bluuebunny/crossref_metadata_2025_split huggingface dataset:
Regulation of Human T Cell Colonies by an Inducing Activity (TCI) Produced by Normal Human and Malignant Mouse Cells
Authors: Gerassi Esther , Sachs Leo 
Published: December 2022

Abstract
Unfractionated human peripheral blood lymphocytes seeded at 5 × 105 cells per 35-mm Petri dish with phytohemagglutinin (PHA) can be induced to form T cell colonies with a cloning efficiency of 1%. Fractionated cells with T cell markers did not form any colonies at this seeding level. T cells were induced to form colonies either by increasing the number of cells seeded, or by adding conditioned medium (CM) from syngeneic or allogeneic T cells cultured with PHA. This CM induced a cloning efficiency of 10% at a seeding level of 5 × 103 cells per Petri dish. The induction of T cell colonies by CM did not require the presence of phagocytic or B cells. The T cell colony-inducing activity in the CM appears to be a trypsin-sensitive protein(s) and was not substituted by thymopoietin. Incubation of T lymphocytes with this inducing activity for 30 min was sufficient to induce colony formation.
Colony-inducing activity for human T cells was also found in CM from normal human unfractionated lymphocytes incubated with concanavalin A, pokeweed mitogen, or lipopolysaccharide, human peripheral blood cells adherent to a Petri dish, Krebs mouse ascites tumor cells, and MGI+D+ mouse myeloid leukemia cells cultured with PHA. The results indicate that the colony-inducing activity for normal human T cells (TCI) can be found in CM from normal human T lymphocytes, human adherent cells, and some malignant mouse cells.
The Structural Heterogeneity among Degraded γ Heavy Chain Disease Proteins
Authors: Franklin Edward C. 
Published: December 2022

Summary
The amino terminal sequence of seven newly studied and three previously reported γ Heavy Chain disease proteins show that they begin at several sites ranging from position 215–234 in the hinge region. The presence of more than one species of molecule in several of the sera and the susceptibility of this region to proteolytic cleavage, taken together with the finding of a blocked Heavy Chain disease protein in the serum of one and the cells of another patient support the concept that these molecules are the result of proteolytic cleavage of typical Heavy Chain disease proteins.
Evidence that the “Mouse Mastocytoma” Cell Line (MCT-1) Is of Rat Origin
Authors: Siraganian Reuben P. , Metzger Henry 
Published: December 2022

Abstract
A rat basophilic leukemia arose in a Wistar rat fed B-chlorethylamine and could be transplanted by subcutaneous inoculation into newborn rats (1). Because these cells (RBL-1) have been adapted for tissue culture (2–4) and have receptors for rat and mouse IgE (2–8), they have become very useful for studies of the IgE receptor (reviewed in 9) and for studies on mediators (e.g., ECFA and SRS-A) (10–13). However, these cells could not be triggered for physiologic histamine release via an IgE-mediated mechanism nor by noncytotoxic doses of compound 48/80 or the calcium ionophore A23187 (14).
Five mastocytomas were found among 99 mice of several different strains that had been treated with pristane and Abelson virus (J. G. Pumphrey, M. Potter, R. Risser and R. P. Siraganian, Manuscript in preparation). These tumors have the morphologic characteristics of mast cells, contain granules, and produce histamine and serotonin.
Discordance among Cell-Mediated Cytolytic Mechanisms in Cancer Patients: Importance of the Assay System
Authors: Catalona William J. , Ratliff Timothy L. , McCool Robert E. 
Published: December 2022

Abstract
ADCC and SCMC directed against Change cell targets that are mediated by lymphocytes having properties characteristic of K cells were impaired in cancer patients. In contrast, ADCC directed against CRBC targets that is mediated by both K cells and macrophages was normal in cancer patients, whereas SCMC against CRBC that is mediated primarily by macrophages was increased. Thus, there was a discordance among cytotoxic mechanisms in cancer patients with K cell-mediated cytotoxic function being impaired and macrophage-mediated cytotoxicity being enhanced. Regression analysis suggested that these perturbations of cytotoxic function occurred independently. Cancer patients had an increased proportion of circulating macrophages and a decreased proportion of eosinophils, but these abnormalities did not correlate significantly with ADCC or SCMC.
Idiotypic Analysis of Anti-Gat Antibodies
Authors: Ju Shyr-Te , Dorf Martin E. , Benacerraf Baruj 
Published: December 2022

Abstract
The humoral response to poly-(L-glutamic acid60, L-alanine30, L-tyrosine10), GAT, in mice is further characterized by both idiotype and fine specificity analyses. The common idiotype on murine anti-GAT antibodies (CGAT) was identified in anti-GAT antisera from seven additional strains of mice. These data confirm that the CGAT idiotype can be induced in all inbred strains of mice.
Using a partially inbred strain of mice selected for their ability to respond to poly-(L-glutamic acid50, L-tyrosine50), GT, we demonstrated that the GT copolymer is capable of inducing antibodies that express the CGAT idiotype. In contrast, antisera directed against poly-(L-glutamic acid60, L-alanine40), GA, bind GAT but lack CGAT idiotype. These results indicate that GAT molecules contain determinants either similar or identical to those on GT molecules, which are responsible for the induction of CGAT idiotypic antibodies. We also demonstrated that both GAT responder and nonresponder strains of mice can produce anti-GAT antibodies with similar fine specificity patterns and CGAT idiotype. In addition, we demonstrate that antibodies of the IgM, IgG1 and IgG2 immunoglobulin classes express the CGAT idiotype.
in Vivo Cooperation of Murine Lymphocytes Sharing One Haplotype of the Transplantation Genes: A Requirement for Tolerance of the Nonshared Haplotype
Authors: Marušić Matko , Perkins Eugene H. 
Published: December 2022

Abstract
The ability of mouse thymus-dependent (T) and bone marrow-derived (B) lymphocytes to cooperate in the (humoral) rejection of the rat Yoshida ascites sarcoma (YAS) was investigated. Mice of two hybrid constitutions that had one parent of the same strain and the other of a different strain were used. T and B cells thus shared one haplotype of the transplantation genes, but the other haplotype was different so that allogeneic recognition could take place in both directions. To investigate the influence of allogeneic recognition on T-B cell cooperation, mice were also made mutually tolerant by establishing long-term radiation chimeras. Erythrocytes and spleen cells of the chimera were shown by serologic analysis to be donor-type. When the chimera was to serve as tumor host and B cell source, it was thymectomized before irradiation and reconstitution with Thy 1.2 antisera and complement-treated bone marrow (TIR). The evidence of tolerance was markedly reduced anti-host-type reactivity in short-term in vivo [3H]thymidine uptake studies. Successful cooperation, manifested by YAS rejection in TIR mice given splenic T cells, was seen a) whenever the transferred T cells and the cells of the TIR recipient were syngeneic, and b) when the T cells were nonsyngeneic with the cells in TIR recipients but were obtained from chimeric donors and injected into chimeric recipients. Chimerism of only T cell donors or TIR recipients was not sufficient for YAS rejection to be induced. The data suggest that the allogeneic recognition on either T or B lymphocytes may thwart otherwise successful cell cooperation.
Stimulation by Granulocyte-Macrophage Colony-Stimulating Factor of Leishmania Tropica Killing by Macrophages
Authors: Handman Emanuela , Burgess Antony W. 
Published: December 2022

Abstract
The intracellular protozoan parasite Leishmania tropica was found to survive unharmed and to multiply for several days in normal mouse peritoneal macrophages. In contrast, when infected monolayers were treated with GM-CSF, there was a continuous decrease in the percentage of infected cells, reaching less than 10% on day 4 in culture, compared to about 30% in normal controls. Microscopic observations showed an increased number of dead parasites in GM-CSF treated infected cells. Within 5 hr of incubation with GM-CSF, almost 40% of intracellular parasites showed morphologic damage, compared to less than 10% in untreated cells. Pretreatment of macrophage monolayers with pure GM-CSF before infection led to an increased level of phagocytosis of L. tropica parasites as reflected by the percentage of infected cells and the increased number of parasites in each infected cell. GM-CSF treated cultures showed 73% infected cells containing a mean of five parasites per cell, as compared to controls in which only about 50% of macrophages were infected with only two parasites per cell. The number of dead parasites per cell was 5-fold higher in the GM-CSF treated cultures at 2 hr. After 24 hr the percentage of infected GM-CSF treated cells was less than one-third that in the control cultures.
Synergistic Cytotoxicity
Authors: Muchmore A. V. , Decker J. M. , Blaese R. M. 
Published: December 2022

Abstract
In a previous paper we demonstrated that freshly obtained human plasma contained a heat labile nonantibody factor that induced human mononuclear cells to become nonspecifically cytotoxic toward xenogeneic but not allogeneic RBC targets. We now present evidence that this factor has a loose affinity for human monocytes and human T cells and can arm them to kill xenogeneic RBC targets. Furthermore, proteolytic enzymes markedly enhance this arming effect. This ability to be armed by a heat labile component found in fresh human plasma and the fact that proteolytic enzymes markedly enhance cytotoxicity clearly dissociate this model of nonspecific cytotoxicity from previously reported NK models.
Soluble Helper Factor(s) Participates in the Generation of Cell Mediated Cytotoxicity Directed against Syngeneic Tumor Cells
Authors: Fyfe Derek A. , Finke James H. 
Published: December 2022

Abstract
Data presented here suggest that one mechanism by which cytotoxic T lymphocytes are generated against certain syngeneic tumors may involve collaboration between pre-killer T cells and helper T cells via a soluble helper factor. Furthermore both lymphocyte-defined as well as cytotoxicity-defined antigens expressed on tumor cells may be involved in stimulating the generation of specific cytotoxic T cells. A lymphoma cell line (CH-1) derived from an SJL mouse stimulates both a syngeneic proliferative and cytotoxic response. However, heattreatment of the CH-1 cells, which is known to functionally inactivate lymphocyte-defined antigens, reduced significantly the ability of such cells to stimulate proliferation and the generation of cytotoxic T cells. The addition of supernatant fluids from either mixed lymphocyte cultures or from cultures in which syngeneic lymph node cells were sensitized against CH-1 tumor cells, restored the ability of heat-treated tumor cells to stimulate a full syngeneic cytotoxic response. The degree of T cell specific cytotoxicity that was generated was dependent in part on the concentration of helper factor(s) added to the cultures. Furthermore, supernatant fluids containing helper activity were not able to stimulate responder cell cytotoxicity in the absence of heat-treated CH-1 cells. The helper activity, detected in cultures where SJL lymph node cells were stimulated by CH-1 cells, appears to be similar to that present in supernates from allogeneic MLC since neither are antigen specific nor H-2 restricted in their ability to assist in the development of cytotoxic T cells.
Suppression of Cytotoxic Response to Histoincompatible Cells
Authors: Gorczynski Reginald M. , MacRae S. 
Published: December 2022

Abstract
The kinetics of appearance of the precursors of SuppA cells (capable of inhibiting CTLp → CTL) or SuppB cells (capable of inhibiting (stem cells → CTLp) in neonatal mice, as well as the appearance of SuppA/SuppB cells in mice given neonatal innoculations of semiallogeneic spleen cells has been investigated. The data obtained are consistent with the idea that SuppA cells have a natural role to play in the induction of neonatal tolerance, whereas SuppB cells may be more important for the maintenance of the tolerant state. Unlike the level of SuppB cells, the level of SuppA cells in tolerant mice seems to be modulated by the presence of the tolerizing determinants. Data are provided to show that SuppB cells, once induced in tolerant mice, can adoptively transfer specific allograft unresponsiveness to newborn syngeneic mice in the absence of added tolerizing antigen, whereas SuppA cells are not able to do so. These data fit the notion that SuppB cells may be responsible for the phenotype of clonal deletion.
Mechanisms of Lipopolysaccharide-Initiated Rabbit Platelet Responses
Authors: Morrison David C. , Oades Zenaida G. 
Published: December 2022

Abstract
The mechanism of bacterial lipopolysaccharide- (LPS) initiated, complement- (C) mediated rabbit platelet lysis has been examined. The results of these studies support our previous observations that activation of the alternative C pathway is required for platelet lysis and that preparations of LPS that activate only the classical pathway (e.g., lipid A) do not cause lysis. The temporal relationship of the interaction of the LPS with the platelet before the addition of plasma suggests a time-dependent association of the LPS with the platelet. On the basis of a number of experiments, including inhibition with polymyxin B, treatment of LPS with alkali, and blocking experiments with polysaccharide-free LPS preparations, it is concluded that the lipid A region of the LPS molecule is responsible for attaching the LPS to the platelet. Finally, a comparison of the activity of lipid A-associated protein-LPS complexes with protein-free LPS demonstrated that an equivalent extent of platelet lysis was achieved with one-one hundredth the concentration of the former as that required for protein-free LPS. The data suggest that LAP facilitates attachment of the LPS to the platelet.
Lymphocyte Function in Experimental African Trypanosomiasis
Authors: Wellhausen Sam R. , Mansfield John M. 
Published: December 2022

Abstract
Cellular mechanisms of immunosuppression were studied in C57BL/6 mice chronically infected with the human pathogen Trypanosoma rhodesiense. Mice lost the capacity to mount primary in vitro splenic PFC responses to sheep erythrocytes (SRBC) within 3 days of infection. The addition of normal mouse spleen cells to infected spleen cell cultures failed to restore responsiveness and, in addition, resulted in the acquisition of unresponsiveness by the normal cells. Parasites present in infected spleen cell cultures were not directly responsible for the suppression observed. Immunosuppression was attributable to suppressor cells present in infected spleens, as assessed by the ability of infected spleen cells to suppress normal spleen cell responses to SRBC. The suppressor cell population could be removed on nylon wool or Sephadex G-10 columns, was insensitive to treatment with anti-Thy 1.2 serum and C, and could be enriched for by adherence to tissue culture dishes. We suggest, therefore, that the splenic suppressor cell is a macrophage. The suppressor macrophage may be present in low concentration within a larger nonsuppressive pool of splenic macrophages since suppressor effects were not evident when &lt;104 adherent cells were transferred to normal cells in dose-response studies. There was good correlation between the appearance of immunosuppression and the presence of suppressor cells in that infected mouse spleen cells exhibited suppressor cell capacity at the time when such cultures became unresponsive to SRBC. Suppressor cells were absent, however, from lymphoid organs other than the spleen, and infected lymph node cell cultures were capable of generating a significant primary in vitro PFC response to SRBC. On the basis of our studies, we suggest that the spleen is the major target organ for immunosuppression in T. rhodesiense infected mice, and that suppression is attributable to the emergence of a suppressor macrophage population that is restricted to the spleen.
Phenotypic and Functional Effects of the Motheaten Gene on Murine B and T Lymphocytes
Authors: Davidson Wendy F. , Morse Herbert C. , Sharrow Susan O. , Chused Thomas M. 
Published: December 2022

Abstract
Lymphoid cells from C57BL/6 mice homozygous for the me gene exhibit multiple phenotypic and functional abnormalities from as early as one week of age. In the B cell population these include a reduction in the frequency of detectable surface Ig+ cells, alterations in the level of expression of surface IgM and IgD, and increase in the frequency of large cells, plasma cells and TNP-specific plaque forming cells, production of anti-thymocyte antibody, and a greatly decreased response to LPS. Together these findings provide strong evidence for polyclonal activation of B cells. The high level of expression of xenotropic MuLV gp70 by me/me spleen and lymph node cells provides further evidence for lymphoid cell activation.
In preliminary studies, me/me T cells appeared to be phenotypically and functionally less affected by the me gene. The distribution of Thy 1.2 on the surface of spleen and lymph node T cells varied from low to normal and the mitogenic responses to Con A and PHA were depressed. It remains to be determined what the basic deficiency in me/me mice is and whether it affects primarily B cells or all lymphoid cells.
Turnover and Shedding of Ia Antigens by Murine Spleen Cells in Culture
Authors: Emerson Stephen G. , Cone Robert E. 
Published: December 2022

Abstract
Lactoperoxidase-catalyzed radioiodination was used to examine the metabolic fate of surface Ia antigens on murine spleen cells in culture. Ia antigens, detected predominately on splenic B lymphocytes, were lost from the cultured cells with biphasic kinetics: a 4 to 6 hr rapid phase, t½ = 5 hr followed by slow release through 20 hr, t½ = 30 hr. The rapid loss of Ia antigens observed was abolished by both harsh iodination conditions and nonphysiologic incubation conditions. The rapid decline in Ia activity was shown to be due to shedding of intact Ia antigens from the cell and to a predominant release of IA subregion-coded proteins. Release of Ia antigens from the cell was accomplished by replacement at the cell surface, and thus reflected net membrane Ia turnover. Ia shedding was shown to be extremely temperature dependent, reflecting both a comparatively high activation enthalpy and entropy requirement for turnover.
Production of Antibodies Against Phosphocholine, Phosphatidylcholine, Sphingomyelin, and Lipid A by Injection of Liposomes Containing Lipid A
Authors: Schuster Brian G. , Neidig Martin , Alving Barbara M. , Alving Carl R. 
Published: December 2022

Abstract
Liposomes were investigated as a combined carrier and adjuvant to promote the immunogenicity of lipid A derived from endotoxin. Lipid A-containing liposomes, or lipid A alone, were injected once into rabbits either subcutaneously or i.v. Antiserum activity was measured by complement-dependent damage to appropriate indicator liposomes containing trapped glucose. Lipid A in liposomes produced a greater immune response against lipid A than that obtained by injecting identical amounts of lipid A alone, and the response to the liposome-lipid A combination was equivalent to that obtained by a frequently used alternative method, in which the antigen consisted of acid-treated bacterial cells coated with lipid A.
Antiserum, or purified IgG antibodies, from rabbits immunized with liposomes containing lipid A also reacted with liposomes lacking lipid A. The antibodies were inhibited by phosphocholine, and the activity was adsorbed by phosphatidylcholine, or ceramide phosphocholine (sphingomyelin). The anti-phosphocholine antibodies did not cross-react with lipid A, but their binding to liposomes was inhibited by the presence of anti-lipid A antibodies on the surface of the liposomes. An “anti-liposome” response was not observed when either lipid A alone, acid-treated bacterial cells coated with lipid A, or liposomes lacking lipid A were injected.
We conclude that one injection of liposomes containing lipid A produces an immune response against lipid A that is equivalent to that produced by other methods of immunization. Injection of liposomes containing lipid A also produces an immune response against phosphocholine, phosphatidylcholine, and sphingomyelin.
Cyclical Changes in Susceptibility of A Myeloma Tumor (LPC-1) to Immune Destruction
Authors: Celis Esteban , Hale Arthur H. , Russell John H. , Eisen Herman N. 
Published: December 2022

Abstract
One of six transplantable ascites tumors of BALB/c mice was found to become periodically resistant to cytotoxic T lymphocytes (CTL). About 12 days after LPC-1, a myeloma tumor, was transplanted it became resistant to lysis by allogenic CTL (anti-H-2d) and by CTL directed to trinitrophenyl groups or minor histocompatibility antigens. Susceptibility to lysis by all of these CTL was regained within 2 to 4 days after transfer of the resistant cells to a fresh BALB/c host. These changes were recurrent: in each transplantation cycle the early LPC-1 cells were susceptible and the late cells were resistant to CTL. Analyses with antisera (B10 anti-B10.D2) showed that the serologically recognized products of the H-2d haplotype were reduced about 10-fold on the LPC-1 cells that were resistant to CTL.
Lymphocyte Activation by the Tumor-Promoting Agent 12-O-Tetradecanoylphorbol-13-Acetate (TPA)
Authors: Abb Jochen , Bayliss Gary J. , Deinhardt Friedrich 
Published: December 2022

Abstract
TPA, a highly active tumor-promoting agent, is an effective mitogen for primate peripheral blood lymphocytes. Optimal stimulation of human lymphocytes was obtained 4 days after the addition of TPA at a concentration of 7.5 ng/ml. Lymphocyte fractionation experiments demonstrated that both T and B cells incorporated 3H-thymidine significantly in response to TPA. Lymphocyte blastogenesis was not due to the reactivation of latent herpesviruses by the tumor promoter, since similar responses to TPA were obtained with virus-genome positive or negative cells. Increased levels of DNA synthesis were observed when TPA was added to marmoset, baboon, rhesus monkey, or chimpanzee peripheral blood lymphocytes. Canine peripheral blood lymphocytes and spleen cells from guinea pigs, rats, and mice were not stimulated by TPA. These observations suggest that TPA-induced lymphocyte blastogenesis may be useful for studies of lymphocyte activation and of the molecular mechanisms of action of tumor-promoting phorbol esters.