bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phorbol ester enhances both interleukin 2 receptor expression and immunoglobulin secretion in human Epstein‐Barr virus‐immortalized B cells
Authors: Polke Christine R. , Lowenthal John W. , Roth Stephan A. , Rohwer Peter , MacDonald H. Robson , Kalden Jochen R. 
Published: February 2007

AbstractThe enhanced expression of interleukin 2 (IL2) receptors by 12‐O‐tetradecanoylphorbol 13‐acetate (TPA) on sublines of an Epstein‐Barr virus‐immortalized human B17 B cell line (M. Steinitz et al., Immunobiology 1979. 156: 41.) was studied by immunofluorescence using the anti‐Tac monoclonal antibody and by binding studies with purified radiolabeled IL2. These studies show that TPA at a final concentration of 5 ng/ml greatly increased Tac antigen expression on a number of sublines of B17. IL2‐binding studies revealed that TPA induced an increase in not only the number of IL 2 receptors per cell but also the affinity of the receptors for IL 2. The number and affinity of IL2 receptors on the C76 subline treated with TPA appear to be similar to those of activated normal human peripheral T cells.Furthermore, TPA‐induced differentiation of these B cell lines was measured by induction of immunoglobulin secretion using an enzyme‐linked immunosorbent assay. The capacity of TPA to induce differentiation in human B cells and the biological significance of IL2 receptor expression by activated B cells are discussed.
Only Tα or Tγ cells can be triggered by IgG or IgA to suppress the production of the matching Ig class
Authors: Bich‐Thuy LĚ Thi , Revillard Jean‐Pierre 
Published: February 2007

AbstractA short exposure of human peripheral blood mononuclear cells (PBMC) to heat‐aggregated IgG (or IgA) was found to inhibit pokeweed mitogen (PWM)‐induced human B cell differentiation into IgG (or IgA)‐producing cells. The present study was designed to investigate the nature of the cells inducible by aggregated (Agg)‐IgG or Agg‐IgA into isotype‐specific suppressors. When T cell‐enriched suspensions were exposed to Agg‐IgG or Agg‐IgA, then thoroughly washed, and cultured with autologous nonrosetting cells in the presence of PWM, a selective suppression of the generation of cells synthesizing and secreting IgG or IgA, respectively, was observed. Conversely, no inhibition was induced by T‐depleted PBMC treated in exactly the same way. Unlike Agg‐IgG, Agg‐F(ab′)2 fragments did not trigger suppression. Finally, in vitro X‐irradiation of T cells pretreated with Agg‐IgG or Agg‐IgA abrogated their suppressive activity. It is concluded that among cells bearing Fcγ or Fcα receptors, only T cells were inducible into suppressor cells by the binding of the matching immunoglobulin class.
Viral recognition by influenza A virus cross‐reactive cytotoxic T (Tc) cells: The proportion of Tc cells that recognize nucleoprotein varies between individual mice
Authors: Pala Pietro , Townsend Alain R. M. , Askonas Brigitte A. 
Published: February 2007

AbstractL cells (H‐2k) transfected with DNA coding for the A/NT/60/68 influenza nucleoprotein (NP) gene have been found previously to provide a target cell for cytotoxic T (Tc) cells. In this report we have studied the repertoire of cytotoxic memory cells in mice of different strains primed by infection with several influenza A subtypes. L cells transfected with NP and Db genes enabled us to estimate the proportion of A virus cross‐reactive Tc cells specific for NP.The most striking feature of our results was variation in the frequency of NP‐specific Tc cells between individuals of an inbred mouse strain. Occasional individuals, although showing a strong A virus cross‐reactive Tc response, had no A virus cross‐reactive Tc cells that recognized NP. The NP‐directed Tc repertoire represented between 0‐40% of lysis of target cells infected with a heterologous type A virus. Thus, a significant proportion of A virus cross‐reactive Tc cells must have different specificities for type A influenza virus. In C3HH‐2o2 mice, Dk is a low responder allele for NP recognition by Tc cells.
The cellular basis for the induction of antigen‐specific T8 suppressor cells
Authors: Morimoto Chikao , Letvin Norman L. , Distaso Judy A. , Brown Howard M. , Schlossman Stuart F. 
Published: February 2007

AbstractThe cellular basis for the generation of antigen‐specific T8 suppressor cells with high doses of antigen has been studied. We separated the T4 subset of human T cells into T4+2H4+ and T4+2H4− subpopulations with a recently developed monoclonal anti‐2H4 antibody. T8 cells could be consistently activated to suppress a primary anti‐2,4‐dinitrophenyl (DNP) antibody response in vitro with unfractionated T4 cells or with the T4+2H4+ subset but not the T4+2H4− subset. In contrast, the T4+2H4− subset functioned as the helper inducer for the anti‐DNP antibody response. With keyhole limpet hemocyanin (KLH)‐stimulated T4+2H4+ cells we could efficiently induce antigen‐specific suppressor activity of fresh T8 cells. In contrast, the T4+2H4+ subset could not effect suppression in the absence of T8 cells. Our findings indicate that the T4+2H4+ subset of human T cells is the suppressor inducer of specific T8 cells in an antigen‐specific DNP‐KLH system.
Antigen‐specific suppression of human antibody responses by allogeneic T cells II. Cell interactions involved in the generation of suppression
Authors: Callard Robin E. , Tiernan Shane L. , Winger Carrie M. 
Published: February 2007

AbstractSpecific antibody responses to influenza virus were obtained in vitro from human blood mononuclear cells (PBMC). Antibody production in these cultures was profoundly suppressed by the addition of allogeneic T cells with the surface phenotype Leu2a+ (CD8+), Leu8−. Suppression by allogeneic T suppressor (Ts) cells required interactions only between T‐depleted B (E−) cells and allogeneic Leu2a+. No evidence was obtained for T‐T cell interactions, or for Ts inducer cells similar to those described for nonspecific antibody responses to pokeweed mitogen. Moreover, allogeneic E+, or allogeneic Leu2a+ cells were able to suppress specific antibody responses by E− cells when help was provided by T cell‐replacing factor showing that the target of suppression was the responding E− cells, and not T helper cells. In contrast to allogeneic T cells, allogeneic E− cells did not suppress antibody production when added to cultures of unfractionated PBMC (E− + E+). That is, Ts cells activated to allogeneic E− were unable to suppress antibody production by the syngeneic E− cells present in the same culture tube. This result shows that alloactivated Ts cells were specific for the allogeneic E− target cells, and that suppression was not mediated by nonspecific allogeneic effects. Allogeneic Ts cells therefore differ from Ts cells in pokeweed mitogen responses by their specificity, and by their activation in the absence of Ts inducer cells.
Kinetics of cellular oncogene expression in mouse lymphocytes: I. Expression of c‐myc and c‐rasHa in T lymphocytes induced by various mitogens
Authors: Schneider‐Schaulies Jurgen , Hünig Thomas , Schimpl Anneliese , Wecker Eberhard 
Published: February 2007

AbstractMurine splenic T lymphocytes display maximal cellular myc gene (c‐myc) expression already 3 h after concanavalin A stimulation and subsequent down‐regulation before the onset of DNA synthesis. Stimulation by leucoagglutinin in the presence or absence of interleukin 2 leads to only low initial levels of c‐myc‐specific RNA which, however, increase later on. A similar pattern of c‐myc expression is shown by the Lyt‐2+ T cell subpopulation stimulated with either concanavalin A or leucoagglutinin in the presence of interleukin 2. Although [3H]thymidine incorporation was identical, the leucoagglutinin‐stimulated Lyt‐2+ T cells were void of any demonstrable c‐myc‐specific RNA at 3 h post‐stimulation. Thus, the kinetics of c‐myc expression in mouse T lymphocytes are not at all uniform, but depend on the mitogen and the subpopulation. In contrast, levels of c‐rasHa‐specific RNA were always low at early times, always increased towards the onset of DNA synthesis and down‐regulation was not observed.
Induction of murine T cell lymphoma expressing specific cytotoxic activity
Authors: Schaaf‐Lafontaine Nicole , Martin Marie Thérèe , Boniver Jacques 
Published: February 2007

AbstractThe present work reports the establishment of an antigen‐specific cytotoxic T cell lymphoma line after immortalization with a murine leukemia virus. Lymph node cells from mice bearing a transplanted syngeneic MCA sarcoma were infected in vitro with radiation leukemia virus and injected intrathymically into congeneic recipient mice. Some lymphomas of donor origin were established as permanent continuous cell lines in vitro. One of them, NS8, expressed Thy‐1.2, Lyt‐1, Lyt‐2 and peanut agglutinin surface markers. These cells were cytotoxic in vitro for the tumor cell line corresponding to the immunizing MCA sarcoma. No significant cytolytic activities against other syngeneic or allogeneic sarcomas or lymphomas, nor against the mastocytoma P815 were observed. After several months of in vitro propagation, the specificity of the cytotoxic activity had degraded and the level of Lyt‐2 or peanut agglutinin receptors dropped. These characteristics were restored with a single in vivo passage. Thus, murine leukemia virus can be used to immortalize antigen‐specific cytotoxic T cells.
Macrophage activation by trehalose dimycolate Requirement for an expression signal in vitro for antitumoral activity; biochemical markers distinguishing primed and fully activated macrophages
Authors: Grand‐Perret Thierry , Lepoivre Michel , Petit Jean‐François , Lemaire Geneviève 
Published: February 2007

AbstractIt was possible to define the effects of trehalose dimycolate (TDM), a glycolipid extracted from Mycobacteriurn tuberculosis, on mouse peritoneal macrophages more precisely using endotoxin‐free culture conditions. TDM‐elicited macrophages, when assayed in vitro in the absence of endotoxin, were unable to limit tumor growth; however, after a short treatment (4 h) with low doses of lipopolysaccharide (LPS; 1‐10 ng/ml), they exhibited a strong cytostatic capacity against P815 mastocytoma cells. Thus, TDM injected in vivo did not activate macrophages fully but it primed them to respond in vitro to low doses of LPS, which provided the final stimulus for activation to antitumor competence. Macrophages elicited by an injection of killed group C Streptococci were also in a primed state; in contrast, thioglycollate‐elicited macrophages were in a nonreceptive state. Besides LPS, concanavalin A (5 μg/ml), MDP (0.2‐1 μg/ml) and the ionophore A23187 (5 μM) can deliver the activation signal to TDM‐primed macrophages.Primed macrophages were found to express several biochemical markers previously described as specific for activated macrophages (low levels of alkaline phosphodiesterase and β‐galactosidase, for example) and, although they were not cytotoxic for tumor cells, they had the capacity to release large amounts of H2O2.However, when pulsed by LPS or MDP, primed macrophages responded by further modifications in their metabolism: the rate of glucose consumption and the labeling of glycoproteins by D‐[2‐3H]mannose were greatly increased and the secretion of a polypeptide of 22 kDa was enhanced. The activation‐associated biochemical markers are thus acquired in two steps. The ability to produce activated oxygen species is expressed earlier than the antitumoral activity.
Human natural killer cell lysis of virus‐infected cells. Relationship to expression of the transferrin receptor
Authors: Borysiewicz Leszek K. , Graham Shek , Sissons J. G. Patrick 
Published: February 2007

AbstractNatural killer (NK) cells lyse tumor and virus‐infected cells yet the nature of the target structure they recognize is unknown. A normal host cell glycoprotein, the transferrin receptor (TfR), has been proposed as a target structure on tumor cells. We therefore investigated whether changes in the number or physiological recycling of the TfR, consequent on virus infection, were related to the differential susceptibility of virus‐infected cells to NK lysis. There was a direct correlation between TfR expression, susceptibility to NK lysis and ability to act as cold target competitors, for human fibroblasts infected with RNA and DNA viruses (cytomegalovirus, herpes simplex, polio, vaccinia and Semliki Forest virus). The NK lysis of human cytomegalovirus‐infected fibroblasts was studied in more detail. NK lysis was increased coincident with human cytomegalovirus early antigen expression and this susceptibility to lysis was associated with increased total and recycling TfR but only a slight increase in surface TfR expression. In addition, susceptibility of uninfected human fibroblasts to NK lysis directly correlated with TfR number. However, we were unable to inhibit NK lysis by either excess iron‐saturated Tf or affinity‐purified TfR. We conclude that there is a direct correlation between total TfR expression and susceptibility to NK lysis of human virus‐infected cells; however, the NK target structure on virus‐infected cells is probably not the TfR itself.
Antigen presentation is a function of all B cell subpopulations separated on the basis of size
Authors: Jelachich Mary Lou , Lakey Ellen K. , Casten Lisa , Pierce Susan K. 
Published: February 2007

AbstractPurified splenic B cells from nonimmune mice were separated by counterflow centrifugal elutriation into 6 subpopulations containing cells of discrete sizes ranging from 119 to 200 μm3. B cells of each subpopulation were competent to process and present a native globular protein antigen, cytochrome c, to a cytochrome c‐specific T cell hybrid. In all cases, the B cells' antigen‐presenting function was radiation sensitive and did not require T cells or T cell products, since B cells fixed with paraformaldehyde effectively presented a carboxyl‐terminal peptide fragment of cytochrome c containing the T cell determinant. Furthermore, the antigen‐presenting function of B cells of each subpopulation was augmented by treatment with submitogenic doses of the F(ab')2 fragment of rabbit anti‐mouse Ig antibodies, in that 10‐30‐fold fewer B cells were required and higher maximal T cell responses were achieved, indicating that B cells of all sizes are capable of being regulated in their antigen presentation function through their surface Ig. In addition, B cells of each subpopulation responded to soluble factors present in the supernatants of activated T cells as evidenced by an increase in volume and by the uptake of [3H]thymidine. These results indicate that B cells, regardless of size, are able to participate in at least two essential phases of T cell‐dependent antibody responses, initiating the interaction by processing and presenting antigen to helper T cells and responding to soluble helper factors secreted by activated T cells.
Modification of lymphocyte migration by sulfated polysaccharides
Authors: Brenan Mary , Parish Christopher R. 
Published: February 2007

AbstractThe role of sulfated polysaccharides in lymphocyte migration has been analyzed in vivo using lymphocytes labeled with an intracellular DNA‐binding fluorochrome Hoechst 33342. The influence of a panel of sulfated polysaccharides on entry (by injecting the sulfated polysaccharide prior to the labeled cells) and displacement from lymphoid organs (by injecting the sulfated polysaccharide after the labeled cells have localized) indicated that different sulfated polysaccharides have selective effects on entry and displacement, and furthermore positioning of subpopulations within organs. Additional experiments suggested that receptors for sulfated polysaccharides on high endothelial venules may interact with complementary structures on lymphocytes. The data supporting this conclusion were: (a) the normal localization behavior of lymphocytes preincubated with sulfated polysaccharides; (b) an inverse relationship between the expression of lymphocyte surface receptors for sulfated polysaccharides and the ability of the lymphocytes to enter lymphoid organs and (c) the selective binding of sulfated polysaccharide‐coupled fluoresceinated beads to high endothelial venules. In this case only the beads coupled with the sulfated polysaccharides that inhibited entry bound to the high endothelial venules. These findings are discussed in terms of a fundamental cellular recognition system utilizing sulfated polysaccharides.
Inability of autoimmune mice with the lpr gene to spontaneously produce interleukin 3
Authors: Kelley Vicki E. , Farber Neal M. , Williams John M. , Strom Terry B. 
Published: February 2007

AbstractA recent report (Palacios, R., Eur. J. Immunol. 1984. 14: 599) indicates that spleen cells from MRL‐MpJ‐lpr/lpr mice spontaneously produce interleukin 3 (IL3) and suggests that this lymphokine could be responsible for promoting the lymphoid hyperplasia regulated by the lpr gene. The present study shows that splenocytes from several murine strains bearing the lpr gene do not spontaneously produce IL3. This has been determined by measuring the amount of this lymphokine by a bioassay and by the detection of IL 3 mRNA using Northern blot analysis. We suggest that another lympbokine is responsible for growth of lymphocytes regulated by the lpr gene.
Immunologic memory to phosphorylcholine (PC) VIII. Expression of the VH−12 gene product in the response to PC‐keyhole limpet hernocyanin
Authors: Rittenberg Marvin B. , Glanville Robert W. , Aebersold Ruedi H. , Chang Sandra P. , Brown Mckay 
Published: February 2007

AbstractThree murine anti‐phosphorylcholine (PC) hybridomas with group II‐like fine specificity patterns isolated during a memory response to PC‐keyhole limpet hemocyanin (KLH) are examined at the molecular level to determine the origins of the VH and VL used by these antibodies. Southern blots of Hind III cut DNA were hybridized with a probe specific for the V1 gene of the T15 VH family. The V1 germ‐line configuration is retained in these hybridomas indicating that this gene which encodes the VH gene product expressed by most group I anti‐PC hybridomas is not used for antibody production. Southern blots of Eco RI cut DNA hybridized to a probe specific for JH1‐JH4 indicated that all three hybridomas PCG1‐2, PCG1‐3 and PCM‐23 share a 5.2‐kb rearranged JH band, suggesting utilization of a common VH gene segment. N‐terminal amino acid sequence analysis of the heavy chains of two of the hybridoma proteins PCG1‐2 and PCG1‐3 indicates that they belong to mouse heavy chain subgroup II and are closest in sequence to a VH−12 isotype anti‐PC hybridoma protein, HPC‐104, derived from BALB/c mice suppressed for the T15 idiotype; PCG1‐2 and PCG1‐3 each differed from HPC‐104 at only 1/20 residues. In addition, these proteins have in common a lysine at position 1 which has not been found previously in 203 other heavy chain sequences reported. N‐terminal sequences of the light chains of PCG1‐2 and PCG1‐3 are each shown to differ at only 1/22 residues from Vx24, and PCM‐23 had previously been shown to use Vx8; both of these light chains have been associated previously with heavy chains derived from the V1 gene in anti‐PC antibodies.These results indicate that the VH−12 isotype can be used during a normal antibody response to PC and thus that heavy chains derived from both subgroup II and subgroup III (the T15 heavy chain) contribute to the molecular heterogeneity observed in memory responses to PC‐KLH.
Human leukocyte function‐associated antigens on lympho‐hemopoietic precursor cells
Authors: Campana Dario , Sheridan Brian , Tidman Nicholas , Hoffbrand A. Victor , Janossy George 
Published: February 2007

AbstractThe expression of human leukocyte function‐associated antigens (HLFA, equivalents of murine LFA‐1) was studied on early lympho‐hemopoietic cells in infant thymus and normal bone marrow by double immunofluorescence methods, cell sorting and colony‐forming assays. Monoclonal antibodies MHM‐24 recognizing the α chain (180 kDa) and 60.3 and 60.1 identifying the β chain (95 kDa) were used. The vast majority of thymocytes including large terminal deoxynucleotidyl transferase (TdT)‐positive blast cells are HLFA positive. On the other hand, most B cell precursors in the bone marrow, identified by the expression of nuclear TdT, do not show surface HLFA which appears at the pre‐B cell stage (cytoplasmic μ positive, surface Ig negative). Cell sorting experiments revealed an enrichment of early myeloid cells (myeloblasts and colony‐forming unit cells) in the HLFA‐negative fraction. Erythroid cells appeared to be completely negative from the burst‐forming unit erythrocyte stage onwards. Anti‐HLFA‐antibodies, capable of blocking T cell and natural killer function, may have therapeutic potential without interfering with precursor cell development in man.
Specific lysis of murine cells expressing HLA molecules by allospecific human and murine H‐2‐restricted anti‐HLA T killer lymphocytes
Authors: Achour Ammar , Begue Bernadette , Gomard Elisabeth , Paul Pascale , Sayagh Brigitte , Van Pel Aline , Levy Jean‐Paul 
Published: February 2007

AbstractThe lysis by human and murine anti‐HLA cytolytic T lymphocytes (CTL) of murine cells expressing class I HLA molecule after gene transfection has been studied using two different murine cells: LMTK− and P815‐HTR‐TK−. Weak but significant HLA‐A11‐specific lysis was found occasionally with human CTL on the HLA‐A11+ L cells. On the contrary, P815‐A11 or P815‐A2 cells were lysed strongly and specifically by HLA‐A11 or HLA‐A2‐specific human CTL. The T8+T4− phenotype of the effector cells was confirmed and the reaction was inhibited by anti‐HLA class I monoclonal antibodies. Despite their higher sensitivity to human CTL, the P815‐HLA+ cells did not express higher levels of HLA antigens than L cells, and the presence or the absence of human β2 microglobulin was irrelevant. Anti‐human LFA‐1 antibodies abrogated the lysis of P815‐A11+ cells showing that the LFA‐1 receptor which is apparently lacking on the L cell surface was on the contrary expressed on P815 cells. On the other hand, murine anti‐HLA CTL have been prepared by immunizing mice against syngeneic HLA‐A11+ L cells. They lysed very efficiently and specifically these cells, but appeared completely devoid of activity against human HLA‐A11 target cells. This barrier was apparently due to the H‐2 restriction of these H‐2k anti‐HLA murine CTL, as shown by their inability to lyse allogeneic H‐2d cells expressing HLA‐A11, and by the blocking of their activity by anti H‐2k antibodies. By contrast, xenogeneic anti‐HLA CTL obtained by immunizing murine lymphocytes against human cells lysed both human and murine HLA+ cells but they reacted with a monomorphic epitope of the HLA molecule in a nonrestricted way. These results show that (a) human cells lyse very efficiently P815 murine cells expressing HLA class I antigens; (b) the higher sensitivity of P815 cells compared to L cells is probably due to the presence of a LFA‐1 receptor on these cells; (c) a class I molecule of human origin can be seen as an H‐2‐restricted minor histocompatibility antigen in another species.