bluuebunny/crossref_metadata_2025_split huggingface dataset:
Target cell heterogeneity in murine leukemia virus infection. II. Demonstration of friend leukemia‐virus‐permissive and non‐permissive subsets of splenic T cells
Authors: Isaak Dale D. , Cerny Jan 
Published: February 2007

AbstractThe permissiveness of normal splenic lymphocytes to Friend murine leukemia virus was determined by enumeration of cells producing infectious MuLV following infection with Friend virus in vitro. The infection was enhanced greatly in the presence of mitogens in the culture medium. The number of infected cells in cultures stimulated with bacterial lipopolysaccharide increased progressively between days 1 and 7 whereas in cultures with concanavalin A, the number of infected cells reached a maximum on days 3–4 post infection and then declined to the level observed in unstimulated cultures. The con‐A‐enhanced infection was absent in cultures of splenocytes from nude mice but was present in cultures from nude mice implanted with thymus glands 6 weeks or more before use as donors of spleen cells. The cells permissive to MuLV upon con‐A stimulation segregated in the nylon‐wool‐adherent fraction (together with B cells involved in the LPS‐dependent infection) whereas the nylon‐non‐adherent fraction, containing approximately 90% T cells, was refractory to in vitro infection. The con‐A‐dependent infectious centers were inhibited by cytotoxic treatment with anti‐Thy 1.2 antibody plus complement. These results indicate the existence of two subpopulations of splenic T cells, a major nylon‐non‐adherent and a minor, nylon‐adherent subpopulation, which are, respectively, non‐permissive and permissive to MuLV‐Friend.
Generation in vitro of ebv‐induced specific cytotoxic T cells in autologous serum avoids complications due to self‐preferred foetal calf serum‐specific t‐cell cytotoxicity
Authors: Misko I. S. , Kane R. G. , Pope J. H. 
Published: February 2007

AbstractA previous report has established that in cultures of human mononuclear leukocytes, foetal calf serum (FCS) is capable of generating high levels of T cells preferentially cytotoxic for the autologous lymphoblastoid cell line (LCL). The present study compared the capacity of Epstein‐Barr virus (EBV) to generate cytotoxic T cells in cultures of mononuclear cells grown in FCS or autologous serum in order to clarify the role of FCS in this system. Five EBV‐seropositive and three seronegative donors were used and cultures were harvested at 14 days. With cultures from seropositive donors, whether grown in FCS or in autologous serum, EBV infection generated T cells cytotoxic for the autologous LCL; the response in uninfected control cultures was markedly lower. With seronegative donor cultures grown in FCS, there was virtually no difference in the capacity of T cells generated in infected or uninfected cultures to lyse the autologous LCL. Moreover, cells from seronegative donors cultured in human serum gave no detectable lysis of autologous LCL in either infected or uninfected cultures, clearly showing the absence of a response to EBV. This evidence shows that it is possible to distinguish the generation of specific cytotoxic T cells by FCS from generation by EBV, and with certain donors the apparently EBV‐induced response may actually include a significant component induced by FCS in the medium. The cytotoxicity patterns of EBV‐induced and FCS‐induced T cells for autologous and allogeneic LCL targets showed a degree of parallelism, stressing the need for caution in interpretation of data obtained from cultures using FCS.
Characterization of ‘h‐2k, d‐like structures’ on mm2 × mouse l cell hybrids. i. ‘h‐2k, d‐like’ alloantigen encoded by the d region and/or to the right of the d region of the h‐2 gene complex
Authors: Kubota Koichi , Manson Lionel A. 
Published: February 2007

AbstractIt was found that anti‐MM2 serum, which had been prepared by immunizing C3H/He mice with syngeneic MM2 mouse mammary ascites tumor, detected molecules of 44–46,000 and 12,000 daltons on EL4 leukemic cells and on C57BL/6 lymph node cells, as well as on somatic cell hybrids between the MM2 and mouse L cells. Experiments with a known rabbit anti‐mouse β2‐microglobulin serum showed that the two molecules detected by anti‐MM2 serum were hydrophobically associated with each other in membrane extracts; thus, the antigen detected by anti‐MM2 serum was structurally similar to H‐2K and D antigens. Preclearing of lysates from C57BL/6 lymph node cells with a mixture of anti‐H‐2.2, anti‐H‐2.33, and anti‐H‐2.28 sera did not remove the ‘H‐2‐like’ antigen, indicating that the antigen was distinct from the H‐2Kb and Db molecules. Neither C3H/He nor B10. BR lymph node cells expressed the ‘H‐2‐like’ antigen, but B10. A(4R) and B10. AM lymph node cells did possess the antigen. Absorption of anti‐MM2 serum with EL4 cells abolished the capacity of the absorbed serum to precipitate the ‘H‐2‐like’ antigen activity on C57BL/6 lymph node cell extracts and reduced the ‘H‐2‐like’ radioactive peaks of the hybrid cells. These results indicate that there are at least two components being recognized by the anti‐MM2 serum in hybrid cells between MM2 tumor and mouse L cells, both of which had originated in the C3H/He mouse (H‐2k). One is the same as or cross‐reactive with an ‘H‐2‐like’ alloantigen of normal C57BL/6 lymph node cells (H‐2d) and the other is another ‘H‐2‐like’ antigen. Experiments with recombinant mice show that the ‘H‐2‐like’ alloantigen on lymph node cells is coded for by the D region and/or to the right of the D region of the major histocompatibility complex (MHC).
Report on international comparative evaluation of possible value of assays for immune complexes for diagnosis of human breast cancer
Authors: Herberman Ronald B. , Bordes M. , Lambert P. H. , Luthra Harvinder S. , Robins R. A. , Sizaret Philippe , Theofilopoulos Argyrios 
Published: February 2007

AbstractThere have been several reports on the possible value of measurement of circulating immune complexes for the diagnosis of human breast cancer. To begin to evaluate this possibility and the comparability of results among laboratories, a cooperative study was organized under the auspices of the International Agency for Research on Cancer and the National Cancer Institute (NCI) of the United States. Investigators from four laboratories performing assays for immune complexes were sent coded aliquots of serum specimens from the NCI‐Mayo Clinic Serum Bank. The serum panel consisted of specimens from 30 patients with breast cancer (including 20 from untreated patients with resectable tumors), 30 preoperative patients with benign breast disease, and 30 normal women. Although some significant differences in levels of immune complexes between cancer patients and controls were seen, none of the assays had sufficient discriminatory capacity to support optimism about the diagnostic value of this approach. To relate the results with immune complexes to those with a widely used cancer marker, the same sera were also tested for levels of carcinoembryonic antigen (CEA). The CEA assay provided significant discrimination between cancer patients and normal donors but did not significantly discriminate between malignant and benign breast diseases.
Induction of differentiation in murine myelomonocytic leukemia cells by the serum of patients with acute myeloid leukemia and other diseases
Authors: Metcalf Donald 
Published: February 2007

AbstractSera from patients with leukemia, lymphomas or other diseases were tested for their capacity to induce differentiation in colonies produced in semi‐solid agar by the mouse myelomonocytic leukemia, WEHI‐3B. Of 949 samples tested, higher than normal differentiating activity was detected in patients with infections (31% of sera tested) and with acute myeloid leukemia in relapse (35% of sera tested). The higher activity of the latter sera was correlated with the concurrent presence of infections in the relapse leukemic patients. Elevated differentiating activity was also observed in sera from patients with neutrophil levels below 1,000/μl even if infections were not present. The study indicates that patients with acute myeloid leukemia are able to elevate serum differentiating activity in response to infections or neutropenia and that the serum differentiating factors could play a role in suppressing myeloid leukemic populations by enforcing differentiation in the leukemic cells.
Studies on the role of cellular immunity and genetics in the etiology of rapidly progressing breast cancer in tunisia
Authors: Levine P. H. , Mourali N. , Tabbane F. , Loon J. , Terasaki P. , Tsang P. , Bekesi J. G. 
Published: February 2007

AbstractIt has been suggested that poussée évolutive (PEV) or rapidly progressing breast cancer (RPBC) represents a failure in the host immune system to control the proliferation of breast cancer cells. To evaluate this possibility, we have performed in vivo and in vitro assays of cellular immunity in Tunisian patients with breast cancer. Studies of delayed hypersensitivity using microbial antigens and in vitro studies including lymphocyte transformation tests and measurements of B and T cells indicated that RPBC patients had an immune response comparable to that of breast cancer patients without evidence of rapid progression. Normal Tunisians were more immunocompetent, however, and appeared to have a higher level of immune activity than normal individuals in the United States. In a second, independent series, an increased frequency of blood group A was found in RPBC patients, suggesting a genetic predisposition to this form of breast cancer. However HLA typing for A, B and DRW antigens revealed no specific RPBC‐associated HLA antigen. Our studies clearly demonstrate that RPBC, or PEV, is not a reflection of immunodeficiency.
Mechanism of enhancement of epstein‐barr virus‐induced transformation of peripheral blood lymphocytes by a tumor promoter, tpa, with special reference to lowering of cytotoxicity of t cells
Authors: Harada Shinji , Katsuki Takato , Yamamoto Hidehiko , Hinuma Yorio 
Published: February 2007

AbstractThe mechanism of the previously observed enhancement of Epstein‐Barr virus (EBV)‐induced cell transformation of human lymphocytes by 12‐O‐tetradecanoyl‐phorbol‐13‐acetate (TPA) was studied. A concentration of TPA (0.5 ng/ml) was used. In cultures of human cord blood lymphocytes infected with EBV in the presence of TPA, a larger number of EBV‐associated nuclear antigen (EBNA)‐positive and/or DNA synthesizing cells was observed than in the absence of TPA. In the virus‐infected lymphocyte cultures of EBV‐seropositive adult donors, in vitro regression of transformation, which is known to be caused by T lymphocytes, was suppressed by TPA. EBV‐specific and ‐non‐specific cytotoxicity of T cells generated in mixed cultures of peripheral blood lymphocytes (PBL) of seropositive adults and autologous lymphoblastoid cell line (LCL) cells was markedly lowered by the presence of TPA in the cultures. However, TPA had little effect on proliferation of T cells in stimulated cultures, and addition of TPA to the reaction mixture for the cytotoxicity test did not lower the cytotoxicity. These results suggest that TPA has an inhibitory effect on T cells which suppress EBV‐transformation. The effect on T cells, together with the direct promoting effect on proliferation of EBV‐transformed cells, may explain the outcome of enhancement of EBV‐induced LCL establishment from PBL of seropositive donors by TPA previously observed.
Characterization of a human papillomavirus from epidermodysplasia verruciformis lesions of a patient from upper‐volta
Authors: Pfister Herbert , Nürnberger Friedrich , Gissmann Lutz , Hausen Harald Zur 
Published: February 2007

AbstractA case of epidermodysplasia verruciformis in a patient from Upper‐Volta is described. Slightly elevated, flat warts were observed on hands, feet, arms and legs, and pityriasis versicolor‐like lesions were found mainly on the trunk. The patient showed no malignant tumors. Histological examination revealed hyperkeratosis, granulosis and moderate acanthosis with large, foamy, basophilic keratinocytes in stratum granulosum and stratum spinosum. Papillomavirus particles could be prepared from these lesions and were differentiated from known papillomavirus types by immune electron microscopy with monospecific antisera and by DNA‐DNA hybridization. The viral DNA was characterized by cleavage with several restriction endonucleases and a physical map of the resulting fragments was established. The virus is designated as HPV 8. Preliminary seroepidemiologic studies with human sera indicate a rather wide distribution of HPV 8. Blot hybridization of DNA from human carcinomas with 32P‐labelled virus DNA detected no HPV 8‐specific sequences.
Clonal analysis of the ability of tumor cells to form colonies in semi‐solid medium
Authors: Brodskaya R. M. , Stavrovskaya A. A. , Stromskaya T. P. , Vasiliev J. M. 
Published: February 2007

AbstractNear‐diploid mouse tumor cells CAK‐25 AGr are characterized by low cloning efficiency in semi‐solid medium: about 10−5 per cell plated in methylcellulose. The properties of cells that have formed colonies in methylcellulose were compared with those of the parental population. Nine of 12 subclones of CAK‐25 AGr picked from methylcellulose retained parental cloning efficiency when retested for growth in semi‐solid medium. Thus most colonies in methylcellulose were not formed by variant cells different from the parental cell population. Cloning efficiency of CAK‐25 AGR and of its subclones on the solid substratum was high. All six sub‐subclones randomly isolated from the solid substratum had the ability to form colonies in methylcellulose at a frequency no lower than that of the parental clone. Thus, most cells of the population had not lost the ability to form colonies in methylcellulose. The results suggest that the probability of a cell's initiating a colony in semi‐solid medium is heritable and identical for most cells of the line under investigation.
Radioisotope assay for evaluation of in vivo natural cell‐mediated resistance of mice to local transplantation of tumor cells
Authors: Gorelik E. , Herberman R. B. 
Published: February 2007

AbstractA radioisotopic assay based on the rate of elimination of [125I]dUrd‐labelled tumor cells from the local site of inoculation was used to study anti‐tumor natural cellmediated immunity in vivo. [125I]dUrd‐labelled YAC‐I, RL♂ I, and M109 tumor cells were inoculated into the footpads of mice and the radioactivity remaining at the site was measured at various times. This method allowed quantitation, in individual mice, of the actual number of tumor cells inoculated and their local clearance. It was found that 90–99% of inoculated YAC‐I or RL♂ I cells were eliminated in the first 24–48 h following transplantation. Participation of NK cells in the local elimination of the transplanted tumor cells was supported by the following findings: (1) The rate of elimination of NK‐sensitive tumor cells was higher than that of the NK‐resistant M 109 tumor cells. (2) There was a positive correlation between the level of in vitro spleen‐cell NK activity of the different strains of mice and the rate of in vivo elimination of YAC‐I. (3) Inoculation of poly I:C or cyclophosphamide increased or decreased, respectively, the clearance of tumor cells in vivo. (4) Local adoptive transfer of normal spleen cells accelerated the rate of tumor cell elimination in vivo. (5) This adoptive transfer of the cytotoxicity was mediated by non‐adherent, non‐T cells that expressed asialo GMI. Despite these correlations between NK activity and the in vivo assay, two major discrepancies were found: YAC‐I cells were eliminated at the same rate in young and old mice, and beige mice were as effective for in vivo clearance of tumor cells as were normal C57BL/6 mice. These data suggested that other natural effector cells may participate in the in vivo destruction of the transplanted tumor cells or that different regulatory processes may operate in vivo. Our findings provide further evidence that natural cell‐mediated immunity can play an important role in the in vivo elimination of the transplanted tumor cells and indicate that this can occur at the local site of tumor inoculation as well as in the lungs or other organs.
Block of a glioma cell line in S by interferon
Authors: Lundblad D. , Lundgren E. 
Published: February 2007

AbstractThe human glioma cell line U‐251 MG, with a well‐characterized defect in growth control, was sensitive to the antiproliferative effects of human (fibroblast) interferon (IFN). IFN inhibited exponentially growing cells by increasing the number of cells in the S stage of the cell cycle. At the same time the number of cells in G0/G1 diminished. The rate of thymidine incorporation was decreased during the first cell cycle, with no prolongation of S. However, in synchronized cultures, the wave of cells with a S‐phase content did not decrease over a time period several hours longer than the length of S measured by pulse labelling. Thus we conclude that, at a sufficient dose, the cells were unable to accomplish cell division as they prematurely stopped synthesizing DNA.
Two human tumor‐associated antigens, p155 and p210, detected by monoclonal antibodies
Authors: Loop S. M. , Nishiyama K. , Hellströ I. , Woodbury R. G. , Brown J. P. , Hellströ K. E. 
Published: February 2007

AbstractBALB/c mice were immunized with human melanoma cells and their spleen cells hybridized with NS‐I myeloma cells. The hybrids were screened for the production of antibodies that bound to melanoma cells. Two hybridomas of interesting specificity were identified and cloned. Hybridoma 5.1 produces an IgG1 antibody that binds to about half of the melanomas and carcinomas tested. The target is a polypeptide with an apparent molecular weight of 210 kilodaltons on sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS‐PAGE). The antigen, denoted p210, is also expressed in normal adult brain and in certain fetal tissues. Hybridoma 6.1 produces an IgM antibody that binds to about 50% of the melanomas, and 80% of the kidney carcinomas tested. The antigen defined by this antibody in melanomas has an apparent molecular weight of 155 kilodaltons and is denoted p155. It has not been observed on any normal adult or fetal tissues. The antigen present in the kidney carcinomas was not p155, but rather consisted of two proteins of approximately 60,000 and 250,000–300,000 daltons. This observation suggests the possibility that the antigenic deteminant recognized by antibody 6.1 may be present on several distinct protein molecules.
Some immunogenic and biochemical properties of tumor‐associated transplantation antigens (TATA) obtained in soluble form or solubilized from two methylcholanthrene‐induced sarcomas, meth A and CI‐4
Authors: Rogers Michael J. , Law Lloyd W. 
Published: February 2007

AbstractThe subcellular distribution of the tumor‐associated transplantation antigens (TATAs) of two highly immunogenic methylcholanthrene‐induced sarcomas, Meth A and CI‐4, were compared. Most of the TATA of CI‐4 was found in the soluble fraction (cytosol) of the cell while the TATA from Meth A was variably distributed between the membrane and cytosol. The soluble fraction TATAs from both tumors were very immunogenic and their strong immunity could not be influenced by administering antigen in a variety of protocols that altered the immune response in other systems. The soluble fraction and membrane‐associated TATAs from both tumors could be specifically bound to liposomes in re‐constitution experiments and the antigenicity of all of the TATAs was significantly enhanced when they were incorporated into these artificial membranes.
Liposomally activated macrophages; subsequent interaction with L1210 leukemic cells
Authors: Luckenbach G. Albrecht , Layton Derek 
Published: February 2007

AbstractThe coincubation of liposomes with mouse leukemia cells or fibroblasts can cause a wide range of effects on their viability. These effects are not particularly specific in terms of destroying the leukemic cells. However, it was observed that the combination of phosphoryl‐choline‐cholesterol (PC‐CHOL)1‐liposomes, which are not toxic by themselves, with alkyl‐lysophospholipids as components of the liposome, can produce the desired specific cytotoxicity for leukemic cells. In this report we show that the cytotoxic effect of vinca alkaloid entrapped in PC‐CHOL‐liposomes was enhanced by syngeneic mouse bone marrow macrophages. In addition, alkyl‐lysophospholipids, which are known to be potent macrophage activators, augment the cytotoxicity. Thus, the macrophage could act as a carrier for liposome‐entrapped drug and, on the other hand, the liposomes partly composed of macrophage activating alkyl‐lysophos‐pholipid and loaded with chemotherapeutic drug seem to be ideal carriers of two effector mechanisms for attacking leukemic cells.
On the mechanism of tumor ‘concomitant immunity’
Authors: Gorelik Eliezer , Segal Shraga , Feldman Michael 
Published: February 2007

AbstractExperiments were carried out relevant to the mechanisms involved in tumor ‘concomitant immunity’. Mice bearing 3LL, B16, EL4 or the methylcholanthrene‐induced T‐10 tumors were capable of completely suppressing the growth of a subsequent intra footpad graft of tumor cells. The observed inhibitory activity exerted by the primary tumor increased with the increase in size of the tumor and reached its maximum at the latest period of tumor growth when the immune response of the tumor‐bearing host was largely suppressed. In T‐cell‐depleted animals (B mice or nude mice), the inhibitory effect exerted by the first tumor on the subsequently implanted tumor graft was as effective as in normal mice. Hence it appears that concomitant immunity is not mediated via a T‐cell‐dependent immune reaction. The observed inhibitory effect was tumor‐nonspecific. Mice bearing a 3LL tumor manifested resistance to the reinoculation of 3LL, B16 or EL4 tumor cells. Similarly, mice bearing B16, EL4 or T‐10 tumors arrested the growth of reinoculated 3LL tumor cells. Hence, concomitant immunity is not a result of specific immune response. Metastases can be considered as ‘naturally’ occurring secondary grafts. Indeed, we found that the local tumors exert a strong inhibitory effect on their lung metastases. Thus, the surgical removal of the local 3LL tumor led to an acceleration of metastatic growth in the lungs. Such acceleration took place even when the local tumor grew in immune‐suppressed mice. It appears, therefore, that ‘concomitant immunity’ and the suppression of metastatic growth exerted by the local tumor, are based on similar mechanisms.