bluuebunny/crossref_metadata_2025_split huggingface dataset:
B cell participation in the recursive selection of T cell repertoires
Authors: Marcos Miguel Angel R. , De La Hera Antóio , Pereira Pablo , Marquez Carlos , Toribio Marisa , Coutinho António , Martinez‐A. Carlos 
Published: March 2007

AbstractNormal BALB/c mice produce 2,4,6‐trinitrophenyl (TNP)‐I‐Ad specific T helper (Th) cells expressing a receptor heterodimer which share with anti‐TNP antibodies an idiotope defined by the F6(51) anti‐idiotypic antibody. Expression of this Th idiotype is controlled by major histocompatibility complex and immunoglobulin heavy chain‐linked genes and results from antibody‐dependent selection of T cell repertoires (Martinez‐A. et al., Eur. J. Immunol. 1986. 16: 417). We now present evidence for the recursive nature of T → B cell repertoire selection and suggest that perinatal B cells, present in adult peritoneal cavity, operate in the early phases of this process. Thus, the Th idiotype is absent in BALB/c mice which are either suppressed from birth with anti‐p antibodies, or reconstituted with autologous bone marrow after lethal irradiation as adults. Supplementation of bone marrow reconstitution with syngeneic Thy‐1−, Ly‐1+ peritoneal B cells, however, selects Th cell repertoires that are undistinguishable from normal mice as to expression of the F6 (51) clonotype. This effect is lost after depletion of Ly‐1− cells in the reconstituting Thy‐1− peritoneal cell population. Interestingly, large in vivo “naturally” activated Ly‐1− splenic B cells can also reconstitute Th idiotype expression if they .are isolated from normal, but not from athymic, nude donors. However, transfer of normal large splenic T cells to adult nude mice “educates” the splenic “large B cell” compartment in these animals such that they acquire the ability to recursively select, upon transfer to bone marrow reconstituted recipients, the Th clonotype. Small resting lymphocytes in either the B or T cell lineage fail to exert these selective effects. These observations constitute formal evidence for recursive repertoire selection in the naturally activated lymphocyte compartment of normal animals.
The human intermediate‐affinity interleukin 2 receptor consists of two distinct, partially homologous glycoproteins
Authors: Herrmann Thomas , Diamantstein Tibor 
Published: March 2007

AbstractIn this report we demonstrate that the human intermediate‐affinity‐type interleukin (IL)2 receptor (IL2R) consists of two distinct glycoproteins designated H1 and H2, whereas the high‐affinity IL2R consists of three chains, H1, H2 and the light chain (L), the Tac antigen. They are neither linked by disulfide bridges to each other nor to the L chain. Similar to the L chain, H1 and H2 apparently carry intramolecular disulfide bonds. From affinity‐labeled IL2 intermediate‐affinity receptor complexes, we deduced an apparent mol. mass of 70 kDa for H1 and of 75 kDa for H2 in sodium dodecyl sulfate‐polyacrylamide gel electrophoresis (SDS‐PAGE) and of 55 kDa for H1 and of 85 kDa for H2 in SDS‐PAGE/urea. As demonstrated by limiting proteolysis, both glycoproteins display high homologies or even identity proximal to the IL2‐binding sites. The areas which are responsible for the striking differences between H1 and H2 in SDS‐PAGE/urea are located distally to the IL2‐binding site and, in contrast to the L chain, are protected from the action of exogenous proteases by the plasma membrane.
Mechanisms of monoclonal antibody‐facilitated tolerance induction: a possible role for the CD4 (L3T4) and CD11a (LFA‐1) molecules in self‐non‐self discrimination
Authors: Benjamin Richard J. , Qin Shixin , Wise Matthew P. , Cobbold Stephen P. , Waldmann Herman 
Published: March 2007

AbstractIn vivo therapy with a CD4 (L3T4) monoclonal antibody is able to provide a tolerogenic milieu for a limited number of protein antigens. In this study we have analyzed the mechanisms of such tolerance to human gamma globulin, and show that tolerance is induced in adult T helper cells without a need for cellular depletion, and that it is probably not maintained by suppressor mechanisms nor by regulatory cellular circuits involving CD8+ (Ly‐2+) cells. Tolerance induction is not a property peculiar to the CD4 molecule, as similar effects can be elicited with a monoclonal antibody directed to the CD11a (LFA‐1) molecule. We suggest that tolerance is maintained by the functional deletion of mature T helper cells and that adhesion molecules, such as CD4, CD8 and CD11a, may play a critical role in T cell discernment of self from non‐self.
Genetic restriction of the murine humoral response to a recombinant Plasmodium vivax circumsporozoite protein
Authors: Nardin Elizabeth H. , Barr Philip J. , Heimer Edgar , Etlinger Howard M. 
Published: March 2007

AbstractThe antibody response of inbred and congenic strains of mice immunized with a recombinant Plasmodium vivax circumsporozoite protein was investigated. Only mice of the H‐2k and H‐2a haplotypes developed antibodies that react with P. vivax sporozoite in an indirect immunofluorescence assay and with the recombinant protein in enzyme‐linked immunosorbent assay. Congenic recombinant strains were used to map Ir gene control to the I‐Ak locus. A similar pattern of genetic restriction was found when congenic strains were immunized with a carrier‐free synthetic peptide corresponding to the repeat region of the P. vivax circumsporozoite protein. The results suggest that the ability of T helper cells to recognize a T cell epitope(s) in the repeat region of the P. vivax circumsporozoite protein is genetically restricted.
The double reactivity of a human monoclonal rheumatoid factor to IgG and histones is related to distinct binding sites
Authors: Pasquali Jean Louis , Azerad Graziella , Martin Thierry , Muller Sylviane 
Published: March 2007

AbstractThe structural basis of the double reactivity of a human monoclonal rheumatoid factor (RF) with both human IgG and histones H1 and H3 was investigated by means of competitive inhibition experiments. The monoclonal RF binding to solid‐phase histones was inhibited by increasing concentrations of heat‐aggregated IgG. However, increasing concentrations of purified histones were almost unable to reduce the RF binding to solid‐phase IgG. Inhibition of antigen binding with two murine monoclonal anti‐idiotopes reacting with distinct idiotopes on the monoclonal RF indicated that the fixation to the different antigens was mediated by distinct binding sites. This result was confirmed by showing the selective sensitivity to mild acid treatment of the histone binding site but not of the IgG binding site. This report provides a structural basis for the existence of polyfunctional combining regions on a human autoantibody.
Co‐expression of Mac‐1 and p150,95 on CD5+ B cells. Structural and functional characterization in a human chronic lymphocytic leukemia
Authors: Hera Antonio De La , Alvarez‐Mon Melchor , Sanchez‐Madrid Francisco , Martinez‐A Carlos , Durantez Alberta 
Published: March 2007

AbstractThe leukocyte adhesion receptors (LAR) Mac‐1 and p150,95 were thought to occur only on myeloid cells, but recently, mouse Ly‐1+ (CD5+) B and pro‐B cells were shown to bind M1/70 monoclonal antibody, an anti‐Mac‐1 antibody. Using immuno‐precipitation, sodium dodecyl sulfate gel electrophoresis, immunofluorescence and flow cytometry, we have studied the expression of LAR in human CD5+ B cells from chronic lymphocytic leukemia (B‐CLL) patients. 170,95 kDa Mac‐1 and p150,95, as well as 180,95 kDa LFA‐1 heterodimers are shown to be co‐expressed on CD5+μ+μ+ B cells from a patient where they retain their known function in homotypic cell‐cell adhesion. Therefore, functional Mac‐1 and p150,95 LAR are not restricted to myeloid cells.
Triggering of the phosphoinositide transduction pathway by a monoclonal antibody specific for the human γ/δ T cell receptor
Authors: Bismuth Georges , Faure Florence , Theodorou Ioannis , Debré Patrice , Hercend Thierry 
Published: March 2007

AbstractWe have developed a monoclonal antibody (mAb), termed anti‐TigammaA, which recognizes an antigenic determinant carried by a variable segment of the T cell receptor (TcR) γ chain. This determinant, encoded by the Vγ9 gene, is expressed on approximately 3% of peripheral blood lymphocytes. In the present study, we have found that binding of anti‐TigammaA mAb to its specific ligand results in the triggering of the phosphatidylinositol (PI) cycle‐related metabolic process. Indeed, an increased labeling of both phosphatidic acid and PI, related to an enhanced turnover of PI cycle‐dependent phospholipids, was observed following exposure of 32P orthophosphoric acid‐labeled cells to anti‐TigammaA mAb. In addition, there was a rapid rise in intracellular free calcium concentrations. Similar experiments have been performed previously on CD3+ TcRα/β−‐cells with an anti‐CD3 mAB. They predicted that signals produced by the interaction between the second TcR and its ligand(s) would be transmitted via the PI cycle‐linked intracellular second messengers. We confirm this hypothesis in an experimental system where stimulation occurs directly through the γ/δ receptor structure.
Protection of neutropenic mice from lethal Candida albicans infection by recombinant interleukin 1
Authors: Van Wout Jan W. 'T , Van Meer Jos W. M. Der , Barza Michael , Dinarello Charles A. 
Published: March 2007

AbstractNatural and synthetic immunomodulators that increase nonspecific resistance to infection are also known to induce interleukin 1 (IL1) production. Previous studies have demonstrated a protective effect of recombinant human IL1β against death from infection caused by Pseudomonas aeruginosa. In the present study we investigated the effect of IL 1β or IL 1α on the survival of neutropenic mice with a lethal Candida albicans infection. Mice with cyclophosphamide‐induced neutropenia were injected with 3 × 105 C. albicans i.v. When 80 ng IL 1β was given as a single i.p. injection 24 h before the infection, survival compared to that in control animals was as follows: 100% vs. 97% at 24 h, 83% vs. 70% at 48 h and 70% vs. 23% at 72 h after the infection (p<0.01). The effect of IL1 was also apparent when it was given 1/2 h before or 6 h after the infection. The results obtained with 80 ng IL 1α given at 24 h before infection were similar to that obtained with IL 1β. The numbers of Candida cultured from the blood, liver, spleen, and kidney were not significantly different in IL 1β‐treated and control animals. Passive transfer of serum obtained from mice pretreated with IL 1 to recipient mice did not provide protection against a subsequent lethal candidal infection. In conclusion, the present study demonstrates that IL 1β and IL 1α prolong survival in neutropenic mice with a lethal C. albicans infection.
Modification of tumor cells by a low dose of Newcastle Disease Virus.
Authors: Hoegen Paul Von , Weber Ernst , Schirrmacher Volker 
Published: March 2007

AbstractThe present study elucidates the mechanism whereby viral xenogenization of highly metastatic ESb lymphoid tumor cells increases tumor immunogenicity and syngeneic tumor‐specific T cell responses in comparison to nonmodified tumor cells. It was found that the frequency of cytotoxic T lymphocytes specific for the ESb tumor‐associated transplantation antigen (TATA) and the cytotoxic anti‐tumor activity in bulk cultures of immune spleen cells were significantly increased (by factor 3 and 25, respectively) when using virus‐modified tumor cells. An amplified response was observed both in vivo and in vitro which might explain the demonstrated effectiveness of this approach for postoperative immunotherapy of ESb metastases.For the stimulation of tumor‐specific cytolytic T lymphocytes (CTL) the ESb tumor cells which are highly metastatic were infected with an avirulent strain of the paramyxovirus Newcastle Disease Virus (NDV). Infection of ESb cells with low amounts of NDV was sufficient to lead to an increase in cytolytic activity of tumor‐specific CTL after sensitization in vivo and restimulation in vitro. In a sensitive limiting dilution mixed leukocyte‐tumor cell microculture system the direct effect of viral modification on the frequency and specificity of CTL was investigated. The number of ESb‐specific CTL per spleen could be raised from about 3300 (without modification) to 9100 by both in vivo and in vitro application of ESb‐NDV. One appliction of ESb‐NDV (in vivo or in vitro) increased the number of CTL to 4900 and 4600, respectively. In split‐type experiments it could be shown at the clonal level that viral modification did not alter the specificity of ESb‐specific CTL. No CTL clones directed against viral antigens or new antigenic determinants were detected. The results indicate that in this system the effect of viral xenogenization is not due to recognition of additional xenoor neoantigens. NDV modification instead led to a selective augmentation of the TATA‐specific CTL response. In this respect it is remarkable since other methods to increase ESb tumor immunogenicity such as mutagenization or co‐expression of minor H antigens were shown before to activate additional CTL clones without affecting the TATA‐specific CTL response.
The differentiation of O‐2A progenitor cells into oligodendrocytes is associated with a loss of inducibility of Ia antigens
Authors: Calder Virginia L. , Wolswijk Guus , Noble Mark 
Published: March 2007

AbstractCurrent data suggest that some astrocytes, one of the 3 main types of macroglia in the central nervous system (CNS), can be induced by interferon‐y (IFN‐γ) to express major histocompatibility complex class I1 antigens (immune‐associated or Ia) and present antigen to T lymphocytes. In contrast, oligodendrocytes, another type of macroglia, cannot be induced to express Ia. The astrocytes which have been shown to express Ia are from a particular glial lineage and are called type‐1 astrocytes. The oligodendrocyte‐type‐2 astrocyte (0‐2A) lineage, which gives rise to oligodendrocytes, also gives rise to a second class of astrocytes called type‐2 astrocytes and the ability of type‐2 astrocytes or the common O‐2A progenitor cell to express Ia is not known. We have now found that both type‐2 astrocytes and O‐2A progenitor cells can be induced to express Ia by IFN‐Γ but Ia expression is not induced in oligodendrocytes in parallel cultures. Thus, it appears that differentiation of O‐2A progenitor cells into oligodendrocytes is specifically associated with a loss of inducibility of Ia. This apparent loss of the capacity for Ia expression, and presumably antigen presentation, in oligodendrocytes (the cells which produce myelin in the CNS) is of particular interest in view of the ability of immunization of myelin components to produce autoimmune‐mediated paralytic disease.
Rapid changes in target cell lysosomes induced by cytotoxic T cells: indication of target suicide ?
Authors: Pitsillides Andrew A. , Taylor Patricia M. , Bitensky Lucille , Chayen Joseph , Helen Muir I. , Askonas Brigitte A. 
Published: March 2007

AbstractAlthough many studies have attempted to elucidate how cytotoxic T (Tc) lymphocytes cause the death of target cells, the mechanism is still controversial. In the present study the effect on the integrity of the lysosomes of the target cell has been investigated. We show here that the specific recognition and attachment of cloned type A influenza‐specific Tc cells to A/X31 influenza virus‐infected target cells caused rapid change in the amount of lysosomal naphthylamidase activity that was bound within the lysosomes, indicating that the lysosomal membianes in the target cells had been totally labilized. Target cells infected with type B influenza virus served as controls. We therefore suggest that the viral specificity of Tc, lymphocytes allows for recognition and intimate membrane contact with suitably infected targets. This intimate contact induces sufficient perturbation of the target cell plasma membrane so as to cause total labilization of the target cell lysosomes which could account for intracellular lysis.
The role of lymphocyte function‐associated antigen 1 (LFA‐1) in the adherence of T lymphocytes to B lymphocytes
Authors: Mazerolles Fabienne , Lumbroso Catherine , Lecomte Olivia , Le Deist Françoise , Fischer Alain 
Published: March 2007

AbstractThe functional role of the LFA‐1 molecule in the interaction between helper T lymphocytes and B lymphocytes was investigated using lymphocytes from patients with leukocyte adhesion deficiency, an inherited immunodeficiency characterized by a defective leukocyte expression of the LFA‐1, Mac‐1 (CR3) and p150,95 molecules. The ability of LFA‐1− T lymphocytes to provide antigen‐specific help for HLA−identical LFA‐1+ B lymphocytes was reduced while their antigen‐specific activation was normal. Antigen‐independent conjugate formation between resting, nonactivated LFA–1− T lymphocytes and LFA‐1+ B lymphocytes was impaired while LFA‐1−B lymphocytes bound LFA‐1+ T lymphocytes normally. Conjugate formation of activated LFA‐1− T lymphocytes was mostly mediated by the CD2‐LFA‐3 adhesion pathway while the ICAM‐1 molecule, a ligand of LFA‐1, had no function. These results demonstrate that LFA‐1 plays a major role in the cognate interaction between helper T lymphocytes and B lymphocytes that cannot be mediated instead by CD2 or other molecules on resting T lymphocytes.
Involvement in the initiation of T cell responses and structural features of an 85‐kDa membrane activation antigen
Authors: Schulz Thomas F. , Mitterer Manfred , Neumayer Heinz P. , Vogetseder Werner , Dierich Manfred P. 
Published: March 2007

AbstractA monoclonal antibody, 7F7, directed at a recently described membrane activation antigen of 85 kDa was found to inhibit the T cell proliferation induced by an anti‐CD3 antibody, phytohemagglutinin A and concanavalin A. The T cell response to allogenic stimulator cells was also weakly inhibited. The inhibition of these T cell responses was only obtained if the antibody was added within the first 8 h (first 24 h in the case of the concanavalin A response) of culture. In addition the antibody inhibited the formation of cellular aggregates seen in stimulated cultures when added within the first 8 h. The membrane glycoprotein recognized by 7F7 is shown to have a slightly different molecular mass on cells of different lineage, a protein core of 55 kDa and to contain 30–50% of N‐linked as well as a small amount of 0‐linked carbohydrates and sialic acid residues. This study suggests that the highly glycosylated membrane activation antigen defined by antibody 7F7 could contribute to the contact between those cells which are involved in the initiation of T cell responses.
Interleukin 6, the third mediator of acute‐phase reaction, modulates hepatic protein synthesis in human and mouse. Comparison with interleukin 1 β and tumor necrosis factor‐α
Authors: Ramadori Giuliano , Van Damme Jo , Rieder Hartmut , Zum Büschenfelde Karl‐Hermann Meyer 
Published: March 2007

AbstractInterleukin 6 ( IL6 ) is the new definition of a group of cytokines previously named according to their biological activity, e.g. B cell stimulatory factor 2 (BSF‐2), hybridoma plasmocytoma‐growth factor (HGF), interferon‐β2 (IFN‐β2), hepatocyte stimulating factor (HSF). It has recently been suggested that IL6 may represent the major mediator of actue‐phase protein response whereas IL 1β and TNF‐α could play a minor role. We compared the effect of the three cytokine on hepatic protein synthesis by performing in vitro as well as in vivo experiments. Human hepatoma cells (PLC/PRFS) were exposed to each cytokine separately for 20 h, and the effect was then studied at the protein and RNA level. All three cytokines reduced albumin and increased C3 and ceruloplasmin biosynthesis. The cytokines induced the same effect at the RNA level indicating that the modulation was pretranslational. The effect of the cytokines was specific since actin gene expression was not changed; furthermore the effect was blocked by specific antibodies against the cytokines. The effect of the single cytokines was dose and time dependent, and quantitatively comparable. None of the cytokines was able to alter αl‐anti‐trypsin synthesis. In vivo experiments with mice showed that IL 1β and TNF‐a both induce serum amyloid A (SAA) mRNA in the mouse liver and increase factor B (Bf) gene expression. Human recombinant IL6 induced SAA gene expression and it also had a weak positive effect on Bf gene expression after i.p. injection. These data demonstrate that the three cytokines studied are quantitatively and qualitatively comparable, and that all three are probably involved in acute‐phase protein response.
Interaction between lymphocytes and cultured high endothelial cells: an in vitro model of lymphocyte migration across high endothelial venule endothelium
Authors: Ager Ann , Mistry Shilaben 
Published: March 2007

AbstractThe interaction between lymphocytes and cultured high endothelial venule endothelium has been studied using light and electron microscopy. High endothelial cells (HEC) in monolayer culture bound lymphocytes 15‐200‐fold more efficiently than aortic endothelium, aortic fibroblasts or serum‐coated glass. Light microscopy of lymphocytes bound to HEC showed two populations. Type I lymphocytes were phase‐light, round and revealed no intracellular detail. Type II lymphocytes were phase‐dark and flattened. The nucleus and cytoplasm of type II cells were clearly visible under high power light microscopy. The relative positions of these two populations were determined by electron microscopy. Type I lymphocytes were attached to the surface of HEC and type I1 lymphocytes were flattened underneath. The transition from type I to type II was accompanied by a loss of surface microvilli and a redistribution of intracellular organelles. This suggested that lymphocytes actively migrated across the HEC layer in this assay.The relationship between migrated lymphocytes and total adherent cells was determined by analysis of surface phenotype. Lymphocytes did not adhere randomly from the cell population plated. After 60 min there was an enrichment for B over T lymphocytes and the adherent T cell population was itself enriched for CD8′ cells over CD4′ cells. Migrated cells were, however, a random subpopulation of lymphocytes which adhered to HEC. This is clear evidence that migration was preceded by specific binding to HEC. Lymphocyte adhesion was independent of viable HEC showing that it was a passive event on the part of the endothelium. Lymphocyte migration was, however, completely dependent on viable high endothelium. We conclude that cultured HEC provide a biologically relevant, 3‐dimensional matrix which supports the specific adhesion of lymphocytes and actively promotes lymphocyte migration. These observations suggest to us that cultured high endothelium provides a novel in vitro model for the study of lymphocyte migration into lymph nodes from the blood.