bluuebunny/crossref_metadata_2025_split huggingface dataset:
Specific suppression elicited by EL4 lymphoma cells in syngeneic mice. Specificity includes self‐antigens on EL4
Authors: Grooten Johan , Leroux‐Roel Geert , Fiers Walter 
Published: March 2007

AbstractIn vivo, subclones derived from EL4 lymphoma cells generate suppressor T lymphocytes specific for anti‐EL4 immune responses. Spleen cells of EL4‐sensitized C57BL/6 mice down‐regulate the in vitro induction of EL4‐specific cytolytic T lymphocytes (CTL). In addition, EL4‐sensitized spleen cells interfere with the antigen response of two T lymphocyte clones. These recognize, in an H‐2b context, a self‐antigen on spleen cells that is also expressed by transformed cells, including EL4. The simultaneous anti‐self and anti‐EL4 specificity of the helper and suppressor activities suggests, therefore, that they are the product of an in vivo autoimmune reaction to EL4. The anti‐self suppression might aim to re‐establish self‐tolerance, at the same time down‐regulating responses against immunogenic epitopes that are co‐expressed with the self‐antigen on the EL4 cells. This agrees well with our observation that suppressor T cells, apparently elicited by suppressogenic epitopes on non‐immunogenic EL4 subclones, down‐regulate the CTL response elicited by immunogenic EL4 subclones. The additional self‐specificity of this suppression indicates that the suppressogenic epitopes at least in part represent EL4 self‐antigens.
Mycoplasma‐induced degradation of IgE bound by Fcϵ receptors of rat basophilic leukemia cells
Authors: Chan Bosco M. C. , Froese Arnold 
Published: March 2007

AbstractPrevious studies from this laboratory have shown that Mycoplasma hyorhinis interacts with some unoccupied, high‐affinity 45‐kDa receptors for IgE on rat basophilic leukemia (RBL) cells to induce the formation of 71‐kDa receptors for IgE. The present study demonstrates that when IgE is bound to the high‐affinity receptors, exposure of RBL cells to mycoplasma leads to a time‐dependent degradation of the cell‐bound IgE into fragments of 186 kDa, 158 kDa and 115 kDa, all of which remain bound to the receptors. Upon reduction, these fragments yield 67‐kDa and 55‐kDa ϵ chain‐derived polypeptides. The degradation appears to start at the N‐terminus of the IgE, leading eventually to a complete loss of L chains. In the absence of mycoplasma, the IgE remains relatively intact throughout the same time period with a molecular mass of 210 kDa. The observed degradation of receptor‐bound IgE by mycoplasma, should it also occur in vivo, could have important consequences as far as the IgE‐dependent mediator release is concerned.
Shared idiotopes between anti‐class II monoclonal antibodies and major histocompatibility complex recognition site of T cells
Authors: Tsuji Moriya , Yagi Junji , Abe Ryo , Asano Yoshihiro , Tada Tomio 
Published: March 2007

AbstractWe have raised a number of monoclonal antibodies (mAb) against idiotopes (Id) on monoclonal anti‐murine class II (anti‐Ak or Ek) antibodies. Two anti‐Id mAb among 31 were found to cross‐react with some T cells but not with macrophages and B cells of H‐2k animals. They were able to block syngeneic mixed lymphocyte reaction (SMLR) and antigen‐induced major histocompatibility complex (MHC)‐restricted T cell proliferation of H‐2k but not of other haplotypes. These results indicated that antibodies were recognizing Id associated with the MHC restriction site of T cells. The injection of these anti‐Id mAb into H‐2k mice resulted in the stimulation of self‐class II‐reactive T cell clones as determined by SMLR. They were also able to stimulate in non‐H‐2k strains to prime H‐2k alloreactive T cell clones. Some animals developed anti‐class II (anti‐Iak) antibodies by the injection of anti‐Id. These results indicated that certain anti‐Id (anti‐anti‐class II) antibodies cross‐reacted with T cell receptors which carried class II restriction specificity and were involved in allorecognition. These antibodies were found to have an ability to alter the T cell repertoire in vivo by stimulating such MHC‐restricted clones.
Kinetics of cellular oncogene expression in mouse lymphocytes II. Regulation of c‐fos and c‐myc gene expression
Authors: Schneider‐Schaulies Jürgen , Schimpl Anneliese , Wecker Eberhard 
Published: March 2007

AbstractNewly isolated lymphocytes from mouse spleens express the c‐fos oncogene even in the absence of mitogen with maximal mRNA levels 60 min post preparation of single cell suspension, whereas c‐myc mRNA levels increase only after mitogenic stimulation with maximal mRNA levels 6 h post stimulation.The half‐lives of c‐fos mRNA are generally very short; they increase from 14 min (after 30 min of culture) to 70 min (after 2 h of culture). The half‐lives of c‐myc mRNA decrease from 50 min (at 2 and 6 h post stimulation with concanavalin A) to 12 min (at 48 h post stimulation).The c‐fos gene transcription is already turned on in time‐0 lymphocytes 10 min after disruption of the organ structure of the spleens and is down‐regulated after 2 h and later. In nuclear run‐on experiments with nonstimulated lymphocytes there is already significant transcription of the first exon of c‐myc, but almost no elongation of the transcript to exon 2 and 3. In concanavalin A‐treated lymphocytes elongation is stimulated about 5‐fold within 6 h and returns to background levels at 48 h post stimulation.The nuclear run‐on analyses of nonactivated lymphocytes showed a signal for RNA complementary to c‐myc mRNA detected with a probe specific for the exon 1/intron 1 boundary of c‐myc, which disappeared with increasing time of concanavalin A stimulation. This anti‐sense transcription may play a role in regulating the elongation of c‐myc transcripts.
Aberrant expression of Ia‐like antigens on tumor cells of regressing but not of progressing Rous sarcomas
Authors: Powell Patrick C. , Hála Karel , Wick Georg 
Published: March 2007

AbstractUnlike many other tumors, experimentally induced Rous sarcomas in chickens have a definite tendency to regress spontaneously. Regression is under genetic control, but it is immunologically mediated although the target antigens that stimulate an immune response are unknown. Tumor cells in regressing sarcomas were found to express class II major histocompatibility complex (Ia‐like) antigens while tumor cells from progressing sarcomas were negative. This suggests that the induction of Ia‐like antigen expression has a role in the initiation or perpetuation of regression, similar to that postulated for class II antigen expression in a variety of autoimmune diseases.
A new V gene expressed in lambda‐2 light chains of the mouse
Authors: Dildrop Renate , Gause Angela , Müller Werner , Rajewsky Klaus 
Published: March 2007

AbstractWe have partially sequenced the light chain variable regions expressed in three IgM‐producing hybridomas generated from newborn mice or from manipulated animals suppressed for IgM production. In these lines a new V gene (V‐lambda‐X), exhibiting less than 60% homology to any known lambda or kappa V gene, is rearranged to J‐lambda‐2. The light chains produced by these cells contain the lambda‐2 constant domain, but are not recognized by goat antisera raised against conventional mouse lambda light chains.
The continuous antigenic regions in the second domain of the β chain of human MHC DR2 antigen: antigenic profile of the entire extracellular part of the chain
Authors: Atassi Hammad , Ulrich Robert G. , Atassi M. Zouhair 
Published: March 2007

AbstractTen consecutive 15‐residue peptides (except for peptide 181–198) that spanned the entire second domain of the HLA DR2 β chain and overlapped by 5 residues were synthesized, purified and characterized. The antibody‐binding activities of the peptides with human alloantisera and with antisera raised in other species were determined by radioimmunosorbent titrations. This established the full profile of peptides having specific antibody‐binding activity with these various antisera. The continuous antigenic sites in this domain were localized within four regions. The localization of the antigenic regions on the second domain completes the description of the antigenic profile of the entire extracellular part of the β chain of HLA DR2. Thus, the continuous antigenic sites on the extracellular part of the DR2 β subunit reside within seven regions with an eighth site being recognized somewhat weakly with some antisera. As was found for the first domain, the immunodominance of a given site varied with the antisera and boundary shifts were present. The submolecular regions recognized on the second domain of the DR2 β were independent of the host species from which the antisera were obtained.
Experimental autoimmune thyroiditis induced by a 5–10‐kDa tryptic fragment from porcine thyroglobulin
Authors: Salamero Jean , Remy Jean Jacques , Michel‐Bechet Marc , Charreire Jeannine 
Published: March 2007

AbstractMonoclonal autoantibodies obtained using the native porcine thyroglobulin (Tg) molecule for immunization were shown to react against a defined epitope of the Tg molecule. Its biochemical characterization was undertaken, using trypsin treatment of Tg, followed by gel filtration, affinity chromatography, sodium dodecyl sulfate‐poly‐acrylamide gel electrophoresis and high pressure liquid chromatography analysis. Immunoreactivity tested by immunoblotting with appropriate monoclonal anti‐Tg antibody allowed the detection of one peptide fragment of 5–10 kDa, after limited proteolysis with trypsin. We demonstrated that this peptide reacts exclusively with monoclonal anti‐Tg antibodies which block in vitro proliferative T cell response; moreover, the 5–10‐kDa tryptic fragments from porcine Tg were able to induce thyroiditis when injected into normal CBA mice, while porcine Tg depleted from these fragments was not able to do so.
Analysis of the human tonsil B cell repertoire by somatic hybridization: occurrence of both “monospecific” and “multispecific” (auto)antibody‐secreting cells
Authors: Logtenberg Ton , Kroon Ali , Gmelig‐Meyling Frits H. J. , Ballieux Rudy E. 
Published: March 2007

AbstractThe purpose of our study was to investigate the (auto)antibody repertoire of human tonsil B cells. To this end, unseparated tonsil B cells and “large” and “small” tonsil B cells, obtained after fractionation on a discontinuous Percoll gradient, were fused with the (human × mouse) heterohybridoma K6H6/B5. The IgM antibodies secreted by individual clones were analyzed in spot‐enzyme‐linked immunosorbent assay for reactivity against a panel of 5 autoantigens and 1 xenoantigen. The results show that both “mono‐” and “multispecific” (auto)antibody‐secreting clones can be obtained by somatic hybridization of unseparated, “small” and “large” tonsil B cells. The patterns of IgM reactivities in these three collections of hybridomas did not differ significantly. Inhibition experiments revealed that “multispecific” antibodies can bind with high affinity to more than one (auto)antigen. The results of these experiments are discussed in relation to the state of activation of tonsil B lymphocytes.
Nickel‐specific T lymphocyte clones derived from allergic nickel‐contact dermatitis lesions in man: heterogeneity based on requirement of dendritic antigen‐presenting cell subsets
Authors: Kapsenberg Martien L. , Res Peter , Bos Jan D. , Schootemijer Annelies , Teunissen Marcel B. M. , Van Schooten Wim 
Published: March 2007

AbstractInflammatory skin T cells were cloned in an antigen‐independent way from lesions of patients with experimentally induced nickel‐contact dermatitis. In three experiments 7–15% of the CD4+8− T lymphocyte clones (TLC) appeared to be specific for nickel in a proliferation assay. These proliferative response of nickel‐specific TLC required the presence of antigen‐presenting cells (APC) and were restricted by HLA class II molecules. All TLC recognized nickel presented by APC from epidermal skin. Remarkably, 5 out of 8 nickel‐specific TLC exclusively recognized nickel when presented by these skin‐specific APC whereas 3 out of these 8 clones could also recognize nickel presented by APC from peripheral blood. The critical APC within the fractions of epidermal cells and peripheral blood appeared to belong to the family of dendritic cells, i.e. Langerhans cells and circulating dendritic cells, respectively.
A new T helper cell specificity within the pigeon cytochrome c determinant 95–104
Authors: Carbone Francis R. , Staerz Uwe D. , Paterson Yvonne 
Published: March 2007

AbstractA T cell hybridoma with unusual antigen specificity has been isolated from B10.BR mice immunized with pigeon cytochrome c. Using synthetic peptide analogues of the pigeon cytochrome c T cell determinant 81–104 we have determined that this hybridoma is specific for residues within the sequence 95–104. However, the mode by which this T cell hybridoma recognizes this determinant in the context of the I‐Ek molecule differs from all previously described T cell clones in that it is not stimulated by the moth cytochrome c analogue 81–103.
Alternative pathway of complement activation by stimulated T lymphocytes. II. Elevation of cytotoxic potential against complement receptor‐carrying cell lines
Authors: Ramos Oscar F. , Sármay Gabriella , Eggertsen Gösta , Nilsson Bo , Klein Eva , Gergely János 
Published: March 2007

AbstractExposure of lectin‐stimulated (concanavalin A, phytohemagglutinin and pokeweed mitogen) blood lymphocytes to human serum or to purified C3 increased their cytotoxic capacity towards complement receptor positive targets such as Raji and Daudi cells. The lysis of complement receptor‐negative lymphoblastoid cell lines was not influenced. The lytic capacity of lymphocytes exposed to 12‐O‐tetradecanoylphorbol 13‐acetate was not elevated by human serum. Lectin‐stimulated lymphocytes were previously shown to activate and bind C3. The results using lymphocytes activated in different ways and targets with or without complement receptor expression suggest that the C3b deposited on lymphocytes binds to the complement receptor on the targets. This contact elevates the avidity between the two cells as indicated also by the increased frequency of the lymphocyte‐target conjugates. On the basis of immune adherence the C3 fragment bound on the lymphocytes was identified as C3b. The increase of the conjugate formation and cytotoxicity was abrogated when the target cells, Raji, were pre‐exposed to purified C3d which occupy the CR2 receptor. The majority of lymphocytes responsible for the cytotoxicity were CD8+.
In vivo generation and function of B cells in the presence of a monoclonal anti‐IgM antibody: implications for B cell tolerance
Authors: Gause Angela , Yoshida Nobuaki , Kappen Claudia , Rajewsky Klaus 
Published: March 2007

AbstractC57BL/6 mice were chronically treated with milligram doses of the noncytotoxic monoclonal anti‐μb antibody MB86 (IgG1,x) from birth or from fetal life. The spleens of the manipulated animals contained large numbers (25% as compared to control mice) of B lineage cells which expressed IgMb on the surface after overnight incubation in vitro. The spleens also contained B cells whose surface IgM was unreactive with antibody MB86. A few such cells were immortalized by cell fusion. They included cells secreting μ together with λ2 chains which apparently prevent recognition by antibody MB86, and a point mutant in the first constant domain of the μ chain, changing the b to the a allotype. Cells expressing MB86− surface IgM did not selectively expand under MB86 treatment over the first few months of life.Serum Ig levels in the manipulated mice were normal except for IgM which was undetectable in most instances. In some animals low levels of MB86− IgM molecules were produced. At 7 weeks of age, mice treated with MB86 from birth produced normal‐size IgG anti‐(4‐hydroxy‐3‐nitrophenyl)acetyl (NP) responses with the usual predominance of λ1 chain‐bearing IgG1 antibodies. At the age of 5–6 months, and also in young mice treated with MB86 from fetal life, the responses were variable and presumably oligoclonal, with a tendency towards the production of antibodies with γ3 heavy and λ2 or λ3 light chains. We interpret these results to mean that B cells hit by antibody MB86 from the time of their generation become unresponsive to T cell‐dependent stimulation, but are still able to expand. Occasionally, they escape functional suppression through class switching (to IgG3) upon mitogenic stimulation. At birth, C57BL/6 mice contain a mature B cell population which mediates normal immune responses under MB86 treatment and eventually dies out.Taken as a model of tolerance induction in B cells, the data provide evidence for “tolerant” cells and support the concept of an early phase of sensitivity to tolerance induction in B cell differentiation.The anti‐NP response under MB86 treatment differed profoundly from control responses in idiotypic terms, but became normal as the animals recovered from suppression. This may reflect blockade by MB86 of idiotypic selection within the B cell population.
Multiple HLA class I‐dependent cytotoxicities constitute the “non‐HLA‐restricted” response in infectious mononucleosis
Authors: Strang George , Rickinson Alan B. 
Published: March 2007

AbstractPrimary Epstein‐Barr virus (EBV) infection, when manifest as infectious mononucleosis (IM), induces a broad‐ranging and apparently non‐HLA‐restricted cytotoxic response whose nature has not been resolved. In the present experiments the ability to cryo‐preserve IM mononuclear cell preparations, after depletion of CD16+ natural killer cells, has allowed detailed analysis of the response on appropriately constructed target cell panels. The results show that IM effector preparations are polyclonal with separate HLA class I antigen‐dependent reactivities against (a) the autologous EBV‐transformed lymphoblastoid cell line (LCL) and (b) particular HLA class I‐mis‐matched LCLs. The autologous LCL‐directed response shows the hallmarks of immunologically specific T cell cytotoxicity; only EBV+ B cell blasts are recognized and the interaction can be blocked by monoclonal antibodies to CD3 and CD8 on the effector cell surface and to HLA class I antigens on the target cell. Such findings demonstrate, for the first time, that the primary cytotoxic response to EBV infection includes a virus‐specific HLA‐restricted component like that found in the T cell memory of persistently infected individuals. Separate components of the response are preferentially active against some (but not all) HLA‐mismatched LCLs, the pattern of reactivity being distinct for each individual IM patient and reproducible on repeated testing. Monoclonal antibody blocking experiments show that these HLA‐mismatched interactions also involve CD3 and CD8 antigens on the effector cell and HLA class I antigens on the target cell. Where tested, such lysis affected both EBV+ and EBV− B cell blasts from the relevant HLA‐mismatched donors. We postulate that a widespread primary infection of the B cell system by EBV leads to a generalized expansion not just of the virus‐specific response but also of other T cell responses coincidentally active at the time. The unusual activity of IM effector preparations against HLA‐mismatched LCLs arises from fortuitous cross‐recognition of allogeneic cells by immunologically specific cytotoxic T cell clones coincidentally expanded in vivo alongside the EBV‐specific response.
Class I H‐2Db determinants are not involved in hybrid resistance to parental H‐2b/Hh‐1b bone marrow allograft
Authors: Milisauskas Vita K. , Kaminsky Steven G. , Nakamura Ichiro 
Published: March 2007

AbstractHybrid resistance to parental H‐2b bone marrow grafts is directed to a cell surface structure controlled by the Hh‐1 locus in or near the H‐2D region. The nature of this surface structure is not known. Since homozygosity at the class I H‐2D locus or loci in this haplotype would seem a necessary but not sufficient condition for the grafts' susceptibility to resistance, we tested whether the expression of this phenotype is dependent on the expression of class I H‐2Db determinants. Cloned variants of H‐2b tumor RBL‐5 were obtained by immunoselection for the absence of H‐2Db expression, as determined by the inability to bind specific antibody and to induce or react with alloreactive cytotoxic T lymphocytes. The three clones used in this study were H‐2Db negative but H‐2Kb positive and were natural killer cell resistant. When tested in vivo as competitive inhibitors the variant cells were capable of blocking hybrid resistance to parental H‐2b bone marrow grafts as were unselected H‐2Db‐positive parental line cells. Therefore, H‐2Db expression is irrelevant for Hh‐1b expression. An incidental observation was that YAC‐1 cells, a non‐H‐2b tumor with pronounced susceptibility to natural killing, were able to block hybrid resistance. This reactivity, not observed in our previous studies, raises the possibility that at least some of the effector cells are cross‐reactive or capable of dual recognition.
CD3+ WT31− peripheral T lymphocytes lack T44 (CD28), a surface molecule involved in activation of T cells bearing the α/β heterodimer
Authors: Poggi Alessandro , Bottino Cristina , Zocchi Maria Raffaella , Pantaleo Giuseppe , Ciccone Ermanno , Mingari Cristina , Moretta Lorenzo , Moretta Alessandro 
Published: March 2007

AbstractWe have applied two‐color fluorescence cytofluorometric techniques to the analysis of the distribution of T44 and CD3 antigens in peripheral blood human lymphoctes. While most CD3+ cells co‐expressed T44 antigen, a small distinct subset was CD3+ T44− (2–10% of CD3+ cells). This cell subset also did not react with the WT31 monoclonal antibody (mAb), specific for an α/β framework determinant of the T cell receptor (TCR). Lack of T44 antigen expression was also observed in purified CD3+ WT31− polyclonal populations that had been cultured in medium containing interleukin 2 (IL2) and as well as >30 clones expressing the CD3+4−8−WT31− surface phenotype. Immunoprecipitation experiments confirmed that expression of T44 molecules was confined to CD3+ WT31+ peripheral blood T cells. While conventional CD3+ WT31+ cells produced IL2 in response to mAb directed to CD2, CD3 or T44 surface molecules, CD3+ WT31− cells did not respond to anti‐T44 mAb but released IL2 following stimulation with anti‐CD2 or anti‐CD3 mAb. Therefore, assuming that anti‐T44 mimicks the effect of a still undefined natural ligand our data suggest that T cells expressing the γ‐gene surface product may be signalled by stimuli which differ, at least in part, from those acting on CD3+ WT31+ T lymphocytes.
Lysis of nonnucleated red blood cells by cytotoxic T lymphocytes
Authors: Lanzavecchia Antonio , Staerz Uwe D. 
Published: March 2007

AbstractTo establish the role of direct membrane damage in cytotoxic T lymphocyte (CTL)‐mediated lysis we investigated whether CTL would be capable of lysing nonnucleated target cells. By antibody‐mediated targeting we show that CTL are indeed capable of lysing sheep and human red blood cells.