bluuebunny/crossref_metadata_2025_split huggingface dataset:
VLA‐1: a T cell surface antigen which defines a novel late stage of human T cell activation
Authors: Hemler Martin E. , Jacobson Jennie G. , Brenner Michael B. , Mann Dean , Strominger Jack L. 
Published: February 2007

AbstractThe VLA‐1 protein complex defines a previously undescribed very late stage of activated T cell differentiation, following either alloantigen or mitogen activation. This protein appears after 2–3 weeks of activation, considerably later than the early T cell activation antigens such as the interleukin 2 (IL2) receptor, transferrin receptor, 4F2 antigen, T10 and HLA‐DR, and has therefore been termed very late antigen‐1 (VLA‐1). Unlike the IL2 receptor, VLA‐1 expression does not require restimulation with antigen, and in fact, VLA‐1 expression was high on T cells that had lost their IL2 receptors. Expression of VLA‐1 was found on all or nearly all long‐term‐activated T cells including T4+ and T8+ clones, bulk cultures, long‐term T cells from adults and newborns and long‐term T cells maintained in pure or crude IL2 preparations. VLA‐1 was also found on HTLV‐1 infected T cell populations. Immunoprecipitation experiments confirmed that the VLA‐1 protein complex (210000/130000 Mr) can be co‐expressed with another protein complex called VLA‐2 (165 000/130 000 Mr) on the same T cell clones. However, co‐expression was not obligatory because in some long‐term cultures little or no VLA‐2 was present relative to VLA‐1. Because VLA‐1 defines a novel late stage of T cell activation, being present on all or most all types of long‐term activated T cells, and not on any other cell types in peripheral blood, it has unique potential as a marker for activated T cells in vivo and may provide a clue towards elucidating novel long‐term T cell functions or growth requirements of this late stage of T cell differentiation.
Splenic dependence of the antibody response to thymus‐independent (TI‐2) antigens
Authors: Amlot Peter L. , Grennan Deirdre , Humphrey John H. 
Published: February 2007

AbstractThe murine antibody response to T‐independent (TI)‐2 antigens [2,4‐dinitrophenyl‐Lys‐Ficoll (DNP‐FIC) and DNP‐hydroxyethyl starch (HES)] was impaired long after splenectomy, while responses to TI‐1 [trinitrophenylated lipopolysaccharide (TNP‐LPS)] and thymus‐dependent [TNP‐keyhole limpet hemocyanin (KLH)] antigens were largely unaffected. The antibody response to these TI‐2 antigens was exclusively against the conjugated epitopes [DNP‐, fluorescein isothiocyanate (FITC)‐ or tetramethylrhodamine isothiocyanate (TRITC)‐Ficoll or ‐HES].Fluorescent conjugates of Ficoll and HES localize selectively to the splenic marginal zone macrophages. This localization was not affected by 750 cGy of X‐irradiation, but the antibody response to the TI‐2 antigens was abrogated for 14 days. Administration of spleen cells restored the antibody response to these TI‐2 antigens in otherwise intact irradiated mice but not if they had been splenectomized.Our findings indicate that the antibody response to TI‐2 antigens depends upon stimulation of B cells in a splenic environment. This probably involves antigen presentation by marginal zone macrophages.
Structure of primary anti‐(4‐hydroxy‐3‐nitro‐phenyl)acetyl (NP) antibodies in normal and idiotypically suppressed C57BL/6 mice
Authors: Cumano Ana , Rajewsky Klaus 
Published: February 2007

AbstractEight monoclonal antibodies from the primary response of C57BLJ6 mice against the hapten (4‐hydroxy‐3‐nitrophenyl)acetyl (NP) were isolated. The antibodies carry λ1 light chains and have similar affinities for the immunizing hapten. Sequence analysis at the level of mRNA reveals that all antibodies express the VH gene 186.2 and all but one the DF116.1 gene segment. The J segment of the heavy chain is JH2 in six cases and JH4 in two. Somatic point mutations are scarcely detectable in the antibodies, but there is extensive sequence variability at the boundaries of the D gene segment, mainly at its 5′ end. However, seven of eight antibodies express tyrosine in position 99 of the heavy chain, encoded either by the 5′ codon of DF116.1 or by presumed N sequences. In the former case, the tyrosine is the first of a stretch of three (positions 99–101). In the latter, a similar stretch (positions 99, 101, 102) is interrupted by aspartic acid, asparagine or cysteine in position 100. These variations profoundly affect idiotypic specificity.Six of the eight monoclonal antibodies came from mice neonatally suppressed by an anti‐idiotope antibody whose target idiotope is regularly expressed in primary anti‐NP responses and depends upon a non‐germ‐line‐encoded aspartic acid in position 100 of the heavy chain. The sequence data show that the mice circumvent suppression by expressing antibodies which lack this aspartic acid but are otherwise structurally very similar to anti‐NP antibodies from normal animals. Since suppression in the animals is partly controlled by regulatory T cells, we conclude that these T cells are highly restricted in their specificity in that they preferentially see a determinant which also depends upon the aspartic acid in position 100. The data suggest that the VH to D boundary serves as a target of idiotypic selection.
Abrogation and reconstitution of nonresponsiveness: a correlation with high network connectivity
Authors: Singhai Rakesh , Hoffmann Geoffrey W. , Levy Julia G. 
Published: February 2007

AbstractA monoclonal antibody (Fd‐B2) to ferredoxin, which bears an idiotype scarcely expressed in any of a wide variety of mouse strains, is able to markedly enhance the response to ferredoxin of both high‐responder and intermediate‐responder strains. A rabbit anti‐idiotype serum to Fd‐B2 also specifically enhances the response to ferredoxin in such mice. Most remarkably, the treatment of nonresponder T cells by either the idiotype (Fd‐B2) plus complement or anti‐idiotype antiserum plus complement causes them to be responsive in adoptive transfer experiments. The two responding populations (idiotype‐treated and anti‐idiotype‐treated) can then be combined to reconstitute the nonresponsive state. When the nonresponders are treated with either Fd‐B2 idiotype plus complement or anti‐idiotype plus complement and subsequently respond, the idiotype of the anti‐ferredoxin antibody produced does not bear the Fd‐B2 idiotype. We interpret the results as being consistent with a model in which the unresponsive state for ferredoxin is a state of high network connectivity of the fer‐redoxin‐specific T cells.
Thymus‐independent induction of idiotype suppression in newborn mice by syngeneic anti‐idiotype antisera
Authors: Lehle Georg , Weiler Eberhardt 
Published: February 2007

AbstractBALB/c and BALB/c nu/nu mice were shown to express to a variable extent in their response against dextran B1355S (Dex), an idiotype which is present on the Dex‐reactive BALB/c myeloma protein MOPC104E. Injection of minute amounts of syngeneic anti‐MOPC 104E idiotype antisera into neonatal euthymic or athymic BALB/c mice suppressed this idiotype in the Dex‐specific response of the adult animals. When spleen cells from suppressed BALB/c mice were transferred into irradi‐ ated BALB Ighb mice the state of suppression persisted. Data are discussed with respect to possible mechanisms regulating expression of this idiotype.
Antibodies against the transferrin receptor block the induction of cytotoxic T lymphocytes. A new method for antigen‐specific negative selection in vitro
Authors: Rammensee Hans‐Georg , Lesley Jayne , Trowbridge Ian S. , Bevan Michael J. 
Published: February 2007

AbstractThe induction of cytotoxic T lymphocytes (CTL) specific for alloantigen in a primary mixed lymphocyte culture (MLC) was used as a model system to study the potential usefulness of monoclonal antibodies directed against the murine transferrin receptor in eliminating antigen‐activated T cells. Two monoclonal antibodies were used which are able to block the transferrin‐mediated uptake of iron by growing cells. One of these antibodies is cytotoxic in the presence of complement (C). Treatment of MLC cells from control, uninhibited cultures with the cytotoxic anti‐transferrin receptor antibody plus C completely knocked out all CTL effector activity showing that all of the effector cells expressed the receptor. However, surviving cells from such antibody‐plus C‐treated populations were not depleted of precursors since they were able to mount a strong CTL response to the original alloantigen upon restimulation. Blocking antibody against the transferrin receptor, in the absence of C, when present during the course of a primary MLC, completely inhibited the generation of effector CTL. Conditions were optimized such that antibody present during the course of the MLC could completely and specifically eliminate all antigen‐activated T cells including precursors as assessed by secondary restimulation with the original, plus third‐ party antigens, in the absence of blocking antibody. This method for producing specifically unreactive T cell populations appears to be superior to previously described techniques.
Inhibition of [3H]thymidine incorporation by Mycoplasma arginini‐infected cells due to enzymatic cleavage of the nucleoside
Authors: Sinigaglia Francesco , Talmadge Kenneth W. 
Published: February 2007

AbstractCulture supernatants contaminated by Mycoplasma arginini inhibit the incorporation of [3H]thymidine ([3H]dThd) by cytotoxic T lymphocyte cell lines. This study presents evidence that the inhibition of uptake of the nucleoside is due to the rapid cleavage of the exogenous [3H]dThd into thymine. Undine and cytidine as well as dThd are degraded by the mycoplasma‐contaminated supernatants, while no cleavage was observed with uninfected supernatants. Cells contaminated by mycoplasma apparently release a pyrimidine‐specific nucleosidase, possibly a dThd phosphorylase, which is responsible for the inhibition.
Isolation and characterization of an Fc receptor from neonatal rat small intestine
Authors: Simister Neil E. , Rees Anthony R. 
Published: February 2007

AbstractReceptors for the Fc region of IgG from neonatal rat intestinal brush borders were solubilized using 3‐[(3‐cholamidopropyl)dimethyl‐ammonio]‐l‐propane sulfonate and purified by affinity chromatography. Analysis of IgG‐binding material by sodium dodecyl sulfate‐polyacrylamide gel electrophoresis under reducing conditions reveals two components with apparent Mr of 41 000‐50 000 and 15 000. The larger component is glycosylated and may dimerize, giving a 100‐110‐kDa band on nonreduced gels. Both proteins are localized in the proximal small intestine, where IgG is specifically taken up during the first three weeks of neonatal life, and disappear when specific transport stops after weaning. Electron irradiation of brush borders shows that the functional unit for IgG binding has a molecular weight in sifu of 110 kDa. These data suggest that a dimer of the 41‐50‐kDa protein together with the 15 kDa and other proteins may mediate intestinal transport of maternal IgG.
Cytolytic T cell hybridomas I. Interleukin 2‐independent noncytolytic variants
Authors: Haas Werner , Kisielow Pawel 
Published: February 2007

AbstractFluorescein‐specific cytolytic hybrids were obtained by fusion of an interleukin 2 (IL2)dependent murine cytotoxic T lymphocyte clone with the thymoma BW5147. The hybrid cells grow and retain cytolytic activity in medium with recombinant IL2. In medium without IL2 rare variants can be selected which grow in the absence of exogenous IL 2; these variants are not cytolytic. Anti‐IL2 receptor antibodies bind to and inhibit the growth of the cytolytic hybrids while they do not bind to and do not inhibit the growth of the variants. The cytolytic hybrids as well as the non‐cytolytic variants produce interferon gamma in response to antigen. These findings indicate that the noncytolytic IL2‐dependent variants lost IL2 receptors but not antigen receptors.
Cytolytic T cell hybridomas II. Interleukin 2‐independent cytolytic variants
Authors: Haas Werner , Kisielow Pawel 
Published: February 2007

AbstractInterleukin 2 (IL 2)‐dependent cytolytic hybrids usually loose IL 2 dependence and cytolytic activity concomittantly. Here we describe an exceptional IL 2‐independent variant which lost IL2 receptor but retained cytolytic activity. When the IL 2‐independent cytolytic hybrid cells were fused with IL 2‐dependent cytolytic clones which express IL2 receptors constitutively, IL 2‐dependent hybrids were obtained. This suggests that the expression of IL 2 receptors can interfere with IL 2‐independent growth mechanisms.
Antigen‐nonspecific T cell‐derived factors in B cell activation: differences in the requirements for interleukin 2 in responses of unprimed and primed B cells
Authors: Kuhara Takatoshi , Haughton Geoffrey , Corley Ronald B. 
Published: February 2007

AbstractThe requirements for interleukin 2 (IL 2) and other T cell‐derived helper factors in the responses of unprimed and antigen‐primed B cells to sheep erythrocytes were investigated. Unprimed B cells required both IL 2 and additional factor(s), hereafter referred to as T cell‐replacing factor (TRF), in addition to specific antigen, for antibody production. IL2 was required only during the early stages (⋍24 h) of culture while TRF was necessary only after this time and was then required throughout the remaining culture period. IL2 stimulated the appearance of Thy‐1+ cells in unprimed “B cell” populations which could substitute for the function of IL2, implicating an indirect role, at least in part, for IL2 in the TRF assay. Furthermore, in contrast to the results with unprimed B cells, primed B cells required only late‐acting TRF for optimal antibody responses. We suggest that IL2 activates residual T cells or precursors of T cells in B cell populations which then function, in the presence of specific antigen, to render B cells receptive to T cell‐derived factors which promote B cell growth and differentiation.
Response of glioma cells to interferon‐gamma: increase in class II RNA, protein and mixed lymphocyte reaction‐stimulating ability
Authors: Takiguchi Masafumi , Tingco Jenny P.‐Y. , Buessow Scot C. , Boyer Cinda , Gillespien Yancey , Frelinger Jeffrey A. 
Published: February 2007

AbstractPrevious results by ourselves and others demonstrated that brain cells and cell lines express major histocompatibility complex class II antigens. We examined interferongamma (IFN‐γ)‐mediated induction of human class II antigen expression on the glioma cells. Purified IFN‐γ induced the expression of HLA‐DR antigens on the surface of the glioma cell lines U‐373 MG and U‐105 MG. Concomitant increase of HLA‐DRα‐and HLA‐DCβ‐specific RNA in the cytoplasm was also observed after treatment with IFN‐γ. Increases of class II antigen paralleled the increased level of class II‐specific RNA. The effect of IFN‐γ on the induction of human class II antigen expression was dose and time dependent. A marked induction of human class II antigen expression was observed when glioma cells were cultured with more than 100 U/ml of IFN‐γ. Little or no induction was observed with less than 50 U/ml of IFN‐γ. Compared to human blood monocytes, glioma cells needed higher concentrations of IFN‐γ for the induction of class II antigen expression.In allogenic mixed lymphocyte cultures, the glioma cell line U‐373 MG stimulated a mixed lymphocyte response (MLR). MLR‐stimulating capacity was augmented by IFN‐γ. The concomitant augmentation of class II antigen levels and MLR‐stimulating capacity suggests that the most relevant factor for MLR stimulation may be antigen density. This is the first report of MLR stimulation by a glioma cell line.
Production and characterization of antibody probes directed at constant regions of the α and β subunit of the human T cell receptor
Authors: Fabbi Marina , Acuto Oreste , Bensussan Armand , Poole Catherine B. , Reinherz Ellis L. 
Published: February 2007

AbstractTo generate antibodies directed at constant regions of the human T cell receptor, purified α and β subunits of a human T cell antigen/major histocompatibility complex receptor from the REX tumor (Ti‐REX) were isolated by preparative sodium dodecyl sulfate‐polyacrylamide gel electrophoresis and utilized to immunize rabbits. H36 (anti‐α subunit) and H38 (anti‐β subunit) antisera were strongly reactive with the denatured subunits and also immunoprecipitated the Ti heterodimer from 125I surface‐labeled lysates of REX, inducer, suppressor and cytotoxic T cell clones, peripheral T lymphocytes and thymocytes. Moreover, immunodepletion experiments showed that such antisera recognized antigenic determinant(s) shared by all Ti molecules expressed in the thymus. Several observations were made with these anticonstant region antibodies. First, peptide map analysis showed that the T cell receptor molecules recognized by the anti‐clonotype and the anti‐constant region heteroantisera on a given T cell clone are identical, thus supporting the view that the T cell receptor undergoes allelic exclusion. Second, since the individual antisera were weakly cross‐reactive with the other denatured subunit, such subunits probably share conserved sequences. Third, the absence of antisera reactivity with intact cells implies that most of these constant region epitopes must be obscured by associated molecules, perhaps including one or more of the 20–25‐kDa T3 subunits. Fourth, the extensive difference in two‐dimensional peptide maps of Ti α subunits from clones of differing specificities makes it likely that the subunit contributes in a major way to antigen/major histocompatibility complex binding.
Isotypes of antibodies induced by plain dextran or a dextran‐protein conjugate
Authors: Seppälä Ilkka , Pelkonen Jukka , Mäkelä Olli 
Published: February 2007

AbstractMice were immunized with a(1→6) dextran or its protein conjugate with monthly intervals, and their antibodies were quantitated with an isotype‐resolved radioimmunoassay. Plain dextran (molecular weight = 5–40 million) induced antibody concentrations varying from 20 to 80 μg/ml (primary response). The resposse to a booster injection was weaker than the response to the first injection. More than 90% of anti‐dextran antibodies were IgM but IgG and IgA responses could be unequivocally demonstrated. IgG1 and IgG3 were the predominant subclasses of IgG. Dextran antibody responses to a conjugate of dextran (molecular weight ≈ 10 000) and chicken serum albumin (CSA) were stronger (80–300 μg/ml) than responses to plain dextran, and anti‐CSA responses to the conjugate were even stronger (up to 900 μg/ml).Three distinctly different isotype patterns were observed. A pattern IgM ≫ IgG1 = IgG3 > IgG2a prevailed in responses to the plain dextran and in primary anti‐dextran responses to dextran‐CSA. Another pattern IgG1 > IgG3 > IgM > IgG2a was observed in late anti‐dextran responses to dextran‐CSA. The third pattern IgG1 ≫ IgG2a > IgG3 ≈ IgM was characteristic of anti‐CSA antibodies. Little IgG2b or IgA antibodies were found. Different isotype patterns can best be explained on the basis of secondary factors such as T cell help.
Effects of soluble aggregates of IgG on the binding, uptake and degradation of the Clq subcomponent of complement by adherent guinea pig peritoneal macrophages
Authors: Veerhuis Robert , van Es Leendert A. , Daha Mohamed R. 
Published: February 2007

AbstractEarlier studies have indicated that Clq, the first subcomponent of complement component C1, is bound to lymphocytes via specific Clq receptor sites. We have recently shown that adherent guinea pig peritoneal exudate macrophages express specific receptors for Clq (Veerhuis, R. et al., Immunology 1985. 54: 801). The present studies were performed to determine whether binding of 125I‐labeled human Clq (125I‐Clqhu) to adherent guinea pig peritoneal exudate macrophages would also result in ingestion and subsequent degradation of 125I‐Clqhu. The binding of 125I‐Clqhu to adherent peritoneal macrophages at 4°C is inhibited fully not only by Clqhu and guinea pig Clq (Clqgp) but also by pepsin fragments of Clqhu. The amount of trichlo‐roacetic acid nonprecipitable radioactivity that appeared in the supernatant was used as a measure for the degradation of 125I‐Clqhu. 125I‐Clqhu is degraded initially into fragments of 25 kDa, after which it is degraded further into small molecular weight peptides. Ingestion of 125I‐Clq by the macrophages occurs before the 125I‐Clq is degraded.In the presence of limited amounts of soluble aggregates of guinea pig IgG2 (AIgG), a known activator of C1, part of the Clq is bound to the AIgG and all of the AIgG in turn is bound to the cellular Fc receptors leading to an enhanced binding of 125I ‐Clq to the cells, a binding that was maximal at near equimolar concentrations of 125I‐Clqhuand 131I‐AIgG. In the presence of a 30‐fold excess of AIgG, however, only a small percentage of the AIgG binds to cellular Fc receptors and the interaction of Clq with its receptor is decreased due to competitive inhibition. The results presented in this report thus suggest that free Clq may be eliminated by specific interaction with Clq receptors present on circulating and tissue phagocytoses and, in addition, that in the presence of immune complexes modulation of elimination of Clq may be encountered.
The defect in delayed‐type hypersensitivity of young adult SJL mice is due to a lack of functional antigen‐presenting cells
Authors: Stohlman Stephen A. , Matsushima Glenn K. , Casteel Nancy , Frelinger Jeffrey A. 
Published: February 2007

AbstractSJL mice exhibit a strain‐specific age‐dependent delay in the maturation of delayed‐type hypersensitivity (DTH) responsiveness. They do not attain “adult” levels of DTH responsiveness until the 10th week of age, which is 4 to 6 weeks later than the other strains of mice tested. In this report we demonstrate that spleen cells, resident peritoneal cells and thioglycollate‐elicited peritoneal exudate cells are all able to transfer DTH responsiveness from naive 12‐week‐old DTH responders to 6‐week‐old nonresponders. Transfer prior to immunization was more efficient at eliciting a response than transfer after immunization. As few as 5 ± 104 cells from 12‐week‐old SJL mice can adoptively transfer responsiveness to unresponsive 6‐week‐old animals. The active cell was found to be adherent, radiation (2000 rds) resistant, I‐A+, Thy‐1− and Mac‐l+. I‐A compatibility between the adoptively transferred population and the nonresponder mice is required. These data suggest that young adult SJL mice lack a functional population of antigen‐presenting cells specific for DTH and that the appearance of these cells is under maturational control.