bluuebunny/crossref_metadata_2025_split huggingface dataset:
Biosynthesis of murine immunoglobulin D: Heterogeneity of glycosylation
Authors: Vasilov Raif G. , Ploegh Hidde L. 
Published: February 2007

AbstractThe biosynthesis of IgD was studied with special reference to aspects of glycosylation in the B1‐8 δ cell line. This cell line was isolated as a spontaneous class switch variant from an IgM‐producing cell line, B1‐8.μ. B1‐8.δ produces both membrane and secretory IgD. The biosynthesis of IgD is unusual in that there is a large degree of heterogeneity in N‐linked glycosylation, most likely involving the number of glycan sidechains that are attached. Similar findings have recently been documented for human IgD. Further modifications of the oligosaccharide side chains follow the pathways established for numerous other glycoproteins. Under conditions where N‐linked glycosylation was inhibited by tunicamycin (TM), the presence of neuraminidase‐sensitive forms of secretory IgD could be shown. Moreover, secretory IgD from TM‐treated cells was susceptible to mild alkaline hydrolysis. Taken together, these findings argue strongly for the presence of O‐linked, sialic acid‐carrying sugars on murine IgD. Both for O‐ and N‐linked carbohydrate side chains, terminal modifications may occur at a different rate and extent for membrane and secretory IgD. For reasons of comparison we also examined some aspects of IgM biosynthesis in the parental cell line and found our results to be in good aggreement with those reported in the literature. Biosynthesis of H‐2K, D antigens was indistinguishable in B1‐8.H μ and B1‐8. δ, suggesting that the unusual features of IgD glycosylation are inherent to this Ig isotype, rather than the consequence of a different complement of glycosyltransfer‐ases or carbohydrate‐modifying enzymes in the Bl‐8.δ cell line. The use of affinity matrices for purification of immunoglobulins allowed us to estimate relative rates for the formation of IgM and IgD molecules capable of binding antigen. The results obtained suggest that Bl‐8 IgM and IgD follow different assembly pathways, IgM most likely through heavy chain dimer formation followed by light chain addition, and IgD through heavy chain‐light chain dimer formation, followed by assembly into full‐sized molecules. Since B1‐8.μ and B1‐8.δ express identical variable regions and light chains, such differences must be attributed to isotypic differences. Inhibition of glycosylation affected neither secretion nor assembly of either IgM or IgD.
Epitope‐specific regulation. III. Induction of allotype‐restricted suppression for IgG antibody responses to individual epitopes on complex antigens
Authors: Herzenberg Leonore A. , Tokuhisa Takeshi , Herzenberg Leonard A. 
Published: February 2007

AbstractMaternal antibody to the paternal Igh‐1b (IgG2a) allotype induces chronic suppression for Igh‐1b (1b) production in (BALB/c × SJL)F1 hybrid mice. These mice characteristically remain incapable of producing lb antibody responses until about 3 months of age and then enter a remission phase during which they produce normal 1b antibody responses to antigens introduced initially at this time. Thus young allotype‐suppressed mice do not produce lb antibody responses to dinitrophenylated keyhole limpet hemocyanin (DNP‐KLH) and 1b anti‐ KLH.The suppression of 1b antibody responses in young allotype‐suppressed mice prevents the expression, rather than the development, of 1b memory for priming antigen epitopes. Furthermore, it not only prevents the expression of such memory cells initially but results in the induction of a continued suppression that specifically prevents their expression after the onset of remission. Thus mice primed with DNP‐KLH while allotype suppression is still active develop normal 1b memory for DNP and KLH but nonetheless fail to produce lb anti‐DNP and 1b anti‐KLH responses, even when restimulated with DNP‐KLH during remission. These mice also fail to produce 1b anti‐DNP when stimulated with DNP on an unrelated carrier molecule, i.e., with DNP‐chicken gamma globulin (CGG).This suppression is both epitope‐specific and allotype‐specific. That is, although 1b responses to DNP on CGG are suppressed, 1b responses to CGG epitopes on DNP‐CGG proceed normally. Furthermore, there is no suppression of other isotype and allotype responses either to DNP or to the CGG epitopes. These data therefore define an Igh‐restricted epitope‐specific mechanism that can be induced to persistently suppress 1b antibody responses to epitopes introduced initially during active (1b) allotype suppression.
Nature of the antigenic complex recognized by T lymphocytes. VIII. Specific inhibition of the stimulatory capacity of antigen‐pulsed hapten‐modified peritoneal exudate cells by anti‐hapten antibody
Authors: Shevach Ethan M. , Chan Christina , Clement Loran T. 
Published: February 2007

AbstractWhen macrophages which were pulsed with soluble protein antigens and then modified with 2,4,6‐trinitrobenzenesulfonic acid (TNBS) were cultured with primed T cells in the presence of anti‐2,4,6‐trinitrophenyl (TNP) antiserum, a marked inhibition of the T cell proliferative response specific for the soluble protein antigen under study was observed. Inhibition of the proliferative response required that the protein antigen under study be easily susceptible to conjugation with TNBS. A lag period of 1‐3 h must elapse following pulse exposure to the protein antigen and prior to TNP modification for anti‐TNP antibody to exert an inhibitory effect, which suggests that processing of antigen in an intracellular site might occur with subsequent reexpression of antigen on the macrophage surface. It was hypothesized that anti‐TNP antibody inhibits T cell proliferation by capping and shedding of TNP‐modified determinants of the nominal antigen as well as TNP‐modified cell surface proteins from the macrophage membrane. The failure of others to demonstrate an effect of anti‐antigen antibody on T cell activation can best be explained as secondary to the low density of antigenic determinants on the macrophage membrane with resultant low‐affinity binding of antibody to antigen.
Human T cell clones specific for tetanus toxoid: Characterization of antigen specificity and HLA restriction
Authors: Schmitt Christian , Ballet Jean‐Jacques , Agrapart Monique , Bizzini Bernard 
Published: February 2007

AbstractT cell blasts isolated from six‐day cultures of peripheral blood mononuclear cells stimulated with tetanus toxoid (TT) were cloned in a two‐layer agar system in the presence of autologous irradiated PBM (iPBM) and TT. Colonies were individually isolated and expanded in interleukin 2‐containing medium. The antigen specificity of three T cell clones was attested by their capacity to proliferate under restimulation by TT and not by an unrelated antigen. The clones were specific for either the α or the β chain of the toxin. T cells from these clones expressed la determinants and antigens of the helper/inducer T cell subset as defined by anti‐T monoclonal antibodies. In the case of the a chain‐specific clone MA 11 from the donor MA, allogeneic iPBM from HLA‐compatible unrelated donors, including seven donors sharing one HLA DR specificity with MA, were found inefficient as antigen‐presenting cells. A familial study, however, demonstrated that antigen presentation could be obtained using nonautologous cells. The presenting capability of cells from relatives of the donor MA segregated in association with the HLA‐DRw6‐bearing maternal haplotype present in MA. Results suggest that MA 11 cells recognized the antigen in the context of a surface determinant closely linked to HLA‐DRw6.
Characterization of human T suppressor‐inducer, ‐precursor and ‐effector lymphocytes in the antigen‐specific plaque‐forming cell response
Authors: Heijnen Cobi J. , Pot Kees H. , Ballieux Rudy E. 
Published: February 2007

AbstractSuppression of an antigen‐specific plaque‐forming cell response of human blood lymphocytes can be effected by Tμ+ cells that have been primed previously by antigen in vitro for 6 days. While lacking the capacity to suppress the plaque‐forming response directly, these primed Tμ+ suppressor‐inducer cells stimulate a subpopulation of unprimed Toy− cells to differentiate to Tγ+ suppressor‐effector cells.The Tμ+, Tγ+ and Tμγ− subsets have been shown to be heterogeneous populations of cells. Therefore, the functionally defined T suppressor‐inducer, ‐precursor and ‐effector cells were characterized by OKT monoclonal antibodies and by the capacity to form rosettes with autologous erythrocytes (ar+). Evidence will be presented that in vitro a T4+μ+ar− cell induces a T8+μγ− ar+ precursor cell to differentiate to a T8+γ+ar− suppressor‐effector cell. A similar T suppressor‐effector cell can also be isolated directly from peripheral blood of normal donors.
Accessory function of human tumor cell lines I Production of interleukin 1 by the human histiocytic lymphoma cell line U‐937
Authors: Palacios Ronald , Ivhed Irene , Sideras Paschalis , Nilsson Kenneth , Sugawara Isamu , Fernandez Carmen 
Published: February 2007

AbstractThe established human histiocytic lymphoma cell line U‐937 spontaneously produced a factor with biological activity similar to that ascribed to interleukin 1 (IL1). Actually, supernatants from U‐937 cells promoted proliferation of thymocytes initiated by concanavalin A (Con A) and replaced the requirement of accessory cells for activation of highly purified circulating T lymphocytes induced by Con A. Phorbol myristate acetate (PMA) significantly increased the titers of the helper factor produced by U‐937 cells as compared to that secreted by non‐PMA‐treated U‐937 cells or PMA‐stimulated P388D1 murine macrophage tumor cells. Generally U‐937 cells did not secrete detectable IL1 activity during the first 24‐48 h of culture. However, after this initial period the level of IL 1 activity increased and reached a maximum at 5‐6 days of culture. Finally, the helper factor released by U‐937 cells had an apparent mol. wt. of 12000‐15000 as determined by Sephadex G‐100 chromatography and lacked interleukin 2 activity as shown by its inability to support growth of IL 2‐addicted T cell lines. To our knowledge this is the first report of an established human cell line capable of producing ILL 1.
Surface markers of cloned human T cells with helper or suppressor activity on pokeweed mitogen‐driven B cell differentiation
Authors: Mingari Maria Cristina , Melioli Giovanni , Moretta Alessandro , Pantaleo Giuseppe , Moretta Lorenzo 
Published: February 2007

AbstractHuman spleen T cells stimulated with pokeweed mitogen (PWM) were cloned under limiting conditions in microculture systems using interleukin 2 and irradiated autologous cells. Clones were screened for helper or suppressor activity on PWM‐dependent B cell differentiation by adding cell aliquots to either isolated B cells and PWM or to mixtures of T and B cells and PWM. Out of 97 clones tested, 14 promoted intense B cell differentiation, as assessed by measurements of secreted IgG, and 6 strongly inhibited B cell maturation induced by spleen T cells.All the selected clones maintained their original activity after shortterm clonal expansion; in addition, a similar (helper or suppressor) effect was detected when the total number of plasma cells per well was evaluated. Suppressor clones had no cytolytic activity on autologous T and B cell blasts, K562 cells or antibody‐coated L 1210 mouse cells. Nine helper and 6 suppressor clones were analyzed for a battery of surface markers. All the clones were E rosette‐positive and expressed HLA‐DR (Ia) antigens. Fcμ eptor was present on a single helper clone, whereas Fcγ receptor was expressed on a suppressor clone only. All but two clones expressed the OKT4+/ OKT8−, a single suppressor clone was OKT8+/OKT4−, whereas coexpression of OKT4 and OKT8 antigens was detected in one helper clone. Thus, the claim that helper T cells are OKT4+/OKT8− and suppressor T cells are OKT4−/OKT8+ is not supported by the analysis of their phenotype at the clonal level.
Cross‐blocking studies with monoclonal antibodies against I‐A molecules of haplotypes b, d and k
Authors: Koch Norbert , Hämmerling Günter J. , Tada Nobuhiko , Kimura Shoji , Hämmerling Ulrich 
Published: February 2007

AbstractFor assessment of the distribution of allodeterminants on I‐A molecules, binding inhibition studies were performed with monoclonal anti‐I‐A antibodies (mAb) in which pairs of labeled and unlabeled mAb were tested for cross‐blocking on spleen cells of H‐2 haplotypes b, d and k. The data suggest that allodeterminants are randomly distributed on the surface of the I‐A molecule. Comparison of mAb with cross‐reactivity for b, d or k haplotypes indicates that the allelic forms of determinants are located in analogous positions on different I‐A antigens.
Effects of anti‐Ig reagents on T cell functions I. Activation of rabbit T cells by anti‐allotype antibodies
Authors: Vaeck Mark , de Smet Walter , Hamers Raymond , de Baetselier Patrick 
Published: February 2007

AbstractRabbit lymphocytes were analyzed by flow microfluorometry, using anti‐T cell and anti‐Ig reagents. Rabbit T cells and cells expressing surface Ig (B cells) appeared to belong to distinct subpopulations which could be separated on the basis of their selective adherence to nylon wool columns or to anti‐Ig‐coated dishes. Using flow microfluorometry, no evidence was obtained for the expression of a allotypes (VH framework) on T cells.Separated lymphocyte populations were functionally characterized using an in vitro proliferation assay. B and T cells from rabbit spleen or peripheral blood responded in a differential fashion to B and T cell‐specific mitogens and to anti‐Ig antibodies. Although such T cells did not respond upon stimulation with anti‐Ig antibodies alone, significant proliferation could be induced by simultaneous addition of anti‐Ig and T cell growth factor. In addition, activated T cells, derived from lymph nodes of immunized rabbits, generated a proliferative response upon stimulation with anti‐Ig reagents alone. The above‐mentioned effects on T cells could be obtained using heterologous anti‐Ig antibodies or isologous anti‐allotype antibodies, directed either against a allotypes (VH framework) or against b allotypes (kappa light chain). Antibodies against the Fc portion of rabbit Ig or against irrelevant allotypic specificities were ineffective in triggering T cells. Fab fragments from anti‐allotype antibodies were equally stimulatory for T cells as compared to intact IgG, indicating that cross‐linking of Ig‐like molecules is not a necessary requirement for anti‐Ig‐induced T cell activation.
Alloactivated long‐term cultured human T lymphocytes express both HLA‐DR and SB antigens but lack lymphocyte stimulation capacity
Authors: Pawelec Graham , Blaurock Mathias , Schneider E. Marion , Shaw Stephen , Wernet Peter 
Published: February 2007

AbstractCell populations obtained from mixed leukocyte cultures of 6‐ or 10‐day duration were found specifically to restimulate primed lymphocytes detecting HLA‐linked SB as well as HLA‐D‐associated antigens. After expansion in vitro (9‐75 days) with medium containing interleukin 2, the cultured cells expressed the T lymphocyte markers detected in indirect immunofluorescence by monoclonal antibodies Lyt‐3, OKT3, OKT4, OKT8, and had high levels of HLA‐DR antigens. In addition, they were shown in cell‐mediated lymphocytotoxicity specifically to express SB antigens of the donor B cell type. Despite their positivity for DR and SB antigens, such cultured T cells failed to restimulate either SB‐ or D‐specific secondary lymphocyte proliferation. Homogeneous cloned populations of cultured T cells also lacked lymphocyte stimulation capacity. In contrast, B cell lines, which also expressed DR and SB antigens, were potent stimulators of both SB‐ or D‐directed proliferation. These data show that the activated T lymphocytes which express both HLA‐DR and SB antigens are by themselves unable to stimulate lymphocyte proliferation.
Clearance of interleukin 2 from the blood of normal and T cell‐depleted mice
Authors: Mühlradt Peter F. , Opitz Hans Georg 
Published: February 2007

AbstractPartially purified, concentrated interleukin 2 (IL2) was injected i.v. into normal and T cell‐depleted mice. At various times after injection IL 2 was determined in the sera of these mice. An interference with the test by a potential inhibitor of IL 2 in the serum was excluded. IL 2 was cleared equally rapidly, with a half‐life of 3 min, from the blood of both groups of mice. It is concluded that IL 2 is a short‐range mediator under physiological conditions, and that clearance was not due to adsorption to T cells.
Murine genotype influences the in vitro production of γ (immune) interferon
Authors: Virelizier Jean‐Louis 
Published: February 2007

AbstractSpleen cells from mice of 6 different strains were stimulated with pokeweed mitogen and the amount of γ interferon in the supernatants was measured. Three strains (BALB/c, A/J and C3H/He) were found to be low producers (less than 50 units) whereas three other strains (C57BL6, CBA and AKR) were high producers (50 to 500 units). F1 hybrids between a low producer strain (A/J) and a high producer strain (C57BL6) were found to produce low amounts of interferon. Nude mice did not produce detectable amounts of pokeweed mitogen‐induced γ interferon. The level of production of this T cell lymphokine is thus under genetic control.
The genetic basis of antibody production: The dominant anti‐arsonate idiotype response of the strain a mouse
Authors: Siekevitz Miriam , Gefter Malcolm L. , Brodeur Peter , Riblet Roy , Marshak‐Rothstein Ann 
Published: February 2007

AbstractImmunization of the A strain of mice with the hapten p‐azophenylarsonate (Ars) results in an immune response in which approximately 50% of the anti‐Ars antibodies share cross‐reactive idiotypic determinants (IdCR). A gene or genes linked to the heavy chain constant region locus is required for the production of this idiotype. The expressed VH gene from a hybridoma cell line which expresses the IdCR has been cloned. DNA hybridization studies utilizing the VH gene have revealed that there are many related genes in both idiotype‐producing and idiotype‐nonproducing strains of mice. However, under stringent hybridization conditions, only a single band of 6.4 kb is present in Eco R1‐digested A strain DNA. Strains of mice which are phenotypically idiotype‐negative either lack this band completely or possess a much weaker one at this position. Utilizing DNA from Igh recombinant strains of mice, it has been shown that the VH locus controlling idiotype expression contains the structural gene information for the idiotype‐positive heavy chains. It has also been shown that DNA at this locus appears to be sufficient for the production of the cross‐reactive idiotype. Utilizing a DNA probe derived from regions flanking the structural gene has confirmed the relatedness of V genes in a variety of mouse strains and revealed a significant degree of polymorphism at the Igh locus.
The role of accessory cells in polyclonal T cell activation. I. Both induction of interleukin 2 production and of interleukin 2 responsiveness by concanavalin A are accessory cell dependent
Authors: Hünig Thomas , Loos Michael , Schimpl Anneliese 
Published: February 2007

AbstractRecent studies from other laboratories have shown that concanavalin A (Con A) acts at two separate steps in polyclonal T cell activation: interleukin 2 (IL2) production, and induction of responsiveness to IL2. Using a combination of techniques for the depletion of accessory cells from lymph node T cells, we have investigated which of these steps, if not both, is responsible for the known requirement for accessory cells in the Con A response. It was found that with increasing T cell purification, first the ability is lost to produce sufficient levels of endogenous IL2, whereas induction of IL2 responsiveness can still take place. Further removal of accessory cells however yields a population of resting T cells that cannot be induced by Con A to become IL2‐reactive. It was concluded that both IL2 production and induction of reactivity to IL 2 are accessory cell‐dependent events.
Modulation of B and T cell subsets in mice treated with fractionated total lymphoid irradiation. II. Tolerance susceptibility of B cell subsets
Authors: Zan‐Bar Israel 
Published: February 2007

AbstractTotal lymphoid irradiation (TLI) results in long‐lasting changes in the characteristics of both T and B cells suggestive of arrested maturation. A characteristic feature of immature B cells is their high susceptibility to tolerance induction. This study examines the susceptibility to tolerance to bovine serum albumin (BSA) of TLI‐treated mice. Two experimental protocols were designed. In the first, tolerance to BSA was induced in TLI‐treated adult (BALB/c × C57BL/6)F1 mice, and the ability of B cells of those mice to respond to BSA was assessed in an adoptive transfer system. In the second experimental protocol, tolerance was induced in adoptive hosts reconstituted with purified B cells originating from TLI‐treated mice and with splenic T cells of normal, untreated mice. Results obtained in these two systems clearly demonstrated that splenic B cells of TLI‐treated mice are highly susceptible to tolerance induction. This high susceptibility of B cells is linked neither with the elevation of immature T cells nor with induced T suppressor cells which arise due to the long‐term malfunction of the thymus. Tolerance could be induced in TLI cells even 4 months after termination of the treatment. Thus, maturation processes of B cells in TLI‐treated mice are arrested for long periods of time.
Isotype commitment in the in vivo immune responses. II. Polyclonal plaque‐forming cell responses to lipopolysaccharide in the spleen and bone marrow
Authors: Björklund Mariana , Coutinho Antonio 
Published: February 2007

AbstractInjection of lipopolysaccharide into adult mice results in a rapid increase in the number of splenic IgM‐secreting plaque‐forming cells (PFC) so that by 60 h they represent roughly 20 times those present in normal mice. Although inhibited for the first two days, IgG3, IgG2b and IgG2a PFC are later selectively stimulated and, by 110 h, they reach numbers that are 100, 40 and 30 times, respectively, those of normal mice. IgG1 PFC are stimulated only marginally and 48 h after the maximal responses of the other IgG subclasses. IgA PFC are selectively inhibited and drop to 20% of normal numbers 4 days after injection. The ability of lipopolysaccharide to selectively stimulate B cells for the production of IgG3, IgG2b and IgG2a was further substantiated by studying athymic mice, and by using adoptive cell transfers that overcome regulatory influences limiting these responses in intact mice. Under these conditions, 16% of all spleen cells are PFC and up to 85% of all Ig‐secreting cells are included in those three isotypes. Similar responses are also detected in bone marrow but they occur 24–48 h after the splenic responses, suggesting that bone marrow PFC are not induced in situ. These results demonstrate a selective in vivo isotype commitment in response to lipopolysaccharide that is polyclonal and, therefore, independent of V region specificities.