bluuebunny/crossref_metadata_2025_split huggingface dataset:
Phorbol 12‐myristate 13‐acetate induces surface expression of T3 on human immature T cell lines with and without concomitant expression of the T cell antigen receptor complex
Authors: Carrel Stefan , Mach J.‐P. , Miescher Guido , Salvi Suzanne , Giuffrè Laura , Schreyer Magali , Isler Patrick 
Published: March 2007

AbstractThe T3 complex is known to be expressed on the cell surface of mature T cells together with either the α‐β heterodimeric T cell receptor (TCR) or the TCR γ protein. In a number of immature T cell malignancies, however, T3 has been described exclusively in the cytoplasm. We have investigated five such T cell lines with cytoplasmic T3 and could demonstrate by biosynthetic labeling the presence of the α and β chains of the TCR in the cytoplasm of two of them, CEM and Ichikawa. No surface TCR α‐β protein could be detected by staining with the WT31 antibody. These observations, therefore, argue against the concept that expression of the TCR α chain controls the surface expression of the T3/TCR complex. Interestingly, phorbol 12‐myristate 13‐acetate (PMA) induced cell surface expression of T3 protein in these two cell lines only. Moreover, on surface‐iodinated CEM cells no association of T3 and TCR molecules could be demonstrated after treatment with PMA, and expression of TCR α and β chains was limited to the cytoplasm. In Ichikawa cells, however, PMA induced surface expression of a mature T3/TCR complex. Our findings indicate that separate regulatory mechanisms may exist for the surface expression of the T3 proteins and for the assembly of the T3/TCR complex.
Analysis of T cell‐replacing factor‐like activity: potent induction of T helper activity for human B cells by residual concanavalin A and interleukin 2
Authors: Sauerwein Robert W. , Van Der Meer Walter G. J. , Aarden Lucien A. 
Published: March 2007

AbstractAt least two factors with the capacity to induce IgM synthesis in human B cells were found to be present in the 15–20‐kDa fraction of the supernatant of mononuclear cells activated with concanavalin A (Con A) and phorbol ester. Previously, it has been shown (Sauerwein, R. W. et al., Eur. J. Immunol. 1985. 15: 611) that interleukin 2 (IL 2) in this material is able to induce T cell‐dependent IgM secretion in normal B cells. Evidence was obtained for the presence of another factor distinct from IL 2 that could replace T cells in the induction of B cell differentiation. We have analyzed this factor with the use of a neoplastic B cell population of prolymphocytic origin that was functionally nonresponsive to IL 2. T cell‐replacing factor (TRF)‐like activity and IL 2 could be separated by ion‐exchange chromatography, although a small amount of IL 2 was recovered in the TRF fractions. This small amount of IL 2 was found to be crucial for the observed TRF activity. Moreover, a substantial amount of monomeric Con A was detected in the TRF preparation. Our studies show that Con A in the presence of IL 2 can act as a potent inducer of helper function in lower numbers of T cells for normal and neoplastic B cells. Functional assays for T cell contamination in B cell suspensions are therefore of limited value because they are determined by the efficiency of the stimulating signal. Particularly in those B cell factor preparations, obtained from mitogen‐activated T cells with an obligatory or unidentified role of IL 2, the possible effect of a contaminating mitogen must be considered.
Interferon‐γ restores T lymphocyte proliferation of nonresponders to IgG1 anti‐CD 3 via the induction of Fcγ1 receptors on monocytes
Authors: Benichou Gilles , Kanellopoulos Jean M. , Wallon Christine , Boue François , Delfraissy Jan‐François 
Published: March 2007

AbstractHuman peripheral blood T lymphocytes are stimulated to grow and divide by some mouse anti‐CD 3 monoclonal antibodies. This polyclonal mitogenesis is dependent on both their immunoglobulin subclass and the presence of monocytes. The unresponsiveness of T lymphocytes from certain individuals to mouse IgG1 (or IgG2a) antibodies is due to a failure of their monocytes to bind these IgG isotypes.In this study, we have selected such nonresponder subjects to IgG1 anti‐CD 3 (UCHT 1) in order to study their monocytes. Two assays were used: IgG1 and IgG2 EA rosettes to evaluate their Fc receptor‐binding capacity, and IgG‐mediated monocyte chemiluminescence to test their receptor‐related activation since mouse anti‐T cell antibodies binding to lymphocytes trigger monocyte chemiluminescence via their Fc receptor.We have observed that in all nonresponder subjects the absence of IgG1 anti‐CD 3 monocyte chemiluminescence strictly correlates with the absence of IgG11 EA rosettes. Thus, the failure to respond to UCHT 1, in all nonresponders tested to date, is due to the absence of Fcγ1 receptors on their monocytes. Treatment of nonresponder monocytes by recombinant interferon‐γ was shown to restore T cell proliferation and monocyte chemiluminescence in nonresponders. This effect of interferon‐γ correlates with the appearance of Fcγ1 receptors on monocytes from these individuals. This work strongly suggests that nonresponder monocytes possess functional genes for Fcγ1 receptors which are not expressed normally at a detectable level but can be induced by interferon‐γ.
Epstein‐Barr virus‐transformed human precursor B cell lines: altered growth phenotype of lines with germline or rearranged but nonexpressed heavy chain genes
Authors: Gregory Christopher D. , Kirchgens Christa , Edwards Carole F. , Young Lawrence S. , Rowe Martin , Forster Alan , Rabbitts Terence H. , Rickinson Alan B. 
Published: March 2007

AbstractA series of lymphoblastoid cell lines (LCLs) have been established by in vitro infection of fetal bone marrow and fetal liver cells with Epstein‐Barr virus (EBV). While most lines showed the usual mature B cell phenotype, a small proportion were cytoplasmic and surface immunoglobulin (Ig) heavy and light chain negative. Analysis of gene rearrangements indicated that the Ig lines were either germ‐line or nonproductively rearranged when probed for JH and were in germ‐line configuration for Cx; no μ or χ mRNA could be detected in such cells. Precursor B cell lines were indistinguishable from their normal Ig+ counterparts in their expression of a wide variety of cell surface markers including “activation” antigens usually associated with the lymphoblastoid state; even the single LCL showing germ‐line heavy and light chain genes expressed B lineage‐specific cell surface antigens. However, the Ig− lines were distinct from their Ig+ counterparts in three important respects: (a) they grew much more slowly and achieved lower saturation densities, (b) they showed unusually high proportions (8–16%) of cells in EBV‐productive cycle, and (c) they contained unusually high proportions (up to 40%) of cells expressing free joining (J) chain. These results suggest that precursor B cells differ in their response to the growth‐transforming effects of EBV such that the virus‐cell interaction in precursor B cell lines is inherently less stable than in conventional LCL. In particular there may be a greater movement of cells out of cycle and along the B cell maturation pathway. It is possible that such movement leads in individual cells either to virus replication or to a “sterile” plasmacytoid differentiation with J chain expression in the absence of Ig synthesis.
Anti‐anti‐IgE idiotypic antibodies mimic IgE in their binding to the Fcϵ receptor
Authors: Baniyash Michal , Eshhar Zelig 
Published: March 2007

AbstractThe binding site of some anti‐idiotypic antibodies (anti‐Id) can appear as a structural image of the antigen and as such may mimic its biologic activity. We raised anti‐anti‐IgE antibodies in an attempt to obtain anti‐Id capable of interacting with the Fcϵ receptor (FcϵR). Guinea pigs were immunized with purified murine monoclonal antibodies (mAb) that had been found to react with epitopes closely related to the site on the IgE molecule which is recognized by the FcϵR. After only two injections, we could detect in the immune sera anti‐Id that inhibited the binding of IgE to the anti‐IgE mAb used as immunogens. However, only after 10 immunizations over a period of about 6 months could we detect antibodies that competed efficiently with the binding of IgE to rat basophilic leukemia (RBL) cells. The “IgE‐like” anti‐Id could be affinity purified from immunosorbents made of the anti‐IgE mAb. F(ab′)2 and Fab′ fragments were as effective inhibitors of IgE binding as the intact anti‐anti‐Id antibodies. Some of the anti‐Id caused RBL degranulation and all of them, like IgE, inhibited the binding of specific anti‐FcϵR mAb to RBL cells. In summary, by hyperimmunization with anti‐IgE mAb we could obtain anti‐Id whose antigen‐binding site is recognized by the mast cell receptor specific to the Fc portion of IgE.
Transcription of a T cell receptor β chain gene in L cell fibroblasts following DNA‐mediated gene transfer
Authors: Sensi Marialuisa , Dembić Zlatko , Steinmetz Michael 
Published: March 2007

AbstractFunctionally rearranged T cell receptor α and β‐chain genes from a fluoresceinspecific cytotoxic T cell clone have been introduced, together with the selectable marker gene neo, into mouse fibroblasts (L cells) by electroporation. Transformed cells were selected for neo gene expression by growth in medium containing the antibiotic G418. Southern blot analysis of DNA from transformed L cell clones revealed that the endogeneous T cell receptor α and β‐chain genes were in germ‐line configuration and that in 4 of the 6 clones examined the exogenously introduced rearranged α and β chain genes were present. The introduced β‐chain gene is transcriptionally active in two L cell clones examined whereas no transcription of the α‐chain gene could be detected in the same transformants.
High‐affinity binding sites for human 26‐kDa protein (interleukin 6, B cell stimulatory factor‐2, human hybridoma plasmacytoma growth factor, interferon‐β2), different from those of type I interferon (α,β), on lymphoblastoid cells
Authors: Coulie Pierre G. , Vanhecke Alain , van Damme Jo , Cayphas Sylvie , Poupart Pascale , De Wit Luc , Content Jean 
Published: March 2007

AbstractThe human 26‐kDa glycoprotein (26K) is a cytokine produced by lymphoid as well as nonlymphoid cells. So far it is active as (a) a potent hybridoma and plasmacytoma growth factor on mouse cells, (b) a B cell differentiating factor on human cells, and (c) (for some authors) an interferon (IFN). Internally labeled recombinant human 26K, obtained by translation of mRNA in Xenopus oocytes, was used to investigate the presence of specific receptors for this new cytokine and to analyze its binding to responsive cells. The results indicate that (a) the 26K‐responsive human lymphoblastoid CESS cells express about 1500 high‐affinity (Kd = 30 pM) binding sites for this cytokine, (b) this binding is not competed for by interleukin (IL)1, IL2, tumor necrosis factor (TNF), IFN‐α2, IFN‐β or IFN‐γ, and (c) these 26K‐binding sites are different from the classical type I (α‐β) IFN receptors by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis.
A phenotypically dominant regulatory mechanism suppresses major histocompatibility complex class II gene expression in a murine plasmacytoma
Authors: Venkitaraman Ashok R. , Culbert Eric J. , Feldmann Marc 
Published: March 2007

AbstractThe expression of major histocompatibility complex (MHC) class II antigens is down‐regulated when B cells differentiate into plasma cells. We have studied the mechanism of down‐regulation of MHC class II expression in a BALB/c strain‐derived murine plasmacytoma cell line, NS1. NS1 cells express MHC class I antigens but not MHC class II antigens. We tested 20 uncloned hybrid cell lines obtained from the fusion of NS1 cells with MHC class II‐expressing splenic B cells prepared from CBA, SJL or BALB/c mice. All the hybrid cell lines expressed MHC class I antigens of either or both parental haplotypes but did not express MHC class II. One NSI × splenic B cell hybrid clone, K3, was used to further validate these results; K3 cells expressed MHC class I but not MHC class II antigens. K3 was fused to the MHC class II‐expressing B lymphoma A20, and the seven resulting hybrid cell lines were again found to express MHC class I but not MHC class II antigens. Since NS1 is a subclone of the P3‐X63Ag8 murine plasmacytoma, we also tested one P3‐X63Ag8 × splenic B cell hybrid, Sp2/0, and two Sp2/0 × splenic B cell hybrids. All were found to express the appropriate MHC class I antigens but did not express MHC class II. Thus, our results suggest that the NS1 plasmacytoma suppresses MHC class II expression by a phenotypically dominant regulatory mechanism. We found that NS1 cells express correctly sized mRNA for the MHC class II genes Aα, Eα and the invariant chain. The co‐expression of MHC class I protein and I‐A and I‐E region gene transcripts provides strong evidence that the MHC gene cluster is structurally intact, and that lack of class II expression is due to a genetic regulatory mechanism. The amounts of class II mRNA expressed by NS1 cells were at least equivalent to those found in splenic lymphocytes. Therefore, this regulation must operate post‐transcriptionally.
Correlation of T cell receptor gene rearrangements to T cell surface antigen expression and to serum immunoglobulin level in scid mice
Authors: Habu Sonoko , Kimura Minoru , Katsuki Motoya , Hioki Kyoji , Nomura Tatsuji 
Published: March 2007

AbstractThe severe combined immunodeficient (scid) mouse which has undetectable serum immunoglobulin (Ig) contains a small number of thymic lymphocytes which express Thy‐1 and IL 2 receptors (IL 2R) but not Lyt‐2 or L3T4 molecules. These thymocytes did not show any rearrangement of T cell receptor (TCR) β‐chain genes. Such thymocyte characteristics in the scid mouse were similar to the 15‐day embryonic thymocytes in ordinary mice, indicating that the scid mouse thymocytes are arrested in the early stage of intrathymic differentiation. However, low or medium level serum Ig was occasionally found in the littermates of the scid mouse. The thymocytes of these mice showed some evidence of TCR β‐chain gene rearrangement and the presence of Lyt‐2+/L3T4+ cells in correlation with the serum Ig level. In the mice with some serum Ig the thymocyte cell number was increased and the proportion of IL 2R+ cells was decreased. Collectively, these results suggest that the rearrangement of TCR β‐chain genes is associated with the expression of Lyt‐2 and L3T4 molecules in intrathymic differentiation and probably with cell proliferation of the migrated lymphoid cells in the scid mouse.
Transient gene expression in untransformed lymphocytes
Authors: Mårtensson Inga‐Lill , Leanderson Tomas 
Published: March 2007

AbstractConditions for transfection of normal, freshly isolated and mitogen‐stimulated spleen cells were established. A sharp optimum of plasmid at 10 μg per 1.5 × 107 transfected spleen cells per transfection was observed. The Ig promoter and the IgH enhancer activity was found to be restricted to cells of the B lineage also in normal, freshly isolated lymphocytes in vitro.
The internal image‐like anti‐idiotypic response to a CD3‐specific monoclonal antibody in primates is dependent on the T cell‐binding properties of the injected antibody
Authors: Jonker Margreet , Nooij Frans J. M. 
Published: March 2007

AbstractMurine monoclonal antibodies used for therapeutic purposes generally elicit a strong antibody response. A large proportion of this response is specific for the idiotype of the injected monoclonal antibody. The CD3 T cell antigen is polymorphic in rhesus monkeys. A monoclonal antibody, FN18, which detects this polymorphism was used to analyze the immune response to FN18 in FN18+ and FN18− animals. The results of this study show that the internal image‐like anti‐idiotypic response predominantly occurs in FN18+ animals. This suggests that this type of anti‐idiotypic response is limited to cell‐binding monoclonal antibodies.
Evidence for a mutual influence of idiotype‐expressing donor cells and recipient lymphocytes in neonatal hosts
Authors: Bösing‐Schneider Rita , Selinka Hans‐Christoph 
Published: March 2007

AbstractNonirradiated recipients do not permit activation of transferred syngeneic lymphocytes. This transplantation barrier gives us insight into the mechanism of the regulatory circuits of the donor's and host's immune network. The present report demonstrates that this barrier depends on the state of differentiation of cells from both donor and host. We measured the expression of anti‐α(1–3)dextran (Dex) correlated idiotypes by cells from responder BALB/c animals (allotype Ig, Dex+, IdDex+) in nonresponder (IgbH, Dex−, IdDex−) congeneic mice. Adult IgbH recipients did not permit activation of either adult spleen or bone marrow cells (isogeneic barrier). Neonatal recipients showed functional tolerance towards adult spleen cells. By contrast, neonates neither permited activation of adult B cell‐depleted bone marrow cells, nor of neonatal immature spleen cells. The results show that the immature system of the neonate is permissive towards mature (adult) congeneic lymphocytes, but not towards immature cells from congeneic neonates or adult bone marrow. It appears that mature adult cell populations are dominant in the immature neonatal host. However, the time required by transferred immature cells to differentiate in the neonatal recipient concomitantly allow the latter to gain maturity and functionally reject the grafted cells.
Xenogeneic recognition of soluble and cell surface HLA class II antigens by proliferative murine T cells
Authors: Viguier Mireille , Lotteau Vincent , Charron Dominique , Debré Patrice 
Published: March 2007

AbstractIn order to characterize the murine anti‐human xenogeneic mixed lymphocyte reactions (MLR), we studied T cell proliferative responses against various human lymphoid cells by immunization of mice either with cellular or purified HLA‐DR antigens. Data presented here indicated that small amounts of soluble HLA‐DR antigen were able to prime mice, and that the xenogeneic MLR depends on the expression of HLA class II antigens on the stimulating cells. Experiments using a mutant call line clearly showed that HLA‐DP molecules were also sufficient in eliciting a primary or a secondary xenogeneic MLR while no secondary proliferative response was obtained with cells expressing only HLA class I molecules.Using a large panel of human cells with various haplotypes, our results also showed that (a) nonpolymorphic determinants of HLA class II antigens trigger dominantly the murine T cells and (b) the xenogeneic response required I‐E and L3T4 accessory molecules and was not inhibited with anti I‐A and monomorphic anti‐HLA class II antigen monoclonal antibodies. Altogether these results suggest that HLA class II antigens act as nominal antigens in triggering a murine anti‐human proliferative response.
T cell activation by processed antigen is equally blocked by I‐E and I‐A‐restricted immunodominant peptides
Authors: Lakey Ellen K. , Casten Lisa A. , Anderson Mark S. , Smolenski Lori A. , Smith John A. , Margoliash Emanuel , Pierce Susan K. 
Published: March 2007

AbstractThe T cell response to a soluble protein requires the processing of the native antigen by an antigen‐presenting cell (APC) to a peptide containing an antigenic determinant, which is transported to and bound on the antigen‐presenting cell surface, where it is subsequently recognized by the specific T cell in the context of the appropriate Ia molecule. Investigating the response of a pigeon cytochrome c‐specific, I‐Ek‐restricted T cell hybrid, which recognizes a determinant present within a 10‐amino acid C‐terminal fragment of the protein, it was previously demonstrated that peptides homologous to the peptide from pigeon cytochrome c, but which were not stimulatory, blocked the T cell response to pigeon cytochrome c as processed and presented by APC. In this report the ability of a series of fourteen, 20‐amino acid overlapping peptides, representing the entire length of staphylococcal nuclease (Nase), were assessed for their ability to block the response of a pigeon cytochrome c‐specific T cell hybrid to antigen‐pulsed presenting cells. Only three Nase peptides blocked the I‐Ek‐restricted pigeon cytochrome c‐specific T cell response. Two of these, Nase 61–80 and Nase 91–110, function as T cell antigens in the I‐Ad and I‐Ab‐restricted response to Nase. The third blocking peptide, Nase 101–120, has not been shown to be a T cell antigen. Two other peptides, Nase 51–70 and Nase 81–100, which are recognized by Nase‐specific T cells in the context of I‐Ek, have no effect on the I‐Ek‐restricted cytochrome c‐specific T cell response. None of these peptides block the higher affinity, heteroclitic response of pigeon cytochrome c‐specific T cells to tobacco hornworm moth cytochrome c. Moreover, the response of an I‐Ak‐restricted T cell to ovalbumin was blocked by the I‐Ek‐restricted cytochrome c peptides from three different species. Thus, peptides with no obvious primary amino acid sequence homology, and which are not capable of being recognized in the context of the same Ia, compete with one another for the sites on the APC necessary for presentation of processed antigen to T cells. These results suggest that there are structures on the APC surface in addition to Ia, which are necessary for effective antigen presentation following processing. One suitable candidate for such a cell surface material is the recently identified peptide‐binding protein, PBP72/74 (Lakey et al., Proc. Natl. Acad. Sci. USA 1987. 84: 1659).
Antigen‐specific T cell unresponsiveness in cloned helper T cells mediated via the CD2 or CD3/Ti receptor pathways
Authors: Lamb Jonathan R. , Zanders Edward D. , Sewell William , Crumpton Michael J. , Feldmann Marc , Owen Michael J. 
Published: March 2007

AbstractWe have investigated the role of the CD2 protein in the negative regulation of immune function and report that similar to antigen and anti‐CD3, the monoclonal anti‐CD2 antibodies (T112 and T113) can induce specific unresponsiveness. Antigen and anti‐CD2 tolerogenic signals both down‐regulated the phenotypic expression of CD3‐Ti. In contrast CD2 surface expression was up‐regulated after exposure to peptide and down‐regulated after anti‐T112 and T113 preincubation. However, in both instances interleukin 2 receptor surface levels were increased. These phenotypic changes could only be partly explained by variations in the levels of the transcripts encoding the CD3‐Ti and CD2 molecules.
A novel strategy for immunotherapy using antibody‐coupled carriers to focus cytotoxic T helper cells
Authors: Ochi Atsuo , Worton Katharine S. , Woods Greg , Gravelle Micheline , Kitagami Keiji 
Published: March 2007

AbstractTargeting of cytotoxic T cells to cell‐bound antigens has previously been reported using bispecific antibodies. In this report we document a novel targeting system whereby cytotoxic T helper (Thc) cells were targeted to a B cell lymphoma by means of an anti‐idiotypic antibody (anti‐Id), specific for the surface immunoglobulin of the B cell, coupled to the carrier protein keyhole limpet hemocyanin (KLH). In this system the anti‐Id‐KLH complex bound to the Id determinant of the surface immunoglobulin of the B cell lymphoma. This complex was then presented in a major histocompatibility complex class II‐restricted manner to the KLH‐specific Thc cell (KLH55) which was induced into its cytolytic pathway through the specific recognition of KLH. The uniqueness of this system was that it utilized the inherent ability of the target B cell to process and present antigen. This offered the distinct advantage that processed antigen re‐expressed on the cell membrane was in a more stable form, thereby enabling the target cell to remain susceptible to cytotoxicity for an extended period of time. Furthermore, as is characteristic of Thc cells in general, bystander kiling was demonstrated and Id (or Ia)‐negative mutants of the target cell did not escape destruction. The adaptation of such a system will have useful implications for future immunotherapeutic strategies.