Id recognizing a distal determinant, changing the radiolabeled proband in inhibition radioimmunoassays results in dramatic changes in relative inhibitory efficacies for certain anti-GAC antibody inhibitors. This observation suggests the possibility that this anti-Id represents an example of a multispecific (polyfunctional) anti-idiotypic antibody.
A reevaluation of rabbit anti-allotype antibody for the presence of cross-reactive idiotypes. I. A species-specific idiotype on rabbit anti-a1 antibody is recognized by guinea pig anti-IdX antibody.
Authors: Roux K H , McCormack W T , Dhanarajan P 
Published: December 2022

Abstract
Rabbit reagents previously thought to display specificity for a cross-reactive idiotype on anti-VHa allotype antibody from all tested rabbits have recently been shown to be contaminated with an induced (latent) molecule similar or identical to the original antigen (rabbit a1 or a2 allotype). In an attempt to circumvent this problem, we have immunized guinea pigs with rabbit anti-a1 allotype antibody to produce heterologous anti-idiotype antibody. The resulting guinea pig antibody (GP anti-R IdX) recognizes anti-a1 antibody from each of 17 immunized rabbits, and in four tested samples reacts with 22 to 100% of the molecules. Neither goat nor guinea pig anti-a1 reacts with the guinea pig anti-R IdX antibody, even though the goat, guinea pig, and rabbit anti-a1 Ab all recognize a similar set of a1 determinants. The reaction between IdX-bearing rabbit anti-a1 and guinea pig anti-R IdX is inhibited by the original antigen (a1 IgG), demonstrating that the IdX is at or near the antigen combining site of anti-a1 antibody. Immunoelectron microscopy of immune complexes supports this conclusion and demonstrates that the reactive site on the GP anti-R IdX is at or near its antigen combining site.
A reevaluation of rabbit anti-allotype antibody for the presence of cross-reactive idiotypes. II. Expression of rabbit a1-like images on goat antibody after immunization with anti-a1 antibody.
Authors: Roux K H , McCormack W T , Dhanarajan P 
Published: December 2022

Abstract
In an effort to generate heterologous anti-idiotype (Ab2) molecules to a suspected IdX on rabbit anti-a1 antibody (Ab1), goats were immunized with either rabbit or guinea pig Ab1. The goat Ab2 preparations reacted with each of 13 rabbit Ab1, as well as two goat Ab1 samples in serologic assays. From 8 to 50% of the molecules in purified rabbit Ab1 preparations reacted with each goat Ab2. Electron microscopy of immune complexes composed of rabbit Fab anti-a1 and goat Ab2 reveals that the Fab anti-a1 binds to the side of the variable region of most goat Ab2 molecules, rather than at the tip (i.e. in the CDR) as expected. This configuration indicates that the goat Ab2 actually represents a population of induced or enhanced Ig molecules expressing a1-like allotypic or isotypic determinants, rather than an anti-IdX Ab or a paratope-associated internal image of a1.
Phagocytosis by mouse peritoneal macrophages plated on monoclonal antibody-coated immune complex-substrates: effects of complexes of different IgG subclasses on Fc receptor functions.
Authors: Sung S S 
Published: December 2022

Abstract
Macrophages plated on immune complex-coated substrates of different mouse IgG subclasses were examined for their capacities to phagocytose sheep red blood cells (SRBC) coated with monoclonal antibodies (MAb) of various IgG subclasses. IgG2a-and IgG2b-coated substrates abrogated macrophage phagocytosis of particles coated with any of the four mouse IgG subclasses. These results were confirmed by the use of two MAb of each of the IgG2a and IgG2b subclasses, with one of the MAb specific for dinitrophenyl groups and the others for SRBC. IgG3-coated substrates reduced the macrophage uptake of IgG2a-but not IgG2b-coated particles. Rabbit IgG-coated substrates ablated the uptake of SRBC coated with all mouse IgG subclasses. Resident and thioglycollate-elicited macrophages showed similar phagocytosis reduction when plated on these immune complexes. The phagocytosis of complement-coated particles was not affected by these IgG-coated substrates. Macrophages plated on both IgG2a-and IgG2b-coated substrates showed reduced immunofluorescence staining by an anti-IgG2b Fc receptor (FcR) Ab, 2.4G2 and reduced E(IgG2a) and E(IgG2b) binding. The results show that substrates coated with various IgG subclasses can abrogate phagocytosis mediated by FcR that do not have binding specificity for the substrate-immobilized Fc ligand, and suggest that the three classes of mouse FcR co-modulate.
Effects of various inhibitors of arachidonic acid oxygenation on macrophage superoxide release and tumoricidal activity.
Authors: Schultz R M , Nanda S K , Altom M G 
Published: December 2022

Abstract
Macrophages release a variety of arachidonic acid metabolites after treatment with various membrane triggers or particulate stimuli. We examined the role of phospholipase and lipoxygenase inhibitors in the modulation of superoxide production and tumor cytolysis by murine macrophages. Superoxide was induced by the soluble stimulus, phorbol myristate acetate (PMA), and the particulate stimulus, opsonized zymosan, and was measured by the reduction of ferricytochrome c with the use of a micro ELISA reader. Macrophage-mediated tumor cytolysis was induced by hybridoma-derived, macrophage-activating factor (MAF) and was quantitated by 51Cr release from P815 target cells. In both assays, 72-hr peptone-elicited macrophages were used. Dexamethasone, and to a lesser degree hydrocortisone, inhibited superoxide release and MAF-induced tumor cytolysis. Inhibition in the superoxide assay required pretreatment with corticosteroid. Only the gold compound, auranofin, inhibited superoxide when given simultaneously with stimulant. Other phospholipase inhibitors, including mepacrine and 4-bromophenacyl bromide, and several lipoxygenase inhibitors, including BW755c, nordihydroguaiaretic acid (NDGA), and 5,8,11,14-eicosatetraynoic acid (ETYA), failed to modulate either macrophage response at nontoxic concentrations. At the concentrations tested in the tumoricidal and superoxide assays, mepacrine and 4-bromophenacyl bromide inhibited the release of 14C-arachidonic acid from macrophages stimulated with opsonized zymosan. Our data strongly suggest that corticosteroids suppress macrophage superoxide production and tumoricidal function by a nonphospholipase-dependent mechanism.
Macrophage colony-stimulating factor (M-CSF) enhances the capacity of murine macrophages to secrete oxygen reduction products.
Authors: Wing E J , Ampel N M , Waheed A , Shadduck R K 
Published: December 2022

Abstract
The capacity of macrophage colony-stimulating factor (M-CSF) to enhance respiratory burst activity in peritoneal macrophages was measured. Macrophages incubated for 48 hr or more with concentrated L cell-conditioned medium as a source of M-CSF released two to three times as much O2- in response to PMA as did unexposed macrophages. Stimulation was noted at concentrations of colony-stimulating activity from 0.1 to 2000 U/ml and was maximal at 10 to 100 U/ml. Purified, endotoxin-free CSF enhanced secretion to a similar degree as unpurified L cell-conditioned medium. Release of O2- by M-CSF macrophages occurred over 60 min and was triggered by opsonized zymosan as well as PMA. H2O2 release was also enhanced in macrophages exposed to both unpurified and purified M-CSF. These data indicate that M-CSF enhances the capacity of mature macrophages to release oxygen reduction products, and they are consistent with reports that CSF can stimulate the release of other secretory products.
Phorbol myristate acetate mediates redistribution of protein kinase C in human neutrophils: potential role in the activation of the respiratory burst enzyme.
Authors: Wolfson M , McPhail L C , Nasrallah V N , Snyderman R 
Published: December 2022

Abstract
Protein kinase C may be important in leukocyte function, because it is activated by phorbol myristate acetate (PMA), a potent stimulus of the respiratory burst in neutrophils. The localization of protein kinase C was compared in unstimulated and PMA-stimulated human neutrophils. Protein kinase C was primarily cytosolic in unstimulated cells but became associated with the particulate fraction after treatment of cells with PMA. The particulate-associated kinase activity did not require added calcium and lipids, but when extracted by Triton X-100 (greater than or equal to 0.2%), calcium and phospholipid dependence could be demonstrated. The EC50 of PMA for stimulating kinase redistribution and activation of NADPH oxidase, the respiratory burst enzyme, were similar (30 to 40 nM). Redistribution of protein kinase C occurred rapidly (no lag) and preceded NADPH oxidase activation (30 sec lag). These results suggest that redistribution of protein kinase C is linked to activation of the respiratory burst in human neutrophils.
Human lymphocyte responses to hepatitis A virus-infected cells: interferon production and lysis of infected cells.
Authors: Kurane I , Binn L N , Bancroft W H , Ennis F A 
Published: December 2022

Abstract
Peripheral blood mononuclear cells (PBMC) from nonimmune healthy donors who did not have antibody to hepatitis A virus lysed hepatitis A virus-infected BS-C-1 cells to a greater degree than uninfected BS-C-1 cells. The predominant effector cells were contained in the nonadherent peripheral blood lymphocyte (PBL) fraction, although some lytic activity was associated with adherent cells. Characterization of the PBL with monoclonal antibodies showed that the responsible effector lymphocytes were contained in Leu-11+ and M1+ subsets, but not in the T3+ or T4+ subsets. The phenotypes of the effector cells active in the lysis of hepatitis A virus-infected cells are similar to those of human natural killer cells that lyse K562 cells. Human PBL produced high titers of interferon-alpha (IFN-alpha) when exposed to hepatitis A virus-infected cells. These results imply that hepatitis A virus infection may be controlled by lymphocyte responses in the liver, i.e., by lymphocyte-mediated lysis of the hepatitis A virus-infected cells, and by the production of high titers of IFN-alpha by lymphocytes exposed to hepatitis A virus-infected cells. Furthermore, these results, along with the observations that hepatitis A virus infection results in a persistent noncytocidal infection in vitro, support the hypothesis that lysis of hepatocytes infected with hepatitis A virus is by lymphocyte-mediated cytotoxicity and not by virus-induced destruction of the liver cell.
Studies on macrophage-activating factor (MAF) in antitumor immune responses. I. Tumor-specific Lyt-1+2- T cells are required for producing MAF able to generate cytolytic as well as cytostatic macrophages.
Authors: Nakajima H , Fujiwara H , Takai Y , Izumi Y , Sano S , Tsuchida T , Hamaoka T 
Published: December 2022

Abstract
In the present study we investigated some of the cellular mechanisms for the generation of macrophage-activating factor(s) (MAF) in immune responses to tumor antigens. C3H/HeN mice were immunized to syngeneic MH134 hepatoma or MCH-1-A1 fibrosarcoma by intradermal inoculation of viable tumor cells, followed by the surgical resection of the tumor. Spleen and lymph node cells from these tumor-immune mice were stimulated in vitro with the corresponding tumor cells, and supernatant from such a culture was tested for an ability to activate macrophages to exert their cytostatic and cytolytic activities as detected on tumor cells unrelated to immunizing tumors. Peritoneal adherent cells as a macrophage source, which were preincubated with supernatant from co-culture of tumor-unimmunized normal spleen and lymph node cells plus tumor cells, failed to exhibit any significant antitumor effect on unrelated X5563 tumor cells, whereas the addition of supernatant from cultures containing immune lymphocytes to adherent cells resulted in appreciably potent cytostatic and cytolytic effects on X5563 tumor cells, indicating the generation of MAF in culture supernatant. The activation of tumor-immune spleen and lymph node cells for MAF generation was tumor-specific, because anti-MH134- and anti-MCH-1-A1-immune lymphocytes produced MAF by the stimulation with the respective but not with the other alternative tumor cells. Such MAF production was abolished by treatment of tumor-immune spleen and lymph node cells with anti-Thy-1.2 or anti-Lyt-1.1 but not with anti-Lyt-2.1 antibody plus complement before culturing. These results indicate that the tumor-specific Lyt-1+2- T cell subset has a crucial role in generating MAF by which an adherent cell population as a source of macrophages acquires the potential for inducing a cytolytic as well as a cytostatic effect on tumor cells.
The events of primary T cell activation can be staged by use of Sepharose-bound anti-T3 (64.1) monoclonal antibody and purified interleukin 1.
Authors: Williams J M , Deloria D , Hansen J A , Dinarello C A , Loertscher R , Shapiro H M , Strom T B 
Published: December 2022

Abstract
A mitogenic anti-CD3 ("T3") monoclonal antibody (64.1), that stimulates polyclonal T cell activation by a mechanism believed to be similar to antigen via binding to the T cell receptor complex, was utilized in soluble (SOL) and Sepharose-bound (SEPH) forms to dissect the role of accessory cells (AC) and interleukin 1 (IL 1) in supporting T cell activation. The T cell activation pathway was dissected into "early" events including expression of interleukin 2 receptors (IL 2R), increased RNA content, IL 2 release, and "late" (DNA synthesis) events. Unseparated peripheral blood mononuclear cells progressed through all stages of activation when stimulated by either form of 64.1. Stringent AC depletion by plastic adherence, nylon wool adherence, and L-leucine methyl ester (selectively lyses AC) prevented early and late T cell responses to either form of 64.1. The addition of highly purified IL 1 replenished both early and late T cell responses to SEPH-64.1 but not to SOL-64.1. Although SOL-64.1 stimulation of purified T cells induced modulation of the CD3 complex, only SEPH-64.1 induced IL 1 responsiveness, and exogenous IL 1 was then able to support synthesis of RNA, secretion of IL 2, expression of IL 2R, and ultimately, DNA synthesis. Therefore, the stages of early T cell activation owing to stimulation of the CD3-T cell receptor complex and IL 1 responsiveness have been dissected.
Calcium ionophore plus phorbol ester can substitute for antigen in the induction of cytolytic T lymphocytes from specifically primed precursors.
Authors: Truneh A , Albert F , Golstein P , Schmitt-Verhulst A M 
Published: December 2022

Abstract
Previous studies indicated that Ca++ ionophores and phorbol esters in synergy could substitute for the initial activation step of normal T lymphocytes or T cell clones leading to increased expression of receptors for the growth factor interleukin 2 (IL 2) and secretion of interleukins, with the mitogenic signal for T cell proliferation being dependent on the presence of IL 2. In this study, the question was addressed as to whether T lymphocytes activated through the Ca++ ionophore ionomycin and the phorbol ester 12-o-tetradecanoyl phorbol 3-acetate (TPA) also acquired the competence to kill relevant target cells. The results indicate that T lymphocytes from primed mice proliferate and lyse the relevant allogeneic target cells after in vitro stimulation with ionomycin plus TPA, and that T lymphocyte preparations enriched for a subpopulation bearing the Lyt-2 marker are dependent on exogeneous sources of IL 2 to proliferate and become competent killer cells, whereas preparations enriched for subpopulations bearing the L3T4 marker grow independently of exogenous IL 2.
Physiology of IgD. V. Enhancement of antibody responses in vivo by allo anti-IgD is due primarily to an indirect effect on B cells.
Authors: Jacobson E B , Xue B , O'Neil M A , Siskind G W , Pernis B , Thorbecke G J 
Published: December 2022

Abstract
Although responses of BALB/c mice to TNP-Ficoll or TNP-Brucella abortus are usually decreased by injection of allo anti-IgD (anti-Igh-5a) given 1 day before antigen, increased responses are obtained if a lymphokine mixture (SN) containing IL 2 is also injected. Simultaneous injection of anti-IgD and SN 4 days after priming with TNP-KLH induces an increase in antibody production similar to that induced by a second antigen injection. Injected together with a second injection of TNP-KLH at that time, anti-IgD and SN cause a synergistic enhancement of the secondary response. In allotype heterozygous (BALB/c X SJL)F1 mice injected with anti-IgD directed against one allotype, this enhancement of the secondary response is seen predominantly in the alternate allotype, because the IgG response of linked allotype specificity is slightly suppressed by the anti-IgD alone and is less enhanced than the alternate allotype by anti-IgD plus SN. Cells from unprimed heterozygous mice, incubated with anti-Igh-5a in vitro and transferred, together with antigen, to TNP-KLH-primed recipients, cause a much greater enhancement of the IgG responses of the Igb than of the Iga allotype in recipients. If, however, SN is also injected into the recipients, the anti-TNP response of both IgG allotypes is greatly enhanced.
B lymphocyte production in the bone marrow of mice with X-linked immunodeficiency (xid).
Authors: Reid G K , Osmond D G 
Published: December 2022

Abstract
CBA/N mice carry an X-linked recessive immunodeficiency (xid) gene manifested by the absence of a B lymphocyte subpopulation, but the manner in which the xid gene exerts its effect on B lymphocyte development is unknown. The production of B lymphocytes in the bone marrow of CBA/N mice has now been compared with that of normal CBA/J mice by using two in vivo assays: immunofluorescence stathmokinetic studies measured pre-B cell proliferation, whereas radioautographic [3H]thymidine labeling was used to evaluate small lymphocyte turnover. Although the total cellularity of CBA/N mouse bone marrow was greater than normal, the absolute number of marrow small lymphocytes, pre-B cells, and B lymphocytes were all similar to those in CBA/J controls. Furthermore, in the bone marrow of CBA/N mice, the proliferation rate of pre-B cells, calculated from their rate of entry into mitosis, and the turnover rate of small lymphocytes, derived from their rate of [3H]thymidine labeling, were not significantly different from those seen in nondefective mice. The present findings that pre-B cell proliferation and small lymphocyte production proceed at similar rates in the bone marrow of xid and normal mice suggest that the xid gene does not act at the level of primary B cell genesis in the bone marrow. The findings are in accord with the view that the xid gene produces a maturation block or a functional abnormality among B lymphocytes in the peripheral lymphoid tissues rather than the deletion of a sublineage of B lymphocytes in the bone marrow.