bluuebunny/crossref_metadata_2025_split huggingface dataset:
Cloned human T lymphocytes with lymphostimulatory capacity preferentially activate suppressor cells
Authors: Pawelec Graham , Schneider E. Marion , Wernet Peter 
Published: February 2007

AbstractA proportion of cloned T cells derived from allogeneic mixed leukocyte cultures (MLC) was found to stimulate rapid primary, but not secondary, lymphoproliferative responses of autologous as well as allogeneic peripheral blood mononuclear cells (PBMC). Of eight major histocompatibility complex (MHC) class II‐specific monoclonal antibodies (mAb), the reagent TÜ39 (which preferentially inhibits allostimulation by SB‐ rather than DR‐ or DC‐associated determinants) most strongly inhibited stimulation by these clones. MAb specific for DC or DR molecules inhibited weakly or not at all. Stimulatory, but not nonstimulatory, clones were found to be strongly suppressive when titrated directly into MLC. Suppression was not MHC restricted, was radioresistant (20 Gy) and was not abrogated by the addition of partially purified interleukin 2 to the test cultures. Transfer of PBMC cocultured with stimulatory, but not with nonstimulatory, clones into a second MLC resulted in its strong suppression, suggesting that a suppressor effector population had been “induced” by the clones. These results are consistent with the hypothesis that SB‐like, rather than DR or DC, determinants present on the surface of certain activated T cells are intimately involved in the regulation of cellular immune responses by rapidly inducing suppressor effector cells in normal lymphocyte populations.
Target structure for natural killer cells: evidence against a unique role for transferrin receptor
Authors: Dokhélar Marie‐Christine , Garson Dominique , Testa Ugo , Tursz Thomas 
Published: February 2007

AbstractThe transferrin receptor (TfR) was recently proposed as putative natural killer (NK) cell target structure. Here data are presented against this hypothesis and it is shown that low TfR expression and high NK sensitivity can occur concommitantly. K562 cells were studied at various stages of cell proliferation. No change in NK sensitivity could be observed between exponential growth and the plateau phase, whereas TfR expression completely disappeared during the latter. Protein synthesis inhibitors such as cycloheximide (1 μg/ml, 48 h) and actinomycin D (50 μg/ml, 48 h), that abolished the TfR expression at the K562 cell surface, had no effect on NK sensitivity. Similarly, hemin induction (0.1 mM, 5 days) did not change NK susceptibility of K562 cells but considerably diminished TfR expression. Moreover, attempts to block NK sensitivity with anti‐TfR monoclonal antibodies were unsuccessful, even when the 42.6 antibody, which is known to bind to the active site of TfR, was used. Finally, no blocking of NK sensitivity could be achieved when K562 cells were preincubated with saturating concentrations of transferrin or when transferrin was added during the NK assay. It therefore seems doubtful that TfR is the unique target structure for NK cells. It remains possible that TfR and NK target structures are often coexpressed on actively dividing cells.
Production of type I (α/β) interferon after virus infection of cloned, alloantigen‐sensitized mouse T lymphocytes
Authors: Cooley Margaret A. , Blackman Michael J. , Morris Alan G. 
Published: February 2007

AbstractMouse T lymphocytes sensitized to alloantigens were cloned by limiting dilution in the presence of interleukin 2. Clones were tested for surface markers Thy‐1, Lyt‐1 and Lyt‐2, and for cytotoxic function. Production of interferon (IFN) by clones either (a) stimulated with allogeneic cells; (b) activated with concanavalin A (Con A); or (c) infected with Semliki Forest virus or Newcastle disease virus were assayed. All clones produced IFN upon Con A stimulation and most after virus infection. Analysis of the IFN produced by a single clone, using anti‐IFN antisera, showed that while Con A stimulation induced production of type II IFN (IFN‐γ), the IFN produced after virus infection was type I IFN (IFN‐α/β).
Human lymphoblastoid cell line producing protective monoclonal IgG1, χ anti‐tetanus toxin
Authors: Tiebout Robert F. , Stricker Elisabeth A. M. , Hagenaars Rien , Zeijlemaker Wim P. 
Published: February 2007

AbstractPeripheral blood lymphocytes from an individual, recently boosted with tetanus toxoid (TT), were transformed with Epstein‐Barr virus. No antigen‐specific selection nor stimulation of B cells was performed prior to transformation. One stable cell line, designated CLB‐Hu‐TT‐1, was established. This cell line has a doubling time of 24 h and yields 10 μg/ml of a monoclonal IgG1,χ anti‐TT antibody in bulk cultures. The antibody is biologically active in that it can protect mice against the effects of tetanus toxin. The cell line has been characterized with regard to some cytoplasmic and membrane markers.
Repopulation of the gut lamina propria with IgA‐containing cells by lymphoid cells isolated from the gut lamina propria
Authors: Tseng Jeenan 
Published: February 2007

AbstractMigration and lodging properties of IgA cells and their precursors of the gut lamina propria (GLP) were studied by transfer of highly purified GLP lymphoid cells between immunoglobulin allotype‐congenic mice (CB‐20 to BALB/c). The donor IgA‐containing (cIgA) cells appeared in the GLP of the recipients at day 1, peaked at days 12–15 (late repopulation peak) and persisted up to day 20 after cell transfer. An additional peak at day 3 (early repopulation peak) was seen only when large numbers of GLP B cells were transferred. Few cIgA cells appearing in spleen and mesenteric lymph nodes were seen mainly at days 12–15. The early repopulation peak was probably formed by the differentiation and accumulation of IgA blasts, recirculating IgA‐bearing cells and some IgA precursors. The former 2 cell types homed directly back, while the later homed indirectly via spleen to the GLP. The late repopulation peak was possibly formed by the homing and differentiation of Peyer's patch IgA precursors arriving in the GLP with membrane immunoglobulins unchanged. These GLP IgA precursors migrated first to the spleen and later back to the GLP, where they differentiated into IgA plasma cells.
Helper T cell activation for the human B cell response to trinitrophenylated polyacrylamide beads: involvement of the T4 antigen
Authors: Delfraissy Jean‐François , Vazquez Aimé , Wallon Christine , Desmottes Rose‐Marie , Galanaud Pierre 
Published: February 2007

AbstractThe monoclonal antibody (mAb) OKT4A (but not OKT4) inhibits the in vitro antibody response of human peripheral blood mononuclear cells. The target of OKT4A mAb is the helper T cell, as the helper cells for the antibody response to trinitrophenylated polyacrylamide beads (TNP‐PAA) are exclusively in the T4 subset. The OKT4A mAb is still suppressive when the anti‐TNP response of cultures of monocyte‐depleted cells is supported by purified interleukin 1. Both the OKT4A mAb and anti‐DR mAb suppress the non‐specific T cell proliferation in the cultures leading to the in vitro mAb response. A parallel inhibition is observed for the autologous mixed lymphocyte reaction, the nonspecific B cell response, but the T cell response to mitogens is not affected. These results suggest that the recognition of self major histocompatibility complex class II determinants by the T4 molecule plays a major role in the activation of T helper cells for antibody production to this particulate antigen.
On the role of I‐A antigens in lectin‐ and antigen‐induced interleukin 2 production
Authors: Larsson Eva‐Lotta , Coutinho Antonio 
Published: February 2007

AbstractThe role of I‐A molecules in lectin‐ and antigen‐induced interleukin 2 (IL2) production has been analyzed using monoclonal antibodies. Both lectin‐ and antigen [plus major histocompatibility complex (MHC)]‐induced IL2 production were profoundly inhibited by monoclonal anti‐I‐A antibodies, whereas monoclonal anti‐D and anti‐K antibodies had no effect. The anti‐I‐A‐mediated inhibition of lectin‐induced IL2 production was fully overcome by addition of interleukin 1 (IL1), while no recon‐stitution was observed in antigen (plus MHC)‐specific induction. Anti‐I‐A antibodies were also found to inhibit the T cell‐independent induction of IL1 production.I‐A antigens appear, therefore, to play two distinct roles in the induction of IL2 production: (a) I‐A molecules are directly involved in mediating activation signals to the macrophages at the level of IL1 production; (b) I‐A epitopes act as restricting elements in specific antigen recognition by T helper cells at the level of IL2 production, a requirement which is overcome by lectin.
In vivo and in vitro studies of thymulin in marginally zinc‐deficient mice
Authors: Dardenne Mireille , Savino Wilson , Wade Sali , Kaiserlian Dominique , Lemonnier Daniel , Bach Jean‐François 
Published: February 2007

AbstractThymulin (or serum thymic factor, FTS‐Zn), a well‐defined thymic hormone previously shown to be a nonapeptide binding the metal zinc, was studied in mice subjected to a long‐term marginally Zn‐deficient diet. In spite of the absence of thymic atrophy, we observed a significant decrease in the serum levels of thymulin as early as two months after the onset of treatment. However, these levels could be consistently restored after in vitro addition of ZnCl2. The analysis of thymuses from Zn‐deficient mice showed that, despite the apparently normal network of epithelial cells, there was a progressive increase in the number of thymulin‐containing cells (assessed by immunofluorescence with anti‐thymulin monoclonal antibodies) that was already significant after two months of treatment. These results are in keeping with those of previous investigators, showing a specific, altered, thymic endocrine function following Zn deprivation. Nonetheless, our results strongly suggest that the nonactive Zn‐deprived peptide is secreted under these experimental conditions. Furthermore, the fact that the augmented numbers of thymulin‐containing cells were observed in the thymuses following a decrease in the peripheral thymulin (biologically active) brings further evidence for the existence of a feedback mechanism for the secretion of this hormone.
The abnormal function of T cells in chronically anti‐μ‐treated mice with no mature B lymphocytes
Authors: Kim K. Jin , Rollwagen Florence , Asofsky Richard , Lefkovits Ivan 
Published: February 2007

AbstractT cells from anti‐μ‐treated mice, normal goat serum (NGS)‐treated mice or untreated control mice were compared with respect to their surface antigenic phenotypes, T cell mitogenic responses, helper function and precursor frequency of helper T cells. Anti‐μ treatment arrested the development of B cells at an immature stage, as determined by flow microfluorometry; it resulted in no serum IgM, but detectable levels of IgG by solid‐phase radioimmunoassay. Proliferative responses to phytohemagglutinin and concanavalin A were significantly decreased in T cells obtained from μ‐suppressed C57BL/6 mice, but not from control mice. When T cells from anti‐μ‐treated mice were tested in vitro for their helper activity to collaborate with B cells from nu/nu C57BL/6 mice to give plaque‐forming cells to sheep red blood cells, they provided far less help than did T cells from control mice. The frequency of T helper cells, as measured by limiting dilution analysis, was much lower in the anti‐μ‐than in the NGS‐treated mice. Cell mixing experiments provided evidence for active suppression of T helper function among splenocytes taken from μ‐suppressed mice.
The role of accessory cells in polyclonal T cell activation III. No requirement for recognition of H‐2‐encoded antigens on accessory cells
Authors: Hünig Thomas 
Published: February 2007

AbstractHighly purified murine lymph node T cells were used to test the hypothesis that polyclonal T cell activation requires the recognition of mitogen‐modified major histocompatibility complex (MHC) antigens on accessory cells (AC) by the T cells. A veriety of tumor cell lines, including macrophage, B and mast cell tumors, as well as thymomas, were shown to function as AC in concanavalin A‐induced T cell activation, even if they expressed only one class of MHC antigens or none at all. In contrast to antigen‐specific responses, where the Lyt‐2+ phenotype is reportedly associated with recognition of class I MHC antigens, T cells enriched for or depleted of Lyt‐2+ cells were not preferentially activated in the presence of class I‐ or class II‐positive AC, respectively.In addition, as shown by others in the guinea pig and in the rat systems, T cell proliferation induced by oxidation of cell surface sugars is equally effective if T cells or AC are oxidized. T cell mitogens, therefore, do not seem to act by altering MHC antigens on AC, but rather by providing T cell‐AC contact via their agglutinating properties.
The invariant chains of mouse class II antigens: biochemical properties and molecular relationship
Authors: Zecher Reinhard , Ballhausen Wolfgang , Reske Konrad , Linder Dietmar , Schlüter Michael , Stirm Stephan 
Published: February 2007

AbstractThe proteins p40 (Mr = 40000), p32 (Mr = 32000), p28 (Mr = 28000), p20 (Mr = 20000) and p10 (Mr = 10000) are described which occur in noncovalent association with the polymorphic α,β heterodimer of class II antigens. They were investigated with respect to their molecular characteristics and their mutual structural relationship. p32, the predominant species of this group corresponds to the invariant chain γ (Ii). In contrast to the polymorphic subunits α and β, proteins p40, p28, p20 and p10 migrated like γ in electrophoretically constant positions, when class II molecules of different subregions and different alleles were assessed by two‐dimensional gel electrophoresis [1st dimension, isoelectric focusing; 2nd dimension, sodium dodecyl sulfate (SDS) polyacrylamide gel electrophoresis]. Analogous to γ, they are therefore designated invariant chains. The low Mr species of this group do not arise from higher Mr forms as preparation artefacts. Short‐term pulse‐chase analysis and cell‐free translation of sucrose gradient‐fractionated mRNA in conjunction with specific immunoprecipitation rendered the possibility unlikely that individual components of this set of proteins existed in a precursor‐product relationship within the cell. Comparative enzymatic fragmentation on SDS polyacrylamide gels as well as tryptic peptide map comparisons by high performance liquid chromatography revealed a high structural relatedness among all members of this group of invariant proteins.
Both Fc receptors and lymphocyte‐function‐associated antigen 1 on human Tγ lymphocytes are required for antibody‐dependent cellular cytotoxicity (killer cell activity)
Authors: Miedema Frank , Tetteroo Pedro A. T. , Hesselink Wim G. , Werner Guy , Spits Hergen , Melief Cornelis J. M. 
Published: February 2007

AbstractA monoclonal antibody, designated CLB‐LFA‐1/1, directed to the human lymphocyte‐function‐associated antigen 1 (LFA‐1) was raised by immunization of mice with the peripheral blood lymphocytes of a Tγ lymphocytosis patient. The monoclonal antibody was selected by inhibition of the natural killer cell and the antibody‐dependent killer cell activity of the patient's Tγ lymphocytes. In addition, the monoclonal antibody was shown to inhibit the cytotoxic activity of T cell clones specific for either class I or class II HLA molecules. The antigen recognized by CLB‐LFA‐1/1 consisted of three polypeptide chains with molecular weights of 180000 (α), 155000 and 94000 (β). The antibody reacted with T cells, B cells, monocytes and granulocytes, and stained normal Tγ cells and Tγ cells of patients with Tγ lymphocytosis two‐ to threefold stronger than normal T cells. It was shown that LFA‐1 and the Fc receptor on Tγ cells did not comodulate and it is therefore concluded that Fc receptors and LFA‐1 are independent membrane structures, both required for the killer cell activity of Tγ cells.
Monoclonal antibodies specific for murine IgM I. Characterization of antigenic determinants on the four constant domains of the μ heavy chain
Authors: Leptin Maria , Potash Mary Jane , Grützmann Rudolf , Heusser Christoph , Shulman Marc , Köhler Georges , Melchers Fritz 
Published: February 2007

AbstractSeventeen monoclonal rat antibodies with specificities for mouse μ heavy chain recognize seven distinguishable determinants that are located on the four constant region domains. All determinants are present on secreted, intracellular and membrane bound IgM, and all but two are expressed on isolated μ heavy chain. One antibody, specific for a site in the first constant region domain, recognizes a determinant that is present on IgM of AKR, C3H/HeJ, C57BL/6J, SJL, DBA/2, BALB/c, NZB and CBA/J mouse strains, but not on IgM of A.TH, A/J and A.CA strains of mice.
Pneumococcal cell wall phosphorylcholine elicits polyclonal antibody secretion in mice
Authors: Bach Mark A. , Beckmann Enrique , Levitt Daniel 
Published: February 2007

AbstractImmunization of mice with phosphorylcholine (PC)‐bearing Staphylococcus pneumoniae Type 2, strain 36a (R36a) results in both a PC‐specific and a polyclonal increase in splenic plaque‐forming cells. The polyclonal increase was observed in all strains tested, including those bearing an X‐linked immune defect resulting in an undetectable anti‐PC immune response. The magnitude of the polyclonal response is directly related to the amount of bacterial surface PC as detected by enzyme‐linked immunosorbent assay. Congenially athymic (nude) mice mount an anti‐PC plaque‐forming cell response after R36a immunization but fail to produce a significant polyclonal response. From our results it appears that PC on the cell wall of a bacterium acts both as a polyclonal activator and a specific antigen, stimulating each by different mechanisms.
Phosphorylcholine on isologous red blood cells induces polyclonal but not anti‐phosphorylcholine plaque‐forming cells in mice
Authors: Beckmann Enrique , Bach Mark A. , Levitt Daniel 
Published: February 2007

AbstractIt has been demonstrated in the preceeding report (Bach, M. A., Beckmann, E. and Levitt, D., Eur. J. Immunol. 1984. 14: 589) that phosphorylcholine (PC) on the bacterium Streptococcus pneumoniae R36a stimulated polyclonal as well as anti‐PC plaque‐forming cells (PFC) in mouse spleen in vivo. In this study, red blood cells from BALB/c mice (MRBC) were either conjugated with PC, 2,4,6‐trinitrophenyl (TNP) or treated with phospholipase A2 (PLA2) to expose PC on the cell membrane (determined by hemagglutination with the anti‐PC myeloma HOPC8). When BALB/c mice were immunized i.v. with the conjugated or enzyme‐treated MRBC, a significant polyclonal antibody response ocurred (p < 0.05) using PC‐MRBC or PLA2‐treated MRBC, but not with TNP‐MRBC or sham‐treated MRBC. No anti‐PC or anti‐MRBC immunoglobulin‐secreting cells developed after immunization. Repeated immunization with PC‐MRBC resulted in similar levels of protein A PFC after each immunization but no anti‐PC, anti‐MRBC or anti‐PC‐MRBC PFC.Thus, PC on R36a or isologous RBC stimulated increased numbers of splenic plaqueforming cells. In the case of R36a, 10‐25% of these PFC produced antibodies directed towards PC. In contrast, PC‐MRBC or PLA2‐treated MRBC, failed to evoke any anti‐PC antibody responses.
Spontaneous production of interleukin 3 by T lymphocytes from autoimmune MRL/MP‐lpr/lpr mice
Authors: Palacios Ronald 
Published: February 2007

AbstractMRL/MP‐lpr/lpr (MRL/lpr) mice develop a lupus‐like autoimmune disease and a massive generalized lymphadenopathy associated with proliferation of nonmalignant Thy‐1+ Lyt‐1+ cells. The mechanism(s) leading to outgrowth of these cells is unknown.We report here that Thy‐1+, Lyt‐1+, Lyt‐2− lymphocytes from spleens of MRL/lpr mice, but not from several strains of normal mice, spontaneously secrete IL3. The presence of IL3 is shown by: (a) the ability of the supernatants from unstimulated spleen cells of MRL/lpr (MRL/lpr SUP) to support growth of IL3 but not IL2 addicted cells and (b) the growth‐promoting activity in MRL/lpr SUP was absorbed with IL3‐dependent cells but not with IL2‐dependent cells. Spontaneous release of IL3 was detected in supernatants from spleen cells of 6‐week‐old MRL/lpr mice and the titers of IL3 activity increased with age.Nylon wool‐enriched cells from spleens of MRL/lpr mice proliferated in response to purified IL3 and IL3 secreted by MRL/lpr T cells, in a manner similar to nylon wool‐passed cells from normal mice. The cells responding to both sources of IL3 were Thy‐1+, Lyt‐1+, Lyt‐2−. Thus, Thy‐1+, Lyt‐1+,2− cells from spleen of MRL/lpr mice spontaneously secrete IL3 and respond normally to this lymphokine.Four Thy‐1+, Lyt‐1+,2− cell lines derived from unstimulated spleen cells of MRL/lpr mice were established in culture with IL3. These IL3‐sensitive T cell lines help syngeneic and H‐2‐compatible normal small “resting” B cells to mature into plasma cells secreting predominantly IgG1, IgG2 and IgA.Taken together, these data and previous findings that T cells from MRL/lpr mice have an impaired production of and response to IL2, strongly suggest that abnormal production of IL3 may account for the outgrowth of Thy‐1+, Lyt‐1+,2− cells in the MRL/lpr mouse. Finally, a mechanism linking abnormal production of IL3 and B cell hyperactivity in these animals is proposed.
Immune recognition of insulin by H‐2b mice: the mutation in the I‐A gene of the B6.C‐H‐2bm12 mouse alters the self‐I‐A‐restricted T cell repertoire
Authors: Hochman Paula S. , Huber Brigitte T. 
Published: February 2007

AbstractThe response to heterologous insulin in H‐2b mice is restricted to the A chain loop determinant(s) of beef insulin. The recognition of this specificity requires the expression of the immune response (Ir) gene epitope Ia. W39 which is absent from the I‐Ab mutant B6.C‐H‐2bm12 (bm12) mice. This restriction could reflect the inability of H‐2b antigen‐presenting cells (APC) to present other insulin determinants or may reflect “self‐major histocompatibility complex”‐dependent influences on the generation of the T cell repertoire. To assess these possibilities we analyzed the genetic control and fine specificity of the insulin‐specific T cell repertoire of H‐2b mice by fusing the AKR thymoma BW5147 with T cells of C57BL/6 mice which had been immunized in vivo and challenged in vitro with beef insulin. The cloned hybridomas that we have produced respond to APC either alone or in conjunction with insulin by the production of interleukin 2. The insulin‐specific hybridomas vary in their fine specificity such that some clones recognize a determinant(s) shared by beef, sheep and pork insulin and the isolated B chain, while other clones recognize a determinant(s) shared by beef and sheep insulin only, likely to involve amino acids 8 and/or 10 of the A chain loop. The presentation of insulin to these hybridomas is restricted by I‐Ab, but not by Ia.W39. This analysis revealed that the insulin‐specific immune potential in H‐2b mice is of greater scope than previously defined and led us to consider, whether insulin nonresponder bm12 mice also possess a latent insulin‐specific immune potential. Our study of the insulin‐specific immune recognition by bm12 mice shows that these nonresponders do possess insulin‐specific T cell clones. Despite the fact that the I‐Ab and I‐Abm12 gene products differ only by 3 amino acids, insulin‐specific C57BL/6 and bm12 hybridomas are restricted to recognize exogenous antigen only in the context of C57BL/6 and bm12 APC, respectively. Furthermore, upon direct analysis of autoreactive subclones, a similar although not complete, restriction was observed. The implications of these findings for understanding the mechanism of Ir gene control are discussed.