bluuebunny/crossref_metadata_2025_split huggingface dataset:
Differences in Kinetic Parameters of Lysis by Syngeneic and Allogeneic T Lymphocytes Immune to the Same Tumor
Authors: Huber S. A. , Lucas Z. J. 
Published: December 2022

Abstract
Kinetic parameters of cell-mediated cytotoxicity (CMC) to the 13762A rat mammary adenocarcinoma were studied by using immune syngeneic (Fischer) and allogeneic (Wistar Furth) spleen cells. Treating the spleen cells with rabbit anti-T cell serum and complement eliminated cytotoxicity. Both types of cytolytic cells bound to tumor cells in Ca2+-free medium but required Ca2+ to lyse them. Cytochalasin A did not interfere with the lysis of target cells already bound to cytolytic cells but it did prevent attachment of cytolytic cells to new targets. Cytolysis of the tumor occurred in three sequential steps: 1) binding of the lymphocytes to the target; 2) production of a lytic lesion in the target by the lymphocyte; and 3) lysis of the target. Allogeneic and in vitro augmented syngeneic lymphocytes required about 30 min for maximum binding to targets compared to 4 hr for syngeneic cells sensitized in vivo. Induction of the lytic lesion required 1 hr for the allogeneic cells and up to 8 hr for both types of sensitized syngeneic cells. Target cell death was slightly faster after incubation with allogeneic (8 hr) than with syngeneic (12 hr) cells. Pretreatment of the tumor cells with mitomycin C or actinomycin D did not enhance target lysis. Despite the many similarities between allogeneic and syngeneic effector cells, the increased time required for induction of the lytic lesion by syngeneic effector cells might indicate employment of a different lytic mechanism or a lower lytic efficiency compared to allogeneic cells.
Enhanced Intracellular cGMP Concentrations and Lectin-Induced Lymphocyte Transformation
Authors: Atkinson John P. , Kelly James P. , Weiss Avery , Wedner H. James , Parker Charles W. 
Published: December 2022

Abstract
On the basis of recent reports that sodium azide, ascorbic acid, nitrosamines, and nitrosoguanidines elevated cGMP levels in some tissues, we examined their effects on cGMP metabolism in human lymphocytes. Sodium nitroprusside (NP), a nitrosoguanidine (MNNG), sodium azide, and ascorbic acid augmented intracellular cGMP concentrations many-fold in the presence or absence of calcium in the extracellular milieu. The response was usually maximal by 30 sec, persisted for at least 1 hr, and occurred in platelet-, granulocyte-, and monocyte-free preparations composed of greater than 90% T lymphocytes. In broken cell preparations these same agents augmented guanylate cyclase activity but had no effect on cAMP or cGMP phosphodiesterase. The magnitude of the increase in cyclase activity was in most cases proportional to the enhancement produced in intact cells, although sodium azide was a better stimulator of guanylate cyclase in broken cell preparations, and ascorbic acid in intact cells. With these agents as positive controls and four separate methods of cyclic nucleotide extraction before radioimmunoassay, significant and reproducible increases in cGMP were not demonstrable with Con A or E-PHA over a wide concentration range. The cGMP agonists did not in themselves produce lymphocyte mitogenesis or modulate E-PHA or Con A-induced transformation at optimal mitogenic concentrations. At supraoptimal concentrations of E-PHA or Con A (&gt;25 µg/ml), NP increased thymidine incorporation and cell number. Cyclic GMP and its analogs alone neither enhanced thymidine incorporation nor modulated mitogen-induced lectin stimulation except for cGMP itself (1 and 0.1 mM) which increased 3H-thymidine transport but not cell number. These data do not support the concept of cGMP being a critical second messenger or having a permissive, positive regulatory role in lectin-induced transformation in human lymphocytes.
Binding Constants of Dextrans and Isomaltose Oligosaccharides to Dextran-Specific Myeloma Proteins Determined by Affinity Electrophoresis
Authors: Takeo Kazusuke , Kabat Elvin A. 
Published: December 2022

Abstract
In polyacrylamide electrophoresis, mobilities of dextran-specific myeloma proteins W3129 and QUPC52 were retarded when dextrans were added to the separating gel. Retardation by dextran was reversed by adding isomaltose oligosaccharides to the gel. From measurements of the extent of retardation by dextran or of reversal by hapten as a function of concentration, association constants of dextrans (Ka) and of oligosaccharides (Kia) were determined.
With W3129, NRRL dextrans B 742 FR.S, B 742 FR.L, N279, B 1355 FR.S, B 1399, B 1299 FR.S, and NRC fractions 6, 7, and 8 have Kα values ranging from 2 to 6 × 104 ml/g. With QUPC52, dextrans in general show lower Ka than with W3129; N279, NRC fractions 6, 7, and 8, and B 1399 have Ka values ranging from 1 to 7 × 104 ml/g, whereas B-742 FR.S, B-1299 FR.S, and B-1355 FR.S have Ka values ranging from 3 to 6 × 102 ml/g. Dextran D3, a completely linear α(1 → 6)-linked glucosyl chain having a m.w. of 36,500 has a relative high affinity for QUPC52 (Ka = 2.3 × 103 ml/g or 8.3 × 104 M-1), although it does not show any affinity for W3129. This result confirms that myeloma protein W3129 is specific for a terminal chain of α(1 → 6)-linked glucosyl residues, whereas QUPC52 reacts with the nonterminal portion of α(1 → 6)-linked glucosyl chains. Kia values obtained coincided with those by other methods reported earlier by Cisar et al. With W3129, affinity increases with chain length up to isomaltopentaose (IM5) with the highest affinity Kia = 6.7 × 104 M-1; Kia of isomaltohexaose (IM6) and isomaltoheptaose (IM7) being 6.3 × 104 and 2.3 × 104 ml/g, respectively. With QUPC52, affinity increases as the number of residues in the glucosyl chain increases, reaching an upper limit with IM6 and IM7, 1.2 and 1.4 × 104 M-1.
This method of affinity electrophoresis is useful for obtaining binding constants ranging from 102 to 106 M-1. It may be performed on antibodies, lectins, and other binding proteins by using not only the purified proteins but also crude protein mixtures such as the ascitic fluid used in this study.
Differential Protective Effects of Immune Lymphoid Cells against Transplanted Line Ib Leukemia and Immune Polioencephalomyelitis
Authors: Duffey Paul S. , Lukasewycz Omelan A. , Olson David S. , Murphy W. H. 
Published: December 2022

Abstract
The capacity of immune cells obtained from the major lymphoid compartments to protect C58 mice from transplanted line Ib leukemia, and from an age-dependent autoimmune CNS disease (immune polioencephalomyelitis = IPE) elicited by immunizing old C58 mice with inactivated Ib cells was quantified. Cells used for comparative adoptive protection tests were harvested from the major lymphoid compartments 14 to 15 days after young C58 mice were immunized with inactivated Ib cell preparations. Regression curves were plotted from survival data and the log10PD50 values were determined. Immune spleen (ISC) and peritoneal cells (IPEC) were significantly more protective against transplanted Ib cells than immune lymph node (ILNC), thymic (ITC), and marrow cells (IMC). In contrast, IPEC and IMC were not protective against IPE and ITC were only marginally protective. ILNC afforded significant protection to transplantable leukemia but were only marginally protective to IPE. When ISC were treated with anti-thy 1.2 serum and complement, protection against transplanted leukemia and IPE was reduced &gt; 99%. When donors of immune lymphoid cells were treated with 12.5 mg of cortisone acetate daily for 2 days before lymphoid cells were harvested, protection against transplanted Ib cells by ISC was reduced by approximately 90% whereas protection against IPE was totally eliminated. Considered together, these results indicate that the protective mechanisms to transplantable leukemia and IPE differ significantly in the same indicator mouse strain.
Activation of Human B Lymphocytes
Authors: Dimitriu Alexandra , Fauci Anthony S. 
Published: December 2022

Abstract
Selective effects of in vitro azathioprine (AZ) on subpopulations of human lymphocytes involved in the pokeweed mitogen (PWM)-induced plaque forming cell (PFC) response against sheep red blood cells (SRBC) have been described. First, it was found that the responding B cell itself was very sensitive to AZ as concentrations as low as 0.01 µg/ml markedly suppressed the PWM-induced PFC responses of unfractionated peripheral blood mononuclear (MN) cell suspensions. The fact that AZ suppresses the PFC response of B cells only when added at the beginning of the cultures suggests that the drug interferes with some early events involved in B cell triggering by PWM. Furthermore, it was demonstrated that higher concentrations of AZ, i.e., 1 and 10 µg/ml selectively eliminated certain regulatory subsets of cells known to act as suppressors of this polyclonally induced PFC response. Preincubation of a) T cell-enriched (TCE) suspensions of cells, b) concanavalin A (Con A)-generated suppressor cells, and c) naturally occurring suppressor cells from nonresponder individuals with 1 and 10 µg/ml of AZ before co-culturing them with fresh MN cells in the presence of PWM caused a differential suppression of suppressor cell function and a selection for a pure helper effect with a resulting increase in B cell responses. Finally, regulatory helper cells were quite resistant to the in vitro effects of this drug as they still expressed their helper activity after pretreatment with 10 µg/ml AZ. Thus, this study demonstrated that B cells are highly sensitive, suppressor cells are less sensitive, and helper T cells are quite resistant to the in vitro effects of AZ.
Antigen-Induced Murine B Cell Lymphomas
Authors: Haughton Geoffrey , Lanier Lewis L. , Babcock George F. , Lynes Michael A. 
Published: December 2022

Abstract
In the accompanying report, we have described the characterization of two unusual murine B cell lymphomas, CH1 and CH2. A heterologous antiserum, which we refer to as “anti-idiotype” serum, has been raised to the detergent-solubilized surface immunoglobulin of CH1. The following criteria have established that this antiserum is specific for the CH1 tumor and that it reacts with V region determinants of the tumor surface IgM: 1) the antiserum reacts with CH1 tumor cells, but not normal mouse lymphoid cells or CH2 tumor cells, in indirect immunofluorescence and C-dependent cytotoxicity testing, 2) capping with the anti-idiotype serum removes all or most of the tumor surface Ig, 3) the antiserum forms a single band of precipitation against serum from CH1 tumor-bearing mice, when tested by double diffusion precipitin analysis, and 4) a single band of precipitation is formed in the electrophoretic migration position of IgM when the anti-idiotype antiserum is tested against serum from CH1 tumor-bearing mice in immunoelectrophoresis. Furthermore, we have demonstrated that this antiserum is useful in monitoring tumor growth and is a potent immunotherapeutic agent. Specifically, 50% of mice injected with a lethal tumor inoculum and given a small dose of anti-idiotype serum 2 days later remain tumor free, whereas all tumor-challenged control mice died within 30 days.
Genetic Control of the Immune Response to the H-2Dk Private Specificity, H-2.32
Authors: Shinohara Nobukata , Hansen Ted H. , Schurko Elizabeth , McKenzie Ian F. C. , Sachs David H. 
Published: December 2022

Abstract
B10.AKM mice (H-2m) when immunized with H-2k cells showed very low cytotoxic antibody responses to the H-2Dk private specificity H-2.32, whereas AKR.M and (AKR.M × B10.AKM)F1 mice that possess the same H-2m haplotype mounted reasonable anti-H-2.32 antibody responses. The genetic nature of the non-H-2 linked gene(s) controlling the anti-H-2.32 response was analyzed on the backcross progeny raised between (AKR.M × B10.AKM)F1 and B10.AKM mice. The anti-H-2.32 antibody response was found to be predominantly controlled by a single locus. This locus segregated independently of the Ig heavy chain locus, the Ly2 locus, and the Mls locus. Despite the observed difference in antibody production, no significant differences between AKR.M and B10.AKM mice were detected in induction of H-2Dk-specific killer T cells. Thus, the defect in the response of B10.AKM mice to H-2.32 can be detected at the level of B cell function and is controlled by a single non-H-2-linked genetic locus, but is not attributable to genes linked to the major immunoglobulin structural genes nor to the Mls locus.
Allergy to Insect Stings
Authors: Sobotka Anne K. , Adkinson N. Franklin , Valentine Martin D. , Lichtenstein Lawrence M. 
Published: December 2022

Abstract
Radioallergosorbent tests (RAST(s)) have been developed and assessed for the diagnosis of insect hypersensitivity by using a purified allergen from honeybee venom, phospholipase A, and crude yellow jacket venom. Sera from 193 patients positive both by history and skin test to one of these insects were compared with various groups of control sera. Eighty percent of sera from skin test-positive patients were RAST positive; positive RAST were found in 16% of sera tested from skin test-negative patients. A highly positive RAST correlates well with a positive skin test and clinical sensitivity, but serum IgE is not measurable in many patients with mast cell or basophil bound antibody. Since biologically important reactions of antigen with IgE require that the antibody be cell bound, skin testing would be preferred to RAST if one were limited to a single test for the diagnosis of insect allergy.
Evidence for a Silent or Null Gene in Hereditary C2 Deficiency
Authors: Pariser Kenneth M. , Raum Donald , Berkman Eugene M. , Alper Chester A. , Agnello Vincent 
Published: December 2022

Abstract
Hereditary deficiency of the second component of complement (C) was the first human inherited C component deficiency state described (1). It also appears to be the most common C component deficiency thus far studied with a gene frequency of 1% (2, 3). The genetic basis for this deficiency is not as yet known. In contrast, the basis for the genetic deficiencies of C3 and C6, which occur much less frequently, have been established. These deficiencies have been shown to be due to inheritance of silent or null genes allelic with the structural genes (4, 5). The approach used in those studies was to identify families with the deficiency that had informative electrophoretic variants of the proteins. Study of the inheritance of the structural variants and the serum levels of C components in such families provided evidence for the silent or null gene mechanism.
Identity of C3- and C5-Receptors on Lymphoid Cells
Authors: Landen Beate , Dierich Manfred P. 
Published: December 2022

Abstract
Tannic acid-treated SRBC, incubated with increasing concentrations of C5 (Etan-C5) can be attached to C3 receptor-carrying (Raji) cells. This binding is dependent on the amount of C5 on Etan-C5 and can be inhibited by pretreatment of the Raji cells with either C5 or C3. Similar inhibition by soluble C3 and C5, respectively, is obtained for the interaction between Raji cells and Etan-C3. In addition, the immune adherence reaction between Ehum and EAC1423b could be blocked by previous treatment of Ehum with C5 or with C3. These results suggest the presence of binding sites for C5 on lymphoid cells and their identity with C3 receptors.
T Cell Helper Defect in Patients with Chronic Lymphocytic Leukemia
Authors: Chiorazzi N. , Fu S. M. , Montazeri Ghodrat , Kunkel H. G. , Rai Kanti , Gee T. 
Published: December 2022

Abstract
Purified peripheral blood T lymphocytes from normal donors were shown to help allogeneic tonsillar B cells to differentiate and secrete specific anti-SRBC antibody in vitro in a plaque-forming assay. Utilizing this system, a comparison was made between the allogeneic helper activity generated by the T cells of normal individuals and patients with various disease states. Allogeneic helper activity was absent when T lymphocytes from patients with CLL were used. Conversely, relatively normal allogeneic helper function was provided by T cells of patients with a variety of other disorders studied. Thus, a functional deficiency was identified in CLL patients in the subpopulation of regulatory T cells responsible for providing helper activity in allogeneic interactions.
Properties of Murine Leukemia-Associated Suppressor Cells
Authors: Grinwich Kazimiera D. , Alexander Thomas S. , Cerny Jan 
Published: December 2022

Abstract
The spleens of BALB/c mice bearing leukemia induced with Moloney leukemia virus contain cells capable of inhibiting the antibody response of normal immunocompetent lymphocytes in Marbrook culture vessels. The immunosuppression requires contact between the cells and appears to be mediated by leukemia-associated suppressor cells rather than by the leukemic cells themselves. Thymus-dependent antibody responses to sheep red blood cells (RBC), horse RBC or trinitrophenol coupled to ovalbumin (TNP-OVA) were inhibited proportionally to the number of suppressor cells added. In contrast, thymus-independent responses to Vibrio cholerae lipopolysaccharide and to TNP coupled to Ficoll were either unaffected or suppressed only with a high number of suppressor cells. The leukemia-associated suppressor cells from BALB/c mice (H-2d) inhibited the anti-sheep RBC response of syngeneic lymphocytes and of allogeneic DBA/2 lymphocytes bearing the H-2d haplotype but failed to inhibit lymphocytes from other allogeneic strains DBA/1 (H-2q), C57BR (H-2k), A (H-2a), and C57BL/10 (H-2b). Experiments with lymphocytes from congenic strains carrying various H-2 gene complexes on the B10 genetic background confirmed that the suppressor effect is restricted by genes in the H-2 complex. Further mapping suggested that the suppression requires identity in the K region between the suppressor and the responder cells. The inability to suppress the allogeneic, H-2 different lymphocytes was retained even when a majority of the leukemic, virus-producing cells were removed from the spleen cell suspension by using a specific cytotoxic antiserum. There was no correlation between permissivity of lymphocytes to infection by the Moloney leukemia virus in vitro and between their inhibition by the suppressor cells. Thus, the nonspecific (polyclonal) leukemia-associated suppressor cells preferentially inhibit helper T cells and the suppression involves a specific interaction with product(s) of K region genes on the surface of the responder cells.
Inhibition of Lymphocyte Blastogenesis by C3c and C3d
Authors: Schenkein Harvey A. , Genco Robert J. 
Published: December 2022

Abstract
The C3 cleavage products C3c and C3d were tested for their ability to alter the immunoproliferative response of human peripheral mononuclear cells to the antigens SLO and SK-SD, and to the mitogens PHA and PWM. It was found that both C3c (30 to 120 µg/ml) and C3d (10 to 40 µg/ml) inhibited lymphocyte blastogenesis in the presence on antigens but not mitogens, when cells were cultured in either autologous plasma or FCS. Similarly, the response to antigens of cell populations enriched for T lymphocytes was inhibited, whereas the response to optimal or suboptimal doses of mitogens was unaffected. When nonadherent (NA) cells were reconstituted with increasing numbers of adherent (AD) cells to potentiate the proliferative response of NA cells to the antigen SLO, the addition of either C3c or C3d abolished the potentiation of the response at low levels of reconstitution. However, at a given dose of C3c or C3d, addition of excess AD cells could restore the proliferative response. These results suggest that both C3c and C3d can inhibit T cell proliferation in response to antigen and that they may act at the level of the monocyte-T lymphocyte interaction to modulate cellular immune responses.
Immunoadjuvant Treatment of Primary Grafted and Spontaneous AKR-Leukemia
Authors: Olsson Lennart , Ebbesen Peter 
Published: December 2022

Abstract
AKR mice grafted with spontaneous AKR leukemia cells and treated with BCG may become leukemic due to graft leukemia or spontaneous leukemia, may die in a wasting-like syndrome, or may appear cured from leukemia and be without signs of wasting-like syndrome. Lymphoid spleen cells from these groups of mice were used at various times from cytotoxicity against AKR leukemia cells, against nonmalignant AKR fibroblasts, and against nonmalignant BALB/c fibroblasts. Spleen cells from cured mice and wasting-like mice were cytotoxic to AKR leukemia cells. The cytotoxic activity could be enhanced by depleting the lymphoid cells of T lymphocytes. AKR leukemia cytotoxic spleen cells were invariably also cytotoxic to AKR fibroblasts, but never to BALB/c fibroblasts. Quantitative differences in sensitivity to cytotoxic attack could be demonstrated between AKR leukemia cells and AKR fibroblasts since the former cell type was about 1000 times more sensitive to cytotoxic attack as compared to AKR-fibroblasts. The insensitivity of BALB/c fibroblasts to cytotoxic attack seemed to be a qualitative characteristic. Addition of lymphoid cells from cured AKR mice inhibited the cytotoxic activity of otherwise cytotoxic cells, thus indicating some suppressor activity in cured mice. It is suggested that successful anti-neoplastic immunoadjuvant treatment depends on a quantitative difference between malignant and nonmalignant cells with respect to cytotoxic attack of self-directed cytotoxic cells.
Activation of the Classical Pathway of Complement by the C3NeF-Stabilized Cell-Bound Amplification Convertase
Authors: Daha Mohamed R. , van Es Leendert A. 
Published: December 2022

Abstract
C3 nephritic factor (C3NeF̄) has been shown to be composed of two heavy and two light chains, like IgG; in addition it shares antigenic determinants with IgG. C3NeF, purified from the sera of eight patients by incorporation of C3NeF into the stabilized fluid phase amplification C3 convertase, C3b,Bb(C3NeF), followed by its release after decay of convertase function, was investigated for its ability to bind 125I-C1q and to activate 125I-C1. It was found that although fluid phase C3b,Bb(C3NeF) is fully capable of binding 125I-C1q, it is not able to activate 125I-C1 even at concentrations of 1.3 × 1012 C3b,Bb(C3NeF) complexes/ml. On the other hand, cell-bound C3b,Bb(C3NeF) is capable of both binding 125I-C1q and activating 125I-C1. This discrepancy between fluid phase and cell-bound C3b,Bb(C3NeF) was found for C3NeF preparations from eight different patients and therefore seems to apply to all C3NeF preparations.
Heavy Chain Variable Region Allotypic Subspecificities of Rabbit Immunoglobulins
Authors: Horng Wayne J. , Knight Katherine L. , Dray Sheldon 
Published: December 2022

Abstract
An a1a2 rabbit (P286-3), neonatally suppressed for the expression of the a1 allotype, was immunized with autologous a1 IgG at 2 months of age. Both auto anti-a1 Ab and a1 IgG molecules were found in the serum of this rabbit after the auto-immunization. The auto anti-a1 Ab and the IgG from the auto anti-a1 Ab-depleted serum were isolated. Of the previously defined a1-AB, a1-AC, and a1-AD Ig subpopulations, the a1 IgG in the IgG preparation from rabbit P286-3 were all of the a1-AB Ig subpopulation. The auto anti-a1 Ab from rabbit P286-3 did not react with the a1-A, a1-B, and a1-C allotypic subspecificities; thus, it was presumably specific for the a1-D allotypic subspecificity. Thus, the a1-AB Ig subpopulation escaped from allotype suppression in rabbit P286-3, whereas the a1-AC and a1-AD Ig subpopulations remained suppressed. The a1-AD Ig subpopulation will probably remain suppressed for a long time and perhaps permanently since rabbit P286-3 has produced circulating auto-Ab specific for the a1-D allotypic subspecificity. These results indicate that the a1 Ig subpopulations are synthesized by distinct clones of lymphocytes under separate control.