bluuebunny/crossref_metadata_2025_split huggingface dataset:
T cell receptor β chain usage in myelin basic protein‐specific rat T lymphocytes
Authors: Chluba Johanna , Steeg Christiane , Becker Andrea , Wekerle Hartmut , Epplen JöRg T. 
Published: March 2007

AbstractMyelin basic protein (MBP)‐specific T cell lines and clones have been established from rats of the major histocompatibility complex (MHC)‐compatible Lewis and BS strains. All lines and clones are MHC class II restricted and share the CD4 phenotype. The cells proliferate specifically in response to either a peptide representing amino acids #68–88 of guinea pig MBP, to residues #47–67 or to an unidentified myelin antigen which is distinct from MBP. All lines and clones specific for MBP express the same T cell receptor (TcR) variable (V) β chain element, which is homologous to the mouse Vβ8.2 gene segment. Three lines/clones with the same antigen fine specificity have identical VβDβJβ junctions on the protein level, a region which represents part of the potential antigen‐binding protion of the TcR; two of the lines express members of the Vα2 family. These results suggest biased usage of TcR Vβ elements in rat T cells specific for MBP. Our findings broaden the basis for a rational therapeutic strategy to specifically intervene in the rodent model system of experimental allergic encephalomyelitis.
L3T4 T cells promoting susceptibility to murine cutaneous leishmaniasis express the surface marker Ly‐24 (Pgp‐1)
Authors: Moll Heidrun , Scollay Roland 
Published: March 2007

AbstractIn a murine model of cutaneous leishmaniasis, the importance of T cell‐dependent immunity has been documented by the susceptibility to parasite infection of athymic nude mice of both genetically resistant and genetically susceptible strains. T lymphocytes from uninfected mice have the capacity to promote resistance to Leishmania major infection in nude recipients, whereas T cells from mice chronically infected with L. major not only fail to mediate protection, but totally abrogate the host‐protective effect of normal mouse lymphocytes. Both these effects are mediated by T cells which have the phenotype L3T4Ly‐2‐. To discriminate between the two activities, we have tried to separate the L3T4 population on the basis of additional cell surface markers and we have found that peripheral L3T4 lymphocytes could be subdivided according to their expression of the Ly‐24 (Pgp‐1) surface marker. In adoptive transfer experiments, both the Ly‐24 and the Ly‐24 subset of L3T4 cells from uninfected mice had the capacity to mediate resistance to infection with L. major. However, diseasepromoting activity was only found in the L3T4Ly‐24 and not in the L3T4Ly‐24‐ subset of cells from mice with chronic cutaneous disease. Moreover, Ly‐24 expression was strongly increased in lymphocytes from chronically infected mice and in vitro limiting dilution analysis confirmed that the vast majority of L. major‐reactive T cells was L3T4Ly‐24. In genetically susceptible mice with chronic cutaneous leishmaniasis, Ly‐24 therefore appears to be a marker for lymphocytes with the capacity to abrogate resistance to disease, these cells being activated and expanding in the course of progressive L. major infection. Ly‐24 expression is a useful tool for phenotypic identification and selective enrichment of antigen‐activated and possibly memory T cells. It may facilitate the isolation of L. major‐specific T cell clones with defined activities.
The autoantigenic response to rabbit cytochrome c
Authors: Cooper Helen M. , Klinman Norman R. , Paterson Yvonne 
Published: March 2007

AbstractIn this report we describe the production and characterization of autoantibody responses to rabbit cytochrome c (cyt c) in rabbits immunized with either the native monomeric or polymerized form of rabbit cyt c. Fine‐specificity analyses of the response indicated that the majority of the response was to the evolutionarily conserved ammo‐terminal region of the molecule. The relative affinity of the autoantibody interaction with rabbit cyt c was assessed by a solid‐phase assay and was found to be lower than that observed for rabbit anti‐horse cyt c antibody populations. These findings are consistent with the prediction that low‐affinity self‐reactive B cells may escape tolerance induction.
MLR3 molecule is an activation antigen shared by human B, T lymphocytes and T cell precursors
Authors: Risso Angela , Cosulich Maria Elisabetta , Rubartelli Anna , Mazza Maria Rosaria , Bargellesi Antonio 
Published: March 2007

AbstractMLR3 molecule is a membrane glycoprotein (mol. mass range 28–34 kDa) present on activated, but not resting human peripheral T cells, B cells and thymocytes. Its kinetics of appearance on the cell surface (3 h after the addition of the inductive signal to the cells) suggests that it is an early activation antigen. The proliferative response of cultured T and B lymphocytes and thymocytes to different activation signals is inhibited by the addition of MLR3 monoclonal antibody. Moreover the antibody in combination with non‐mitogenic doses of phorbol myristate acetate leads to proliferation of thymocytes and resting B and T lymphocytes. In the latter, synthesis of interleukin 2 is also induced. Biochemical analysis of MLR3 antigen indicates that it is a phosphorylated protein with N‐linked sugar moieties. Together these data suggest a role for MLR3 antigen in the signal transduction process during activation, both for mature lymphocytes and for T cell precursors.
The gene for human lymphocyte homing receptor is located on chromosome 11
Authors: Forsberg Ulla HÉLena , Ala‐Kapee Minna Maria , Jalkanen Sirpa , Andersson Leif C. , Schröder Jim 
Published: March 2007

AbstractThe mouse monoclonal antibody Hermes‐3 recognizes the human lymphocyte homing receptor. A panel of mouse‐human T lymphocyte hybrids, carrying all mouse chromosomes and a limited number of human chromosomes, was analyzed for expression of human homing receptor by indirect immunofluorescence and immuno‐precipitation of radiolabeled cell lysates with Hermes‐3 antibody. Karyotypic analysis of the tested clones showed that the expression of human homing receptor correlated to the presence of human chromosome 11 in all but one clone. However, con‐canavalin A induced a weak to moderate expression of the homing receptor in this clone, but not in a chromosome 11‐ clone. Another clone, heterogeneous for the expression of homing receptor, was separated into a Hermes‐3 and a Hermes‐3‐ fraction with a fluorescence‐activated cell sorter. Karyotypic analysis performed after sorting showed human chromosome 11 to segregate with the Hermes‐3 antigen. To confirm these data we correlated the expression of two chromosome 11‐coded antigens, Trop‐4 and Leu‐7, with the expression of the homing receptor. In our hybrid clones these three antigens were expressed concordantly. The gene coding for the human lymphocyte homing receptor recognized by Hermes‐3 is thus assigned to chromosome 11.
Anti‐viral protection and prevention of lymphocytic choriomeningitis or of the local footpad swelling reaction in mice by immunization with vaccinia‐recombinant virus expressing LCMV‐WE nucleoprotein or glycoprotein
Authors: Hany Manuela , Oehen Stephan , Schulz Manfred , Hengartner Hans , Mackett Michael , Bishop David H. L. , Overton Hilary , Zinkernagel Rolf M. 
Published: March 2007

AbstractThe viral antigen specificity of primary cytotoxic T cell responses (CTL) of H‐2b, H‐2k, H‐2q, H‐2s, H‐2f and some H‐2‐recombinant mice against lymphocytic choriomeningitis virus (LCMV‐WE isolate) as well as the specificity of some CTL clones and T cell lines was defined on target cells infected with vaccinia‐recombinant virus expressing nucleoprotein (Np) or glycoprotein (Gp). Np was recognized together with H‐2q (Dq), H‐2d (DLd), H‐2s and H‐2b (Db). Gp specificity was restricted to H‐2f and H‐2b (Kb and Db); H‐2k‐restricted CTL anti‐LCMV responses were neither Gp nor Np specific.The anti‐viral protective immunity induced by vaccinia‐Gp or vaccinia‐Np recombinants was evaluated in mice. In vivo protection was T cell mediated by class I restricted Ly‐2 T cells; it correlated well with the CTL specificity defined in vitro. Some of the CTL‐nonresponder H‐2 allele plus Np or H‐2 plus Gp combinations were, however, protected to variable and low degrees by vaccinia‐recombinant viruses, indicating that anti‐viral protection is a more sensitive readout for CTL activity than the in vitro assay. For example, B10.D2 H‐2d mice generated measurable CTL responses only to Np; after immunization with a vaccinia‐Np recombinant, LCMV titers were 104 times lower in spleens than in vaccinia‐primed controls. Although vaccinia‐Gp‐immunized BALB/c mice revealed no CTL activity in vitro, they nevertheless had 102 times lower LCMV titers in spleens than controls. Anti‐viral protection, particularly in low‐responder combinations, was usually short‐lived and diminished after 3 weeks. In a high‐responder situation, protection was of a longer duration (> 8 weeks). Vaccination with vaccinia‐Np or Gp recombinants protected mice against lethal T cell‐mediated lymphocytic choriomeningitis induced by LCMV or prevented the local footpad swelling reaction; these in vivo effects were H‐2 dependent and followed the identical roles established for CTL recognition in vitro.
Serological detection and molecular localization of allelic HLA‐DP supertypic epitopes
Authors: Colonna Marco , Tanigaki Nobuyuki , Tosi Roberto , Ferrara Giovan Battista 
Published: March 2007

AbstractA DP serological allospecificity was identified using 125I‐labeled preparations of HLA class II molecules isolated from cells of HLA homozygous typing cell lines, SLE (DRw6, DQw1, DPw3) and WT46 (DRw6, DQw1, DPw2), and depleted of DR molecules by absorption with an anti‐DR monoclonal antibody. The specificity, provisionally called WT, was carried by class II molecules possessing the characteristics of DP molecules on sodium dodecyl sulfate‐polyacrylamide gel electrophoresis, and detected primarily in DPw1, DPw3 and DPw5 cells and exceptionally in some DPw2 cells including WT46 and DPw4 cells on a large panel of DP‐pretyped B cell lines mostly derived from the 10th International Histocompatibility Workshop B cell reference panel. It was apparently allelic to another DP serological specificity BUT previously defined on DP molecules isolated from cells of DPw2 HLA deletion mutant cell line LCL 721.82. On the same cell panel, the BUT specificity was negative in all DPw1, DPw3 and DPw5 cells, and positive in all DPw2 and DPw4 cells and also in DPw2B and DPw4B cells except the cells typed WT. This DP association pattern was similar to that of the known allelic sequences, GGPM and DEAV, in DP ß F segment, one of the six variable segments in the second exon of DP ß gene. Thus, genomic DNA from 22 B cell lines pretyped for BUT and WT specificities were enzymatically amplified for the second exon of DP ß gene by the use of locus‐specific oligonucleotide primers and hybridized with 32P‐labeled oligonucleotide probes corresponding to the F segment sequence variations. This oligonucleotide typing showed perfect one‐to‐one correlation with the BUT and WT serological typing. The typing also revealed that WT46 cells, although typed DPw2, have the DEAV sequence common to DPw1, DPw3 and DPw5.
Feedback regulation of murine Ly‐1 B cell development
Authors: Lalor Paul A. , Herzenberg Leonore A. , Adams Sharon , Stall Alan M. 
Published: March 2007

AbstractStudies presented here, conducted with allotype homozygotes, demonstrate the existence of a feedback mechanism that regulates development of Ly‐1 B cells from immature progenitors. In the preceding study (P. A. Lalor et al., Eur. J. Immunol. 1989. 19: 501), conducted with allotype heterozygotes, we showed that treating neonates with monoclonal antibody to the paternal allotype IgM depletes roughly half of the neonatal B cell population (i.e. those expressing the paternal IgM allotype) and that paternal allotype Ly‐1 B cells specificically remain depleted for the life of the animal. Here we show that treating allotype homozygotes with the same antibody depletes all (rather than half) of the B cells and that, under these conditions, relatively normal numbers of Ly‐1 B cells reappear shortly after the treatment antibody disappears. This recovery, we also show, is prevented by restoring allotype‐congenic Ly‐1 B cells to the treated homozygotes, i.e. by reconstituting treated neonates with allotype‐congenic peritoneal cells, sorted Ly‐1 B cells or a monoclonal population of Ly‐1 B “tumor” cells.These findings in essence reveal a feedback mechanism through which mature Ly‐1 B cells prevent further Ly‐1 B cell development from Ig‐ precursors. This feedback regulation is independent of Ig secretion by the mature Ly‐1 B cells, since the monoclonal Ly‐1 B “tumor” population that prevents endogenous Ly‐1 B development does not secrete Ig. Furthermore, it appears to be independent of Ly‐1 B surface Ig specificity, since a monoclonal population is sufficient to block all Ly‐1 B cell development. This mechanism appears to operate normally to fix the composition of the Ly‐1 B population, which survives through self‐replenishment in adults, in accord with conditions that influence Ly‐1 B development during neonatal life.
The majority of mouse spontaneous rosette‐forming cells of thymic origin belong to the Ly‐2+ subset
Authors: Lepault Françoise , Fache Marie‐Pierre , Gagnerault Marie‐Claude , Bach Jean‐François , Dardenne Mireille 
Published: March 2007

AbstractSpontaneous sheep erythrocyte rosette‐forming T cells (T‐sRFC) found in normal mouse spleen are specific for the xenogeneic species of red cells and are distinct from human E rosettes as illustrated by their persistence after sheep red blood cell (SRBC) incubation with anti‐LFA‐3 monoclonal antibodies directed against SRBC molecule binding to the E rosette receptor. We confirm here using monoclonal antibodies that T‐sRFC are Thy‐1+CD3+. Additionally, using cell separation techniques based on panning and cell sorting, it is shown that the vast majority of spleen sRFC have the L3T4−Ly‐2+ phenotype. As already shown for anti‐Thy‐1 antibodies, anti‐CD3 and anti‐Ly‐2 antibodies block rosette formation, whereas antibodies to more abundant cell surface antigens (T200, H‐2Db) are not inhibitory. These data suggest that the interaciton of T‐sRFC with SRBC occurs at or near the T cell receptor.
A monoclonal antibody to murine CD45R distinguishes CD4 T cell populations that produce different cytokines
Authors: Bottomly Kim , Luqman Mohammad , Greenbaum Laurence , Carding Simon , West Jeff , Pasqualini Theresa , Murphy Donal B. 
Published: March 2007

AbstractCD4 T cell clones have been shown to be functionally heterogeneous in the mouse. However, it is not known if normal CD4 T cells are also functionally heterogeneous, or whether functional specialization is a result of cloning and long‐term culture. To approach this question, a monoclonal antibody reacting with a subset of CD4 T cells has been prepared by immunization of rats with different cloned T cell lines all sharing the same functional activity. This monoclonal antibody reacts with a subset of CD45 (T200) molecules by binding to a determinant requiring the expression of the second variable exon of the CD45 molecule. Some CD4 T cells bear high levels of this marker, while others react only weakly. This antibody was used to separate CD4 T cells into two subpopulations. The brightly staining population was found to produce interleukin (IL) 2 and not IL 4, while the weakly staining population produced IL 4 and not IL 2. These data demonstrate that CD 4 T cells in normal mice are already functionally committed, and that they differentially express forms of CD45 that contain the second variable exon.
A monoclonal antibody to LFA‐3, the CD2 ligand, specifically immobilizes major histocompatibility complex proteins
Authors: Bierer Barbara E. , Golan David E. , Brown Carl S. , Herrmann Steven H. , Burakoff Steven J. 
Published: March 2007

AbstractT cells are activated when the antigen‐specific T cell receptor recognizes antigen in association with major histocompatibility complex (MHC) proteins. The T cell surface protein CD2 (T11, LFA‐2, the T erythrocyte receptor) and its target or stimulator cell ligand, lymphocyte function‐associated antigen‐3 (LFA‐3), are also involved in T cell adhesion and activation. The molecular mechanisms by which the CD2/LFA‐3 interaction affects T cell adhesion and activation are unclear. The CD2/LFA‐3 interaction may be modeled by the interaction between LFA‐3 and anti‐LFA‐3 monoclonal antibody (mAb). We used the fluorescence photobleaching recovery technique to investigate the effect of anti‐LFA‐3 mAb on the lateral mobility of MHC proteins in plasma membranes of JY, a human Epstein‐Barr virus‐transformed B cell line. Anti‐LFA‐3 mAb induced immobilization of class I MHC proteins labeled with bivalent but not monovalent fluorescein‐conjugated W6/32 mAb. Anti‐LFA‐3 mAb also caused immobilization of class II MHC proteins labeled with bivalent fluoresceinated LB3.1 mAb. In contrast, anti‐LFA‐3 mAb did not affect the mobilities of either a B cell membrane protein labeled with bivalent fluoresceinated anti‐CD45 (human leukocyte antigen) mAb or a membrane lipid analogue. Unlike anti‐LFA‐3 mAb, anti‐LFA‐1 mAb did not affect class I MHC protein mobility. These results suggest that CD2 binding to LFA‐3 may trigger a physiological response in which target cell MHC proteins, cross‐linked by receptors on the T cell surface, are immobilized at and thereby localized to the T cell‐target cell interface.
The molecular context of determinants within the priming antigen establishes a hierarchy of T cell induction: T cell specificities induced by peptides of β‐galactosidase vs. the whole antigen
Authors: Shivakumar Sumati , Sercarz Eli E. , Krzych Urszula 
Published: March 2007

AbstractThe antibody response following priming with a macromolecule or a peptide will depend on the regulatory T cells that become activated by the antigenic determinants available. In this report, activation of T helper (Th) and T suppressor (Ts) cells by determinants on β‐galactosidase (GZ) was examined by comparing native GZ [1023 amino acid (a.a.) residues per monomer] with peptides from the immunodominant region encompassing residues 3 to 187. Each immunogen established its characteristic hierarchy of dominance of determinants within it: in particular, GZ and CB‐2–3 (a. a. 3–187) each induced immunodominant Th cells which could not be induced by T8 (a.a. 60–140). Hierarchies of suppressor determinant are also created: T8‐Ts suppresses all Th specificities and therefore can be deemed immunodominant: T8–2‐Ts and T8–3‐Ts have a more selective suppressor activity and can be considered subdominant. We conclude that the outcome of immunization shifts with a change in the nature of the immunogen and the context within which the determinant lies will crucially influence its expression. A particular ‘context’ presumably determines the likely order of processing of that molecule which leads to a characteristic relationship among the Ts, Th and B cell determinants involved.
On the cellular source and function of interleukin 6 produced in the central nervous system in viral diseases
Authors: Frei Karl , Malipiero Ursula V. , Leist Thomas P. , Zinkernagel Rolf M. , Schwab Martin E. , Fontana Adriano 
Published: March 2007

AbstractInterleukin 6 (IL 6) was found to be produced in the central nervous system (CNS) of ICR +/+ mice infected with lymphocytic choriomeningitis virus (LCMV) or with vesicular stomatitis virus (VSV). When infecting athymic ICR nu/nu mice which cannot develop T cell‐mediated meningitis after LCMV infection, no significant synthesis of IL 6 was detected in the CNS. IL 6 was found, however, to be produced intrathecally in ICR nu/nu mice infected with VSV, which causes a T cell‐independent acute encephalitis. This suggested that IL 6 may also originate from cells not belonging to the T cell compartment. Indeed, in vitro assays showed that both virus‐infected microglial cells and astrocytes secreted IL 6. In astrocytes, the infection resulted in the induction of the 1.3‐kb messenger RNA IL 6. Besides its effect on the development of B cell immunity in the brain, IL 6 may be involved in repair mechanisms initiated in the course of viral‐induced tissue damage. As shown here, IL 6 induced an increase of the secretion of a neurotrophic factor, nerve growth factor by astrocytes. Thus, the intrathecal synthesis of IL 6 may be part of the host response to infection favoring immune‐mediated elimination of the infectious agent as well as trophic support for neurons.
The role of anti‐idiotypic antibodies in the induction of experimental systemic lupus erythematosus in mice
Authors: Mendlovic Shlomo , Fricke Harald , Shoenfeld Yehuda , Mozes Edna 
Published: March 2007

AbstractWe have recently reported the induction of experimental systemic lupus erythematosus (SLE) in mice by a human anti‐DNA monoclonal antibody (mAb) that bears a common idiotype, the 16/6 Id. In the present report we investigated the role of the idiotypic network in the induction of experimental SLE by using a murine anti‐idiotypic mAb specific for the 16/6 Id. This anti‐idiotypic mAb induced experimental SLE similarly to the 16/6 Id. Thus, following immunization, in addition to 16/6 Id+ antibodies, the mice produced antibodies to various nuclear antigens: single‐stranded DNA, double‐stranded DNA, poly(I), poly(G), Ro, La, Sm and ribonucleoproteins. Similarly to the 16/6 Id‐immunized mice, the mice injected with the anti‐16/6 Id mAb exhibited elevated erythrocyte sedimentation rate and leukopenia. The murine anti‐16/6 Id mAb was found to be more effective than the 16/6 Id, in causing earlier onset of proteinuria and renal damage. These results suggest that the idiotypic network and particularly anti‐idiotypic antibodies specific for anti‐DNA common idiotypes found in SLE, play an important role in the induction of SLE in mice.
Interleukin (IL) 4 counteracts the helper effect of IL 2 on antigen‐activated human B cells
Authors: Llorente Luis , Crevon Marie‐Claude , Karray Saoussen , Defrance Thierry , Banchereau Jacques , Galanaud Pierre 
Published: March 2007

AbstractWe tested the effect of interleukin (IL)4 on the specific IgM antibody response induced by trinitrophenylated‐polyacrylamide beads (TNP‐PAA) in cultures of human B cells. T cell help was provided by exogeneous IL2. IL4 profoundly suppressed the response to optimal concentrations (50 U/ml) of IL2, with a 50% inhibitory concentration of 6 U/ml. This was due neither to a shift in the kinetics nor to a switch to an IgG response. The production of anti‐TNP antibody (as measured by an enzyme‐linked immunosorbent assay in the culture supernatant) was inhibited to the same extent as the generation of plaque‐forming cells. The effect of IL4 was completely abolished by a neutralizing antibody toward IL4. Kinetic studies showed that IL4 had to be present during the first 48 h of culture to fully inhibit the response. The sequential stimulation of B cells by antigen and by IL2 showed that IL4 does not negatively interfere with signaling through membrane Ig but counteracts the effect of IL2 on antigen‐activated B cells.