bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fine specificity and idiotype expression of antiphosphorylcholine IgE and IgG antibodies
Authors: Weber Ernst A. , Heusser Christoph H. , Blaser Kurt 
Published: February 2007

AbstractThe immune response to the phosphorylcholine (PC) hapten elicited in BALB/c mice by PC‐keyhole limpet hemocyanin (KLH) is composed of 2 groups of antibodies with specificity to PC and phenyl‐PC, respectively. They were designated as group I and group II anti‐PC antibodies. In this report we demonstrate that anti‐PC IgE antibodies elicited by PC‐KLH or PC‐ovalbumin belong to the group II and do not express the T15 idiotype. Anti‐PC IgG1, IgG2a, and IgG2b antibodies express group I characteristics in the primary response and bear the T15 idiotype. Later, after 5 weeks and 3 injections of PC‐KLH or PC‐ovalbumin, a change in these isotypes to group II antibodies is observed. In contrast, anti‐PC IgE is a group II antibody throughout progression of the immune response. The regulation of group I and group II antibody expression in serum is independent of the genetic background of the animals.
Multiple pathways for antigen‐independent activation of a T helper hybridoma
Authors: Torbett Bruce E. , Skidmore Barry , Clark William R. 
Published: February 2007

AbstractAn important question in mitogen activation of T cells is whether the T cell must interact with a major histocompatibility complex product during the activation process. The T helper hybridoma AODH 7.1 is specific for human gamma globulin in the context of IEd, and when activated secretes interleukin 2. The mitogen concanavalin A (Con A) can activate AODH 7.1 cells directly, but two other standard T cell mitogens, phytohemagglutinin (PHA) and neuraminidase‐galactose oxidase, cannot. However, Con A, PHA and neuraminidase‐galactose oxidase could all activate AODH 7.1 when presented on various cloned class II+ cell lines. There was an absolute requirement for the presentor cell to be class II+, and the activation signal on mitogen‐treated class II+ presentor could be blocked by monoclonal antibody to the class II antigens. To determine if class II molecules were absolutely required for the presentation of a mitogen activation signal we used class II− LtK− L cells and two LtK− cell class II gene transformants as presentor cells. Only the class II+ transformants, but not the class II− LtK− cells, could present either Con A or PHA. The class II requirement cannot be bypassed through provision of soluble factors. However, when Con A was used to activate AODH 7.1 cells directly, it appeared to be acting in a transmembrane fashion. It was not the case that AODH 7.1 cells were responding to Con A on a neighboring AODH 7.1 cell, and no class II antigens were involved. These results are consistent with the idea that different routes of activation exist for T cells, at least at the level of signal recognition.
Effect of anti‐Ia treatment on the production of anti‐DNA antibody by NZB mice
Authors: Klinman Dennis M. , Lefkowitz Michael D. , Raveche Elizabeth S. , Steinberg Alfred D. 
Published: February 2007

AbstractA cell transfer system was used to study the effect of anti‐Ia antibodies on anti‐DNA‐producing B cells. B cells from autoimmune New Zealand Black (NZB) mice were necessary and sufficient to transfer anti‐DNA antibody production to congenic NZB. xid recipients. Anti‐Ia treatment of either donors or recipients led to a significant reduction in the number of B cells secreting anti‐DNA antibody. This effect was detectable after as little as 3 days of treatment and persisted for at least 1 month after the cessation of therapy. In this system, we could find no evidence of suppressor cell induction. These data suggest that anti‐Ia antibodies directly suppress autoantibody‐producing B lymphocytes.
The immune response to bacterial dextrans III. Ontogenic development and strain distribution of specific clonal precursors
Authors: Lundkvist Inger , Holmberg Dan , Ivars Fredrik , Coutinho Antonio 
Published: February 2007

AbstractThe frequencies of B512 dextran (Dex)‐specific B cell precursors were determined by limiting dilution analysis in a number of mouse strains originally described as “high responder”, “low responder” and “nonresponder” to this antigen. No significant difference in the frequencies of Dex‐specific precursors was found in C57BL/6, B10.BR, C3H/Tif, BALB/c and A/Sn adult mice. Together with the large intra‐strain variability in the magnitude of anti‐Dex PFC responses in vivo, these results established that differential reactivity in vivo cannot be ascribed to genetically controlled absence or wide variation in the frequency of Dex‐specific immunocompetent precursors.A similar analysis of the Dex‐specific precursor frequency was carried out in C57BL/6 mice between 1 week and 3 months of age. While no Dex‐specific antibody response was detected in vivo before the age of 3 weeks, clonal precursor analysis revealed that the appearance of these specificities parallels the development of competent (IgM‐ producing) B lymphocyte clonal precursors, such that no significant difference in absolute frequencies of Dex‐specific precursors could be observed among these age groups. This is interpreted to suggest that the late development of the Dex‐specific antibody responses is regulatory rather than due to late rearrangement and activation of the appropriate V genes and a sequential expression of antibody specificities in ontogenic development.
Structural implications of the location and stability to proteolytic enzymes of immunodominant determinants of the human leukocyte common molecule
Authors: Dalchau Rosemarie , Flanagan Brian F. , Fabre John W. 
Published: February 2007

AbstractIn this report, we use 8 different mouse monoclonal antibodies to define 3 immunodominant determinants of the human leukocyte common (LC) antigen, and by defining the relative location and the stability to proteolytic enzymes of these determinants we make some structural predictions about the LC family of molecules. One lineage‐restricted determinant is expressed predominantly on B lymphocytes and is located on the two higher (210 and 195) kDa bands of LC, with possibly some expression on the 180‐kDa band. The two other determinants, one of which is a complex of 3 partially overlapping sites, are expressed on all leukocytes and found on all four (210, 195, 180, 160 kDa) LC bands. Pronase and trypsin treatment of peripheral blood lymphocytes and of Daudi cells gave complete cleavage of the lineage‐restricted determinant from the cells, but the two common determinants were, surprisingly, left intact on the cell surface. By contrast, pronase and trypsin treatment of pure, detergent‐solubilized LC resulted in rapid degradation of the common determinants, while the restricted determinant was sensitive to pronase but not to trypsin. Purification of the LC molecule from pronase‐treated Daudi cells yielded a 130‐kDa lentil lectin‐binding protein, while undegraded LC from Daudi cells has a molecular mass of 210 kDa. Our results demonstrate that both common and restricted determinants are at least partly protein in nature and that the restricted determinant is external to and therefore on the presumed amino terminal side of the common determinants. Moreover, because LC has been reported to have a large (approximately 100 kDa) intracellular component, our data suggest the presence of a relatively small (approximately 25 kDA) membrane proximal domain containing both of the common LC determinants and at least one N‐linked oligosaccharide chain. This domain is potentially susceptible to proteolytic cleavage, but it is interesting that on the intact cell it is both protected from proteolytic degradation and unable to be cleaved from the cell surface.
Inhibition of lipopolysaccharide‐induced monocyte interleukin 1 secretion by gangliosides
Authors: Cavaillon Jean‐Marc , Fitting Catherine 
Published: February 2007

AbstractGangliosides known to be potent immunosuppressors are shown to inhibit the secretion of interleukin 1 (IL1) by human monocytes stimulated with lipopolysaccharide (LPS). The inhibitory activity was observed either with mono‐, di‐ or trisialogan‐gliosides. The inhibition of LPS‐induced IL 1 secretion was obtained in the presence of indomethacin, indicating that the ganglioside inhibitory capacity was not due to prostaglandin induction. Indeed the inhibitory activity seems to be mediated by an interaction with LPS molecules, preventing their ability to deliver a signal to monocytes for IL 1 secretion.
IgE receptors on human lymphocytes III. Expression of IgE receptors on mitogen‐stimulated human mononuclear cells
Authors: Delespesse Guy , Sarfati Marie , Rubio‐Trujillo Manuel , Wolowiec Terry 
Published: February 2007

AbstractHuman peripheral blood mononuclear cells (PBMC) were tested for the expression of Fee‐receptor (FcεR) after stimulation with various mitogens in the absence of IgE. FcεR were found on virtually all the cells from 19 Epstein‐Barr virus‐transformed B cell lines including those derived from cord blood, from one agamma‐globulinemic patient and VDS‐0 pre‐B cells. Hence, the data clearly indicate that FcεR may be expressed on very immature B cells. PBMC cultures stimulated with either pokeweed mitogen (PWM), phytohemagglutinin (PHA) or concanavalin A displayed an early increase of their content in FcεR‐bearing cells followed by a decrease to levels below those of the control cultures. After fractionation of the PWM‐stimulated cultures into T and B cell‐enriched preparations, most of the FcεR+ cells were in the B cell fractions and the same low levels of FceR+ cells were found in the T cell fractions isolated from the PWM‐stimulated and from the control cultures. Double‐labeling experiments, employing biotinylated F(ab')2 monoclonal antibody to FcR and either fluorescein isothiocyanate‐conjugated B1 or Mo2 monoclonal antibodies, indicated that PWM mainly exerted its effect on B cells and on monocytes. This effect was T cell dependent and it was mediated by soluble factors of T cell origin. At the peak of the PHA or concanavalin A response, most of the FceR‐bearing cells were found in the B cell fraction but the T cells isolated from mitogen‐stimulated cultures contained significantly more FcεR+ cells than those from the control cultures, suggesting that T cell mitogens had increased the expression of FcεR on some T cells. This view was supported by the finding of a higher proportion of FceR+ cells in PHA‐stimulated than in control cultures of highly purified T cells with a maximum response at the end of the culture period. Double‐labeling experiments at the peak (day 2) of the peripheral blood mononuclear cell response indicated that the expression of FcεR was increased on B cells (Bl+) and on monocytes (Mo2+). By using the same approach at the peak of the T cell response (day 7), it was found that T cells isolated from PHA‐stimulated cultures expressed more FcεR than those isolated from control cultures. Moreover, in unstimulated cultures, FcεR was mainly expressed on T helper cells (Leu 3+) whereas in PHA‐stimulated cultures FcεR was expressed on both T helper and T suppressor/cytotoxic cells (Leu 2+).
Demonstration of C3b receptor‐like activity and of decay‐accelerating factor‐like activity on rabbit erythrocytes
Authors: Horstmann Rolf D. , Muller‐Eberhard Hans J. 
Published: February 2007

AbstractC3b receptor activity and decay‐accelerating activity for the C3 convertase, C3b, Bb, were demonstrated on rabbit erythrocytes (erab). Particles bearing C3b agglutinated ERAB if the C3b was of rabbit origin, but not if it was of human origin. The reactivity of rabbit C3b was abolished by enzymatic conversion of C3b to C3bi. Deposited on ERAB. rabbit C3b, but not human C3b, was cleaved by factor I in the absence of factor H. Similarly, decay acceleration of the C3b, Bb complex on ERAB occurred when the complex was of rabbit origin, but not when it was of human origin. Soluble immune complexes in the presence of rabbit serum were bound to and then released from the erab. Binding of the complexes is presumed to be mediated by immune complex‐bound C3b and release to be the consequence of degradation of C3b by Factor I. These findings suggest that ERAB, like human erythrocytes, are endowed with membrane‐associated complement regulators that protect these cells against homologous complement attack and participate in the clearing mechanism of circulating immune complexes.
Azacytidine‐induced reactivation of adenosine deaminase in a murine cytotoxic T cell line
Authors: Castellazzi Marc , Vielh Philippe , Longacre Shirley 
Published: February 2007

AbstractIn C57BL/6 mice, cytotoxic T lymphocyte (CTL) lines have previously been found to exhibit low (< 150 U/mg) or undetectable (< 20 U/mg) adenosine deaminase (ADA) levels (Minkowski, Castellazzi and Buttin, J. Immunol. 1984. 133: 52) in contrast to what has been seen in T helper lines (1770 ± 340 U/mg; Minkowski and Bandeira, Cell. Immunol. 1985. 95: 380). Treatment of one of these CTL ADA− lines with the demethylating agent 5‐azacytidine gave rise to an ADA+ population. Subsequent cloning allowed the recovery of pure ADA+ clones showing a rather narrow range of activity with an average value of 2030 ± 504 U/mg. The restored ADA+ activity is stable over several months of continuous growth. It is identical to the activity of C57BL/6 thymic cells or C57BL/6 T tumor lines regarding (a) its sensitivity to ADA inhibitors 2‐deoxycoformycin and erythro‐9‐(2‐hydroxyl‐3‐nonyl)adenine, and (b) its electrophoretic mobility under nondenaturing conditions (starch gel and isoelectric focusing). An ADA‐specific, 1.4‐kb mRNA is present in the reactivated clones but is undetectable in the CTL ADA− parental line. These results demonstrate that the ADA− phenotype is due to an extinction of the corresponding gene. They suggest that the extinction of the ADA gene which appears to be specific for CTL and to take place in vivo during T cell differenciation may result from increased methylation in or near the ADA gene. This extinction seems to affect specifically ADA since nucleoside phosphorylase, the enzyme which follows ADA in the purine salvage pathway, is present at equivalent levels in the ADA− and ADA+ CTL clones.
Structural requirements for inducing in vitro B lymphocyte activation by chemically synthesized derivatives related to the nonreducing D‐glucosamine subunit of lipid A
Authors: Kumazawa Yoshio , Matsuura Motohiro , Maniyama Tokuei , Yuzuru Homma J. , Kiso Makoto , Hasegawa Akira 
Published: February 2007

AbstractMitogenic and polyclonal B cell activation (PBA) activities of 16 synthetic compounds related to the nonreducing D‐glucosamine (GlcN‐II) subunit of lipid A were investigated. Among compounds possessing the GlcN backbone, a 4‐O‐phosphorylated GlcN derivative carrying N‐linked 3‐tetradecanoyloxytetradecanoyl [C14‐O‐(C14)] and 3‐O‐linked tetradecanoyl (C14) groups, GLA‐27, expressed the highest degree of both activities. Omission of the 3‐O‐linked C14 group from GLA‐27 and transfer of the C14group to the C‐6 position induced critical changes in expression of activities. Both 4‐ O‐phosphorylated compounds carrying an N‐linked C14 or 3‐hydroxytetradecanoyl (C14OH) group instead of the C14‐O‐(C14) group in GLA‐27 showed no detectable activity. Substituting a 3‐O‐linked C14 group in GLA‐27 for the C14‐O‐(C14) group also markedly decreased mitogenic and PBA activities. Change of phosphorylation site from the C‐4 to the C‐6 position and bisphosphorylation at the C‐4 and C‐6 positions induced somewhat weak depression. Much weaker activities were observed in a compound carrying N‐linked 3‐dodecanoyloxydodecanoyl [C12‐O‐(C12)] and 3‐O‐ dodecanoyl (C12) as fatty acid substituents. No detectable activity was seen in a compound carrying N‐linked 3‐hexadecanoyloxyhexadecanoyl [C16‐O‐(C16)] and 3‐O‐ hexadecanoyl (C16), indicating that the most suitable carbon chain length for expressing the activities is C14. Regarding structural change of the GlcN backbone, a 1‐deoxy derivative of GLA‐27 exhibited stronger activity than did GLA‐27 itself. Mitogenic and PBA activity of GLA‐27 were stronger than those of lipid X, which corresponds to the reducing D‐GlcN (GlcN‐I) subunit of Escherichia coli lipid A and is a 1‐O‐phosphorylated GlcN derivative carrying N‐ and 3‐O‐linked C14OH groups. These results indicate that N‐linked acyloxyacyl and 3‐O‐linked acyl groups and phosphorylation are critical for expressing both mitogenic and PBA activities.
Ligand binding by the pl50,95 antigen of U937 monocytic cells: properties in common with complement receptor type 3 (CR3)
Authors: Malhotra Vivek , Hogg Nancy , Sim Robert B. 
Published: February 2007

AbstractU937 cells (a monocytic cell line) grown in the presence of phorbol myristate acetate were surface labeled with 125I and the iC3b‐binding proteins isolated by affinity chromatography on iC3b‐Sepharose in the presence of divalent cations. Three polypeptides of 170, 150 and 95 kDa were found to bind specifically to iC3b‐Sepharose. The polypeptides of 170 and 95 kDa were identified as the α and the β subunits of CR3 by immunoprecipitation with OKM1 monoclonal antibody. The 150‐kDa polypeptide was not immunoprecipitated by antibodies to the α subunit of CR3 or LFA‐1. However, the 150‐kDa polypeptide, together with the 95‐kDa polypeptide, was immunoprecipitated with an anti‐β subunit‐specific antibody IB4, which immunoprecipitates LFA‐1, CR3 and pl50,95. These results indicated that the 150‐kDa polypeptide is the a subunit of the pl50,95 antigen. The binding of pl50,95 and CR3 to iC3b‐ Sepharose is specific as neither binds to C3u‐Sepharose.A monoclonal antibody, 3.9, which immunoprecipitated the 150 and a 95‐kDa polypeptide from U937 cells was characterized as being directed against the α‐subunit of the pl50,95 antigen. Phorbol myristate acetate‐stimulated U937 cells form rosettes with EAC3b and EAiC3b but not with EAC3d cells. Monoclonal antibody 3.9 does not inhibit either type of rosetting, but we were unable to exclude a role for pl50,95 in adherence of iC3b‐coated particles. Since there is no rosetting with C3d‐bearing particles it is unlikely that pl50,95 is a receptor for C3d, a role for pl50,95 which has been suggested by others (Wright, S. D., Licht, M. R. and Silverstein, S. C, Fed. Proc. 1984. 43: 413).
Early arrest of B cell development in nude, X‐linked immune‐deficient mice
Authors: Karagogeos Domna , Rosenberg Naomi , Wortis Henry H. 
Published: February 2007

AbstractMice simultaneously expressing the nude and xid mutations have a severe deficit of both mature T and B cells. We now report studies designed to determine at which point in B cell differentiation development is arrested. Nude‐xid mice have normal numbers of hematopoietic colony forming units (CFU‐s) but lack two early pre‐B cell markers: susceptibility to transformation by Abelson murine leukemia virus (A‐MuLV) and production of cytoplasmic μ (Cμ) heavy chain. Thus, there is a defect in lymphocyte development prior to or early in pre‐B cell differentiation but after hematopoietic stem cell formation. The monoclonal reagents DNL 1.9, 14.8 and RA3–3A1/6.1, which react with the surface protein B220 (Ly 5) on pro‐B, Cμ− pre‐B, Cμ+ pre‐B, and surface Ig+ B cells, revealed the presence of positive cells in nude‐xid mice. The bone marrow of nude‐xid mice contains more B220+ cells than Cμ+ cells. Our data suggest that the developmental block in these mice occurs at the earliest identifiable step in the B lymphocyte lineage, after the appearance of B220+ Cμ− pro‐ B cells, but before the differentiation of Cμ‐bearing (pre‐B) cells.
Characterization of suppressor‐inducer cells which control the production of rat erythrocyte‐induced anti‐erythrocyte autoantibodies
Authors: Watt Graham J. , Elson Christopher J. , Healey Donald G. , Oryan Ahmad , Craig Hooper D. 
Published: February 2007

AbstractMice immunized with rat erythrocytes produce autoantibodies to their own red blood cells, distinct anti‐rat agglutinins and autoantigen‐specific suppressor cells. Suppressor cells were detected by adoptive transfer of rat erythrocyte‐immunized spleen cells to naive recipients. Such recipients failed to make erythrocyte autoantibodies after immunization with rat erythrocytes although their anti‐rat erythrocyte response was unimpaired. Depletion and enrichment studies were performed to identify the cell type(s) which transfer suppression. B cell depletion of rat erythrocyte‐immunized spleen cells by passage over Ig/anti‐Ig‐coated bead columns abrogated the transfer of suppression. However, suppression was still transferred after rat erythrocyte immunized spleen cells were passed over beads coated with a complex of 4‐azido‐2‐ nitrophenyl (NAP)‐mouse IgG‐rabbit IgG anti‐NAP suggesting that T cells bearing Fcγ receptors are not responsible for suppression. Positively selected B cells from rat erythrocyte‐immunized spleen cells caused some suppression of erythrocyte autoantibodies but only after high numbers of cells were transferred. Neither positively selected Lyt‐l+2− nor Lyt‐1–2+ T cell subpopulations transferred suppression. By contrast, rat erythrocyte‐immunized spleen cells which contained a mixture of B memory and T cells were suppressive and retained their suppressor activity after removal of Lyt‐1–2+ but not Lyt‐l+2− cells. It is proposed that these Lyt‐l+2− T cells belong to a distinct population of suppressor‐inducer cells which together with memory B cells stimulate the generation of effector T suppressor cells in naive recipients.
Biosynthesis of the subcomponents Clq, Clr and Cls of the first component of complement (Cl) by guinea pig hepatocyte primary cultures
Authors: Ramadori Giuliano , Heinz Hans‐Peter , Martin Harry , Buschenfelde Karl‐Hermann Meyer Zum , Loos Michael 
Published: February 2007

AbstractThus far, the synthesis of Clq by liver cells has not been demonstrated. To investigate this possibility, viable hepatocytes were isolated from the liver of guinea pigs and primary cultures were established. The cells (106 cells/ml) were cultured under serumfree conditions for 8 days and the culture medium was changed every 24 h. The few contaminating Kupffer cells were lysed by preincubating the cell cultures with a monoclonal (22C4–8) antibody directed against a nonpolymorphic la determinant and preabsorbed rabbit serum. The hemolytic activity of Cl and its subcomponents Clq and Clr/Cls was tested in the supernatants. Guinea pig hepatocyte primary cultures synthesize and secrete up to 3 × 103 effective Clq molecules/cell/24 h and 34 ± 103effective Clr/Cls molecules/cell/24 h. The synthesis of Clq and Clr/Cls could be reversibly inhibited by cycloheximide (50 μg/ml). Furthermore, to demonstrate de novo synthesis of the Clq subcomponent, endogeneous labeling with 3H‐proline (or 14C‐proline) was performed. The immunoprecipitated Clq from cellular lysates and culture medium was analyzed by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis and fluorography. Compared to biosynthetically labeled guinea pig Clq from peritoneal macrophages, three corresponding bands (30, 28 and 24 kDa, respectively) were detectable in the fluorograph. The data show that guinea pig hepatocytes are able to synthesize Cl subcomponents, whereby the synthesis of Clq and Clr/Cls occurs independently.