bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transfer of allergic encephalomyelitis with spleen cells from donors sensitized with myelin basic protein in incomplete Freund's adjuvant.
Authors: Namikawa T , Richert J R , Driscoll B F , Kies M W , Alvord E C 
Published: December 2022

Abstract
Myelin basic protein (BP) emulsified in incomplete Freund's adjuvant (BP/IFA) is relatively nonencephalitogenic in Lewis rats. Furthermore, repeated injections of BP/IFA prevent subsequent induction of experimental allergic encephalomyelitis (EAE) by BP emulsified in complete Freund's adjuvant (BP/CFA). In spite of this, spleen cells from rats injected repeatedly with BP/IFA transfer EAE after they are cultured with BP almost as effectively as BP/CFA spleen cells. However, unlike the latter, BP/IFA spleen cells do not proliferate in response to BP in culture. Furthermore, BP/IFA spleen cells are unable to transfer EAE after culture with concanavalin A (Con A), in contrast to BP/CFA spleen cells. Both populations of spleen cells undergo a strong proliferative response to Con A in culture. For BP/IFA cells, at least, a proliferative response to BP in vitro is not a prerequisite for enhanced transfer of EAE in Lewis rats.
OT-CLL: a human T cell chronic lymphocytic leukemia that produces IL 2 in high titer.
Authors: Friedman S M , Thompson G , Halper J P , Knowles D M 
Published: December 2022

Abstract
This report identifies and describes a human T cell chronic lymphocytic leukemia, OT-CLL, which can be triggered by selected mitogens (either PHA or Con A) to produce IL 2 in high titer. Optimal IL 2 production requires culturing OT-CLL cells at 2 to 5 X 10(6)/ml for 24 hr in the presence of 1 to 2% PHA-M. Under these conditions, the titer of IL 2 generated is greater than 20-fold that obtained from conventional sources, e.g., from mitogen-activated tonsillar lymphocytes. Two lines of experimental evidence suggest that the tumor cell product(s) is IL 2. First, in functional assays, suprenatants derived from cultures of PHA-activated OT-CLL cells trigger the proliferation and long-term growth of IL 2-dependent human TCL cells. Second, a partial biochemical purification of the active moiety(ies) derived from OT-CLL demonstrates marked similarity to conventional human IL 2. Thus, the biologically active material(s) precipitates in 50 to 70% saturated (NH4)2 SO4 solutions; elutes from DEAE-Sepharose in the presence of 0.04-0.08 M NaCl; and has an apparent m.w. of approximately 14,000, as determined by Sephadex G-100 gel filtration. In addition, analysis of OT-CLL cells by indirect immunofluorescence, utilizing a panel of monoclonal antibodies, confirms not only that these tumor cells are of T cell lineage but that they display surface antigens that define the normal human peripheral T cell subset subserving helper or inducer function: OKT3+, OKT4+ , OKT8-.
Identification of human CML target. HLA-B locus (B12) antigen variants defined by CTL generated between B locus-identical (B12) responder-stimulator pairs.
Authors: Kato S , Iványi P , Lacko E , Breur B , Du Bois R , Eijsvoogel V P 
Published: December 2022

Abstract
The genetics of human CML targets were studied by seven CTL generated in combinations iun which the responder/stimulator difference was limited to one (or two) HLA-A, -B, or -C antigens. Unstimulated peripheral blood lymphocytes were used as targets. CTL sensitized against antigens A11, Aw31, or B17 lysed all cells bearing the respective target from a large panel of cells from unrelated individuals. Hence, at least one CTL clone was directed against the HLA antigen molecule. However, all CTL also exerted cross-kill to cells not sharing the stimulating HLA antigen. For two CTL, the target of the cross-kill was not clarified. Five CTL were found where the cross-kill was directed against antigen HLA-B12 (Bw44 and Bw45). All these cTL were generated in R/S pairs identical for B locus antigens (Bw44/Bw35 heterozygotes). The individual CTL lysed different parts of the panel of B12-positive target cells. The interpretation is that these CTL detect subtypes of HLA antigens, but alternative possibilities are also considered. Four B12 subtypes are described, tentatively designated as B12-related CML targets. Identification of HLA-B-related CML targets represent CML "typing" of HLA-antigen differences that were not detected serologically. The subtypes can now be tested for their possible functional significance.
Anti-idiotype as antibody against the formyl peptide chemotaxis receptor of the neutrophil.
Authors: Marasco W A , Becker E L 
Published: December 2022

Abstract
Anti-idiotypic antibodies have been produced in mice, guinea pigs, and goat against rabbit antibodies to the chemoattractant f Met-Leu-Phe. The anti-idiotypic antibodies were demonstrated by their capacity in the presence of preimmune rabbit serum to block the binding of 125I anti-f Met-Leu-Phe to f Met-Leu-Phe-human transferrin absorbed to microtiter plates. Goat anti-idiotypic antibodies were further demonstrated by their ability, when absorbed to Staphylococcus aureus, to selectively bind 125I anti-f Met-Leu-Phe. In addition, some of the goat anti-idiotypic IgG was able to bind nearly all rabbit and rat anti-f Met-Leu-Phe antibodies examined. This was shown by 1) the ability of antibodies produced in rabbits immunized with either f Met-Leu-Phe conjugated to goat IgG or f Met-Leu-Phe conjugated to keyhole limpet hemocyanin (KLH) when adsorbed to S. aureus to bind the 125I F(ab')2 goat anti-idiotype, and 2) the ability of various rat anti-f Met-Leu-Phe antibodies to block the binding of 125I rabbit anti-f Met-Leu-Phe to goat anti-idiotype absorbed to S. aureus. Finally, goat anti-idiotypic antibodies can also cross-react with the receptor on the rabbit neutrophil for the formyl peptides as evidenced by 1) the direct binding of goat anti-idiotypic IgG to the PMN, 2) the ability of F(ab')2 fragments to goat anti-idiotype to partially inhibit the binding of f Met-Leu-(3H)Phe to rabbit PMN, and 3) loss of anti-idiotype and anti-PMN receptor activity after passage over an anti-f Met-Leu-Phe column. These data support Jerne's hypothesis of "internal image" and suggest a feasible experimental approach for producing anti-cell receptor antibody without purifying the receptor.
Modulation of the immune response to lipopolysaccharide.
Authors: Hiernaux J R , Baker P J , Delisi C , Rudbach J A 
Published: December 2022

Abstract
Mice given a single optimally immunogenic dose (20 micrograms) of bacterial LPS make an antibody response that is characterized by cyclic (oscillatory) patterns. This kinetic pattern is dose as well as mouse strain dependent. LPS can induce a secondary response in BALB/c mice that is also cyclic, although it differs in amplitude as well as periodicity from a primary response. To rule out the involvement of B cell mitogenic activity of LPS in the expression of such cyclic patterns, the responses produced by both C3H/HeN and C3H/HeJ mice to a single injection of LPS were compared; the latter do not give B cell proliferative responses to LPS and also have been reported to give low LPS-specific responses in vivo. Both strains gave an oscillatory kinetic pattern. By contrast, BALB/c nu/nu mice given an optimal immunogenic dose of LPS (2 micrograms) do not present a cyclic immune response. This indicates that mature T cells are required for the generation of an oscillatory anti-LPS response.
Activation of Fc receptor-bearing lymphocytes by immune complexes. I. Stimulation of lymphokine production by nonadherent human peripheral blood lymphocytes.
Authors: Neville M E , Lischner H W 
Published: December 2022

Abstract
Activation of human peripheral blood lymphocytes by incubation with particulate immune complexes or aggregated human gamma-globulin was studied by measuring the release of leukocyte migration inhibitory factor (LIF) activity. LIF-active supernatants were consistently produced when nonadherent lymphocytes containing less than 1% surface immunoglobulin-bearing cells and less than 0.2% nonspecific esterase-positive monocytes were incubated in the presence of RBC sensitized with rabbit or human antibodies or with pooled heat-aggregated human gamma-globulin. This immune complex-induced lymphokine production (ICLP) was dependent on the presence of cells bearing receptors for the Fc portion of IgG (Fc gamma). ICLP could not be demonstrated with lymphocyte preparations enriched for B cells even though the latter showed vigorous LIF production in the presence of complement-sensitized erythrocytes. ICLP was dependent on the concentration of lymphocytes and of stimulant as well as on the duration of coincubation, and it required active metabolic processes and RNA and protein synthesis but not DNA synthesis. Ca++ but not Mg++ was obligatory. ICLP by non-B Fc gamma receptor-bearing lymphocytes may play a role in antibody-dependent protective inflammation and immunologic injury phenomena, which is similar to that of lymphokine release by antigen-activated T cells in delayed hypersensitivity responses.
Immunotherapy of a chemically-induced sarcoma in rats: characterization of the effector T cell subset and nature of suppression.
Authors: Fernandez-Cruz E , Gilman S C , Feldman J D 
Published: December 2022

Abstract
Chemically-induced sarcomas (BC5), established subcutaneously and growing progressively in BN rats, were completely eliminated by i.v. infusion of syngeneic effector cells. The effector cells were generated from BN spleen cells immune to BC5 in a mixed lymphocyte-tumor cell culture (MLTC). Generation of a high yield of effector cells that were efficacious in eliminating BC5 in vivo necessitated: depletion of macrophages from immune spleen populations, before preparation of MLTC; addition back to MLTC of a small number of macrophages from normal spleens to attain a level of 0.5% of the spleen cells in culture; and addition of T cell growth factor on day 5 of MLTC. With these conditions a subset of T cells was expanded. They were blast cells with surface markers W3/25 and Ia, which exhibited no cytotoxic activity in vitro, and probably functioned as a helper or amplifier element in the tumor-bearing host. Effector cells generated in MLTC with BC5, treated with mitomycin C, were specific for BC5 in vivo and did not affect growth of a viral-induced BN tumor.
Cellular and genetic restrictions in the immunoregulatory activity of alpha-fetoprotein. III. Role of the MLC-stimulating cell population in alpha-fetoprotein-induced suppression of T cell-mediated cytotoxicity.
Authors: Peck A B , Murgita R A , Wigzell H 
Published: December 2022

Abstract
Alpha-fetoprotein (AFP), a normal component of fetal and newborn sera, exerts selective suppressive effects on various functions of thymus-derived (T) lymphocytes, including the T cell-mediated cytotoxic reaction. In the present study, AFP-induced suppression of the T cell-mediated allogeneic response was examined to define more precisely the mechanism by which AFP acts. Data presented indicate that AFP elicits its effect within the first 25 to 36 hr of culture. However, AFP apparently has no direct effect on T lymphocytes. T cells incubated in the presence of AFP retain full capacity to respond in MLC and CML. In contrast, AFP induces major changes in the functional status of monocyte-enriched, MLC-stimulating cell population. This monocyte-enriched population, after pretreatment with AFP, possesses strong stimulating capacity for the T suppressor cell limb of the immune response, while at the same time, suppresses the activity leading to the normal generation of cytotoxic T lymphocytes. These data correlate with the immune activity present in the newborn mouse.
Unfolded transferrin polypeptide chain is immunologically crossreactive with similar derivatives of serum albumin and alpha-fetoprotein.
Authors: Pekkala-Flagan A , Ruoslahti E 
Published: December 2022

Abstract
Radioimmunoassays utilizing reduced and carboxymethylated (RC) proteins as antigens reveal a cross-reactivity between alpha-fetoprotein (AFP) and albumin. Similar assays were used to study the relationships of AFP and albumin to other serum proteins. Of the several serum proteins tested, transferrin showed the most similarity with AFP and albumin. There was no cross-reactivity of the native proteins, but antisera prepared against RC-albumin and RC-AFP bound 125I-labeled RC-transferrin at high titers, and antiserum to RC-transferrin bound labeled RC-AFP but not RC-albumin. Inhibition assays utilizing binding of 125I-RC-AFP or 125I-RC-transferrin to anti-RC-albumin showed that the RC derivatives of AFP, albumin, and transferrin were equally efficient inhibitors, whereas other serum proteins inhibited much less. The serum vitamin D carrier protein (Gc protein) showed intermediate reactivity. The reactivities of the antisera to RC-albumins with RC-transferrin and RC-Gc protein were corroborated by immunostaining of proteins separated by sodium dodecyl sulfate/polyacrylamide gel electrophoresis and transferred to nitrocellulose filters. These antisera stained the bands formed by RC derivatives of albumin, AFP, transferrin, and Gc protein, but not other proteins tested. AFP and albumin are known to have amino acid sequence homology. Our results suggest that transferrin and possibly also Gc protein may be structurally related to AFP and albumin.
Antigen-specific suppression of cytotoxic T cell responses: an idiotype-bearing factor regulates the cytotoxic T cell response to azobenzenearsonate-coupled cells.
Authors: Greene M I , Ratnofsky S , Takaoki M , Sy M S , Burakoff S , Finberg R W 
Published: December 2022

Abstract
When A/J mice are injected subcutaneously with azobenzenearsonate- (ABA) coupled spleen cells, their splenocytes contain primed ABA-specific cytotoxic T lymphocyte (CTL) precursors. Animals that are not primed in vivo do not develop vigorous CTL activity when assessed after in vitro culture with ABA-coupled stimulators. Suppressor molecules derived from ligand-induced first-order ABA-specific suppressor T cells were evaluated for their ability to limit cytolytic T cell development. We have shown that an idiotype-bearing, hapten-specific suppressor factor suppresses priming for CTL in an H-2-unrestricted but allotype-restricted manner. The implication of these studies to regulatory networks is discussed.
Cyclic nucleotides regulate the morphologic alterations required for chemotaxis in monocytes.
Authors: Stephens C G , Snyderman R 
Published: December 2022

Abstract
The initial morphologic response of human monocytes to chemoattractants is a change in shape from round to a triangular "motile" configuration (polarization). At doses chemotactic in vitro, chemoattractants induced rapid (t 1/2 = 45 sec), sustained (greater than 40 min) polarization of monocytes in suspension. Extracellular Ca++ was not required for polarization induced by chemoattractants, but in the absence of Ca++ kinetics were slowed (t 1/2 = 6.5 min). Phenylephrine, carbamycholine, serotonin, and ascorbate also caused rapid polarization of monocytes. Unlike chemoattractants, polarization by the pharmacologic agents was unsustained (less than 15 min), absolutely required extracellular Ca++, and affected about 50% of the cells responsive to chemoattractants. Based on relative sensitivities to alpha 1- and alpha 2-adrenergic agonists and antagonists, polarization caused by adrenergic agents was mediated by alpha 2-receptors. Muscarinic and alpha 2-adrenergic agonists, serotonin, and ascorbate enhanced the rate and number of monocytes polarizing to suboptimal doses of chemoattractants. Thus, the initial morphologic changes induced by chemoattractants appear to utilize an activation pathway shared with a variety of agents that enhance cGMP levels and inhibit adenylate cyclase. In contrast, theophylline, histamine, and isoproterenol, all agents that activate adenylate cyclase and elevate cAMP levels, inhibited monocyte polarization to chemoattractants. As in PMN, pharmacologic agents that increase cAMP levels inhibited monocyte chemotaxis in vitro, whereas those that inhibit adenylate cyclase and increase cGMP enhanced monocyte chemotactic responses. Thus, the initial morphologic response of monocytes to chemoattractants as well as the processes required for sustained directional motility are modulated by cyclic nucleotides.
Heterogeneity of allogeneic restriction of human cytotoxic T cell clones specific for Epstein Barr virus.
Authors: Tanaka Y , Sugamura K , Hinuma Y 
Published: December 2022

Abstract
Clones of human cytotoxic T cells (Tc) specific for Epstein Barr virus (EBV) were isolated from peripheral blood lymphocyte (PBL) cultures stimulated repeatedly with autologous EBV-transformed lymphoblastoid cell line (LCL) cells in vitro. The method employed to clone EBV-specific Tc was a limiting dilution technique utilizing T cell growth factor (TCGF). The EBV specificity of Tc clones was determined by showing that they were significantly cytotoxic for autologous LCL cells but not for either autologous PBL or (natural killer-sensitive) K-562 cells. Eight EBV-specific Tc clones derived from a single donor exhibited distinct cytotoxic patterns against allogeneic LCL targets. Two clones were cytotoxic to LCL targets sharing both HLA-A26 and B15 antigens with effectors, and killing by two other clones was strongly restricted to autologous LCL cells. The four remaining clones showed cytotoxicities against various allogeneic LCL targets irrespective of HLA antigen expression. Eight EBV-specific Tc clones derived from a second donor also exhibited a wide spectrum of cytotoxicity to allogeneic LcL targets. We conclude that EBV-specific Tc, induced in vitro, consist of a number of clones with respect to restrictions imposed by the major histocompatibility complex. The determinants regulating these restrictions may include not only private HLA antigenic determinants that are defined by the HLA serotyping, but also undefined HLA antigenic determinants.
Inhibition of human antibody-dependent cellular cytotoxicity, cell-mediated cytotoxicity, and natural killing by a xenogeneic antiserum prepared against "activated" alloimmune human lymphocytes.
Authors: Neville M E , Hiserodt J C 
Published: December 2022

Abstract
Xenogeneic antiserum (RH1) was prepared in Lewis rats by hyperimmunization with concanavalin A- (Con A) activated alloimmune human lymphocytes. The antiserum RH1 effectively inhibited human antibody-dependent cellular cytotoxicity (ADCC), cell-mediated cytotoxicity (CMC), and natural killing (NK) in the absence of complement (C). Inhibition by RH1 was dependent on the dilution of antiserum employed and the number of cytotoxic lymphocytes present during cytolysis. Pretreatment of lymphocytes with RH1 or the presence of RH1 in culture did not inhibit lymphocyte proliferation stimulated by Con A, phytohemagglutinin, or allogeneic cells; lymphokine production as measured by leukocyte-inhibiting factor production; antibody-dependent C lysis; or CMC mediated by murine cytotoxic T lymphocytes. Analysis of the mechanism of inhibition of cytotoxicity by RH1 revealed that 1) RH1 was not cytotoxic for human lymphocytes at 37 degrees C in the absence of C; 2) purified F(ab')2 fragments were equally inhibitory as whole serum; 3) pretreatment of lymphocytes with RH1 effectively inhibited their capacity to mediate ADCC, CMC, or NK, and this effect was reversible by culturing the cells overnight at 37 degrees C; 4) RH1 did not inhibit target cell binding by K cells, effector cells of ADCC, or alloimmune T cells, but did inhibit binding by NK cells; and finally, 5) the addition of RH1 to preformed lymphocyte-target conjugates in a single cell cytotoxicity assay inhibited killing of the bound target cells in all three systems without disrupting the conjugates. Collectively, these findings suggest that RH1 antiserum interacts with structures present on the surfaces of cytotoxic lymphocytes that are involved in the activation of the lytic mechanism(s) or with the actual lytic molecule or molecules themselves. Furthermore, the ability of RH1 to inhibit ADCC, CMC, and NK during the post-binding cytolytic phase of these reactions indicates that binding and cytolysis are distinct and separate events in all types of cell-mediated cytolysis.
Interactions between lymphocyte membrane molecules. II. Characterization of an interaction between B lymphocyte surface IgD and Fc IgG receptors that differs from the surface IgM-Fc IgG receptor interaction.
Authors: Dickler H B , Kubicek M T , Finkelman F D 
Published: December 2022

Abstract
The B lymphocyte surface membrane receptors IgD (sigD) and Fc IgG receptors (Fc gamma R) were evaluated for interactions by means of immunofluorescence. Ligand-(F(ab')2 anti-delta) induced capping of sIgD resulted in co-capping of Fc gamma R if the latter were occupied during the capping process by soluble antigen-antibody complexes (which themselves provided insufficient cross-linking to result in capping), but not if the Fc gamma R were occupied by monomeric IgG or unoccupied. Capping of Fc gamma R by highly cross-linked complexes did not cause co-capping of sIgD occupied by monomeric F(ab') anti-delta. The interaction between sIgD and Fc gamma R was specific in that cross-reactions between ligands were excluded and ligand-induced capping of sIgD did not cause co-capping of ligand-occupied sIgM or I-A antigens. The sIgD-Fc gamma R interaction occurred on only approximately 60% of B lymphocytes, and this B cell subpopulation did not correlate with other B cell subpopulations (CBA/N strain B cells and B cells bearing either large or small amounts of sIgD). The sIgD-Fc gamma R interaction differed from the sIgM-Fc gamma R interaction in that co-redistribution of the Fc gamma R was occupied by monomeric IgG and involved nearly all B lymphocytes. The qualitative and quantitative differences between the sIgD-Fc gamma R and sIgM-Fc gamma R interactions suggest a mechanism whereby the two antigen receptors could provide different signals to the B lymphocyte.
Antibody restores human alternative complement pathway activation by mouse erythrocytes rendered functionally deficient by pretreatment with pronase.
Authors: Moore F D , Austen K F , Fearon D T 
Published: December 2022

Abstract
Activation of the human alternative pathway of complement (C) by surfaces requires the initial deposition of C3b by fluid-phase C3 convertase and sustained C3 cleavage by C3 convertases fixed to the surface. Nonactivating particles have previously been characterized by an inability to sustain the function of C3 convertases on their surfaces because these sites were susceptible to the regulatory action of the control proteins. Pronase converts the mouse erythrocyte (E) from an activator to a nonactivator by markedly decreasing the ability of the cell to affix C3b generated by a fluid-phase C3 convertase; this conversion is unrelated to the action of the control proteins on bound C3b. The capacity of antibody and its F(ab')2 or Fab' fragments to restore the alternative pathway-activating function of pronase-treated mouse E indicates that the contribution of antibody is mediated by its combining site without a requirement for bridging or for the Fc portion. The fab'-dependent activation of the alternative pathway of C relates to the deposition of C3b on the particle surface, which is a first and continuing step in alternative pathway activation. The antibody effect is not directed to the action of the regulatory proteins. Thus, particle-dependent activation of the alternative C pathway has been shown for the first time to be abolished and restored by cell surface-directed mechanisms that function independently of the regulatory proteins.