bluuebunny/crossref_metadata_2025_split huggingface dataset:
The alloantigenic organization of RT1Aa, a class I major histocompatibility complex molecule of the rat
Authors: Diamond Austin G. , Larkins Audrey P. , Wright Bruce , Ellis Susan T. , Butcher Geoffrey W. , Howard Jonathan C. 
Published: February 2007

AbstractOver 300 monoclonal IgG alloantibodies have been prepared against RT1Aa, the class I major histocompatibility complex molecule of the DA rat. In this study a combination of techniques is exploited to show that all these antibodies can be allocated to 9 antigenic sites which form a continuous antigenic surface, that is, no site is completely isolated from the rest. The results suggest that techniques for the identification of antigenic sites using competitive inhibition of monoclonal antibody binding are generally valid, in the sense that competition between antibodies appears most commonly to represent competition between combining sites for a structural feature of the antigenic surface. From the distribution of antibodies between sites, it is clear that the RT1Aa molecule has three immunogenic areas against which nearly all the antibodies studied were directed. Of these areas one is both antigenically complex, consisting of four closely spaced sites, and remarkably immunodominant. Antibodies directed at sites between the major areas are extremely rare.
Immunodominant protein epitopes I. Induction of suppression to hen egg white lysozyme is obliterated by removal of the first three N‐terminal amino acids
Authors: Wicker Linda S. , Katz Michael , Sercarz Eli E. , Miller Alexander 
Published: February 2007

AbstractThe lack of response to hen egg white lysozyme (HEL) by C57BL (H‐2b) mice has been demonstrated previously to be related to the induction of suppressor T (Ts) cells which recognize the amino terminal region of HEL. In this report, the nature of the protein determinant required for Ts cell induction is more precisely detailed using des‐1,2,3‐HEL (AP‐HEL) prepared with an aminopeptidase purified from Aeromonas proteolytica. Remarkably, the removal of just these three amino acids obliterates the ability of HEL to induce Ts cells specific for HEL. Additionally, in contrast to HEL, AP‐HEL is able to prime for an in vitro T cell proliferative response to either AP‐HEL or HEL. Thus, removal of a very limited region of a protein antigen can drastically alter its immunogenic properties.
Pre‐B cells in bone marrow: peanut agglutinin binding and separation of cytoplasmic μ chain‐bearing cell populations in normal, post‐irradiation and polycythemic mice using fluorescence‐activated cell sorting
Authors: Osmond Dennis G. 
Published: February 2007

AbstractMouse bone marrow cells exposed to fluorescein‐conjugated peanut agglutinin (PNA) showed subsets of highly labeled cells when analyzed in a fluorescence‐activated cell sorter. After separating three cell fractions of large and small PNA‐binding cells and PNA‐nonbinding cells, respectively, the B lymphocyte precursor (pre‐B) cells, having cytoplasmic μ chains (cμ) without surface μ chains (sμ), were recovered solely in the PNA‐binding fractions. Only a minority of sμ+ small lymphocytes having the lowest densities of sμ bound PNA. Small and large cμ+sμ− pre‐B cell populations were separated in high degrees of purity in the PNA‐binding fractions, especially when obtained from bone marrow undergoing lymphoid regeneration after sublethal X‐irradiation and during stimulation of lymphocyte production in post‐polycythemic erythroid suppression. Characteristic shifts in the size distribution profile of PNA‐binding cells reflected changes in the maturation stage of the pre‐B cells. The results demonstrate that surface membrane components with strong PNA‐binding capacities characterize cμ+sμ− pre‐B cells in the bone marrow during both normal and perturbed primary B lymphocyte genesis. The PNA‐binding sites become undetectable soon after the first expression of sμ. This property permits the isolation from the bone marrow of high concentrations of subsets of large and small cμ+sμ− cells in a viable state suitable for use in further functional studies.
Poly(Glu60, Ala30, Tyr10) (GAT)‐specific T cells do not express B cell public idiotopes but can be primed by monoclonal anti‐idiotypic antibodies
Authors: Bismuth Georges , Sommé Gérard , Roth Claude , Gougeon Marie‐Lise , Thèze Jacques 
Published: February 2007

AbstractEight monoclonal anti‐idiotypic antibodies directed against public idiotopes have been further characterized: (a) they bind to public idiotopes with a high affinity; (b) they recognize all anti‐poly(Glu60, Ala30, Tyr10) (GAT) antibodies as measured by inhibition of the anti‐GAT plaque‐forming cell response. This has been verified in three strains of mice. These reagents were not able to detect idiotope expression on eight GAT‐specific helper T cell lines and clones. This result was obtained by two techniques: (a) idiotope expression at the T cell surface was measured by indirect immunofluorescence using a cell sorter with surface antigens H‐2D, Thy‐1.2, Lyt‐1 and L3T4 as positive controls; (b) after immunoadsorption of [35S]methionine‐labeled cellular extracts from two lines, no unique molecule was retained by the HP‐idp22 monoclonal anti‐idiotypic antibody coupled to Sepharose. Despite these negative results, this antibody was found to prime lymph node cells in vivo, which were able to proliferate specifically in response to GAT. Two T cell lines derived from this lymphocyte population do not express any of the idiotopes tested. These results suggest that monoclonal anti‐idiotypic antibodies may be influencing T lymphocyte activity indirectly.
Monoclonal anti‐cardiolipin antibodies bind to DNA
Authors: Rauch Joyce , Tannenbaum Hyman , Stollar B. David , Schwartz Robert S. 
Published: February 2007

AbstractBALB/c mice immunized with the phospholipid, cardiolipin, produced anti‐cardiolipin and anti‐DNA antibodies. Seven hybridomas derived from spleen cells of the cardiolipin‐immunized mice produced cardiolipin‐binding monoclonal antibodies that also bound to the polynucleotides DNA, poly(dT), and poly(I). The seven cardiolipin‐induced monoclonal antibodies shared idiotypic determinants with a high frequency idiotypic marker of spontaneously expressed anti‐DNA autoantibodies of lupus‐prone MRL‐lpr/lpr mice. The monoclonal antibodies presumably bound to phosphodiester phosphate groups that occur in both polynucleotides and phospholipids. The results imply that production of anti‐DNA autoantibodies does not require immunization by DNA.
Analysis of gp140, a C3b‐binding membrane component present on Raji cells: a comparison with factor H
Authors: Frade Raymond , Barel Monique , Krikorian Laure , Charriaut Christiane 
Published: February 2007

AbstractIn a previous report (M. Barel et al. FEBS Lett., 1981. 136: 111) using radiolabeling methods, we characterized from the membrane of the human B lymphoblastoid cell line Raji, a 140000‐Mr glycoprotein (gp140) carrying a C3b‐binding activity with 125I‐labeled C3b or Sepharose‐bound C3b. The facts of absence on Raji cells of CR1, the C3b receptor purified from human erythrocytes, the observations made by others that H‐like activity (the 150000 Mr C3b binding serum protein) was present in Raji cells and the same molecular weight range of H and gp140, led us to investigate the relationship between both antigens.A rabbit antibody anti‐5.4 was prepared against gp140, highly purified from Raji cells. However, anti‐H specificities were detected in crude anti‐5.4 IgG, while anti‐serum H IgG did not react with gp140 antigen. The crude anti‐5.4 IgG fraction, anti‐gp140 IgG or F(ab′)2 and anti‐H specificities present in anti‐5.4 IgG, separated by absorption on Sepharose‐bound H, and anti‐serum H IgG were tested on Raji cells by immunofluorescence techniques, by measuring the inhibition of specific cytotoxic assays and the inhibition of specific binding of soluble or particle‐bound C3b to the cell surface and on solubilized antigens by immunoblotting techniques. All the data obtained support that: (a) anti‐H specificities are not shared by antibodies bearing anti‐gp140 specificities and their presence in crude anti‐5.4 IgG is more likely due to a contamination by H antigen of gp140 antigen used in the immunization process, and (b) gp140 antigen is highly expressed on Raji cell surface, whereas H antigen can not be detected under the same conditions. Molecular analysis of gp140 and H antigens confirmed differences between both antigens in molecular weight, trypsin sensitivity and charge properties.All the results presented herein support the notion that gp140 is not identical with the H molecule and that C3b binding to gp140 is not mediated by H. The relationship between gp140 and C3 receptors described by others is discussed.
The interaction of high endothelial venules with T and B cells in peripheral lymph nodes after antigenic stimulation
Authors: Kraal Georg , Twisk Agaath 
Published: February 2007

AbstractThe influence of an ongoing immune response on the specific interaction of high endothelial venules (HEV) in peripheral lymph nodes with T and B cells was determined using short‐term homing experiments and an in vitro HEV adherence assay. It was demonstrated that stimulation with various antigens did not change the receptor specificity of the HEV. However, the retention and/or the efflux of immigrant cells in the stimulated lymph nodes had changed.
Allosuppression: evidence for the involvement of both “noncytotoxic” and cytotoxic T cells
Authors: Zamoyska Rose , Waldmann Herman 
Published: February 2007

AbstractAllogeneic suppressor cells were generated by priming to a minor histocompatibility antigen. C57BL/10 female mice were primed to the male‐specific minor transplantation antigen, H‐Y. After boosting, anti‐male‐primed cells could potently suppress the secondary antibody response of male spleen cells in vitro. Anti‐male suppressor cells were H‐2‐restricted, radiation‐resistant T cells which could act on either T or B cells in the responding population. Mapping the restriction elements for anti‐male suppressor cells revealed two distinct subpopulations of effector cells. The majority subpopulation was restricted to H‐Y in the context of the H‐2Db molecule. These cells were probably cytotoxic T cells as they were inhibited by culture of the suppressor cells in pyrilamide (a histamine1 receptor antagonist, which prevents the maturation of cytotoxic T cells from their precursors). The second subpopulation of suppressor cells was restricted to H‐Y in the context of H‐2K or I region‐coded molecules. As neither H‐2Kb nor H‐2Ib molecules can act as restriction elements for anti‐male‐specific cytotoxic T cells, this subpopulation was almost certainly not composed of conventional cytotoxic cells. Furthermore, these cells were not affected by culture in pyrilamide. Together these two populations act to completely inhibit the anti‐trinitrophenyl (TNP) plaque‐forming cell response of male spleen cells in vitro.
Specificity, duration and mechanism of idiotype suppression induced by neonatal injection of monoclonal anti‐idiotope antibodies into mice
Authors: Takemori Toshitada , Rajewsky Klaus 
Published: February 2007

AbstractMonoclonal antibodies detecting idiotopes on the germ line‐encoded anti‐(4‐hydroxy‐3‐nitrophenyl)acetyl (NP) antibody B1‐8 were injected at various doses into newborn mice and the expression of B1‐8 idiotopes was measured in anti‐NP responses in later life. Suppression was long lasting, and a 100‐fold increase in the dose of anti‐idiotope delayed recovery from suppression by 5‐6 weeks. Upon injection of a single anti‐idiotope, suppression was observed for all B1‐8 idiotopes to various degrees. Certain idiotopically defined antibody phenotypes were much more efficiently suppressed, and later recovered from suppression, than others. This specificity pattern was observed at the level of both B and T cells from the manipulated animals, as demonstrated in cell transfer experiments in which such cells were mixed with normal T and B cells. In these experiments, there was evidence for suppression mediated by regulatory T (and possibly also B) cells. Whereas the B cells from the manipulated animals were idiotypically unresponsive in a T cell‐dependent adoptive primary response, the frequency of lipopolysaccharide‐reactive B cells expressing the target idiotype was only slightly reduced in these animals as compared to control mice.Together with data on the elimination of anti‐idiotope antibody from the neonatally injected animals these results are interpreted in the following way: idiotype suppression is induced through the reaction of anti‐idiotope with idiotopes expressed on the surface of newly generated B cells, at microgram concentrations of anti‐idiotope. When the concentration of anti‐idiotope falls below that level, recovery from suppression sets in. Two types of suppression are induced. The first, namely, direct blockade of B cell maturation, is short‐lived. The second involves the induction of regulatory cells, perhaps through idiotope‐bearing antibody V regions complexed by anti‐idiotope. This type of suppression is long‐lived and its specificity depends upon the distribution of the target idiotope in the antibody repertoire and/or peculiarities of the T cell receptor repertoire. It impinges on the selection of the B cell repertoire in the animal as expressed in T cell‐dependent (and possibly other) responses and is thus hardly seen at the level of lipopolysaccharide‐reactive (immature) cells. Idiotype suppression by regulatory cells may be perpetuated by antigen interacting with idiotypic antibodies on the B cell surface and may therefore play a role in establishing tolerance not only for the expressed antibody repertoire, but for self antigens in general.
Low sialic acid‐bearing mouse thymocytes do not express helper T cell properties in vitro
Authors: Herron Lynne R. , Collins Janet M. , Abel Carlos A. , Campbell Priscilla A. 
Published: February 2007

AbstractImmature, presumably cortical, mouse thymocytes were isolated by removing mature thymocytes by agglutination with the sialic acid‐specific lectin, lobster agglutinin 1 (LAg1). These immature cells do not respond to the mitogenic effects of concanavalin A (Con A), even in the presence of interleukin 2. Moreover, they do not exhibit two properties of helper T cells; they do not secrete interleukin 2 when stimulated with Con A, nor do they provide T help for an in vitro immune response by spleen B cells to the T‐dependent antigen, sheep erythrocytes. LAg1‐negative thymocytes fail to provide T help even though Con A is added to the cultures, regardless of the number of LAg1‐negative thymocytes added per culture, and even in the presence of exogenous macrophages. Unseparated thymocytes, LAg1‐positive thymocytes and cortisone‐resistant thymocytes all provide T cell help under these conditions. These experiments indicate that immature, presumably cortical mouse thymocytes, isolated by virtue of their low levels of surface sialic acid, are inherently unable to provide T cell help in vitro.
Feedback regulation of immune suppression by a suppressor factor
Authors: Ikezawa Zenro , Nagy Zoltan A. , Klein Jan , Arden Bernard 
Published: February 2007

AbstractMouse hybridomas generated by fusion between a lactate dehydrogenase‐B (LDH‐B)‐specific B10.A(2R) T suppressor (Ts) cell line and the BW5147 thymoma secrete two suppressor factors, TsF‐A and TsF‐E. The factors carry the same antigen‐binding chains but different major histocompatibility complex (MHC) chains (Aβ‐like and Eβ‐like, respectively). The TsF‐A suppresses the proliferation of A‐restricted, LDH‐B‐specific T helper (Th) cells. In this report we demonstrate that the addition of the TsF‐E (isolated on immunosorbent columns with Ek‐ or Jk‐specific antibodies) to the culture of LDH‐B‐primed B10.A(2R) lymph node cells turns the nonrespnder (suppressed) cultures into proliferating ones, and that this change is antigen specific. This enhancing effect occurs in the early phase of the cell culture; the factor has no effect when added 2 days after the initiation of the culture. Because pretreatment of the Ly‐2+ but not of the Ly‐1+2− cells with TsF‐E induces responsiveness, it is very likely that the targets of the factor are the Ts cells or their precursors that belong to the Ly‐2+ subset. An incubation period of about 4 h is necessary for the TsF‐E to expert its action. The enhancing effect of the TsF‐E is abrogated by monoclonal antibodies specific for Ek and Jk antigenic determinants. However, only some of the antibodies that retain the TsF‐E on the immunosorbent column neutralize the factor in a functional test. Antibody blocking studies also indicate that the MHC determinants involved in the interaction between the antigen‐presenting and the Ts cell during Ts cell activaton, and in the TsF‐E Ts cell interaction are either very similar or identical. We interpret the data as indicating that the Ts cells or their precursors recognize the TsF‐E with the same receptors as they use for the recognition of LDH‐B together with the Ek on the antigen‐presentign cells. The recognition of the TsF‐E inactivates the Ts cell so that proliferation of Th cells then occurs unhindered. Thus, the production of the TsF‐E may provide a feedback mechanism that regulates the activation of the Ts cells and, consequently, the degree of suppression in the response to LDH‐B.
Macrophage‐chemotactic factor‐producing T cell hybridomas reactive to phosphorylcholine in I‐E‐restricted manner
Authors: Sugimura Shingo Harita, Kazuhisa , Watanabe Takeshi 
Published: February 2007

AbstractMacrophage‐chemotactic factor (MChF)‐producing T cell hybridomas were established. These hybridomas produced MChF upon the specific antigenic stimulation with phosphorylcholine (PC)‐conjugated protein in the presence of I‐Ed‐positive antigen‐presenting cells. The hybridomas also secreted MChF after co‐culture with concanavalin A in the absence of antigen‐presenting cells. The MChF‐secreting hybridomas were positive for Kd, Dd, Lyt‐1.2 but negative for I‐Ad, Lyt‐2.2. The molecular weight of MChF produced by the hybridomas was 43000 and the factor was focused at pH 6.6‐6.8 in the chromatofocusing procedure. The MChF was protease sensitive but resistant to neuraminidase treatment, and it was stable by heating at 80°C for 15 min. The MChF‐producing hybridomas established in this study did not produce macrophage migration inhibitory factor (MIF), macrophage‐activating factor (MAF) or interleukin 2, suggesting molecular nonidentity between MChF and these lymphokines. The MChF‐producing T cell hybridomas reactive to specific antigens (PC) will be promising tools for analysis of molecular nature of MChF as well as molecular aspects of antigen recognition mechanism of T cells.
Interactions between immunoglobulins and I region antigens on the B lymphocyte membrane
Authors: Forni Luciana 
Published: February 2007

AbstractModulation and co‐modulation of membrane‐bound IgM and IgD and of I region‐encoded antigens (I‐A and I‐E) were studied by immunofluorescence with the use of monoclonal antibodies. The two sets of molecules displayed different ability to be redistributed, by divalent ligands: immunoglobulins could be easily redistributed, while this was not the case for I‐A and I‐E molecules. After short periods of activation, however, this property was found to change drastically: I‐region antigens were redistributed into polar caps, and immunoglobulins were modulated without clear polar redistribution.Cross‐linking and removal of one of the molecules always resulted in the modulation of at least one other, often two membrane molecules. Concomitantly, an additional molecule was expressed in higher amount. The results are compatible with the existence of specific interactions at the level of the B cell membrane, involving the four molecules in the order I‐A → IgM → I‐E → IgD. Such interactions, probably reversible in the unperturbed state, are likely to change in affinity when one molecule interacts with a ligand. The possible relevance of membrane interactions between immunoglobulin and class II antigens in the regulation of the B cell is discussed.
Surface carbohydrate epitopes of Thy‐1.1 and Thy‐1.2 thymocytes are distinguished by a monoclonal antibody with a specificity common to peanut agglutinin
Authors: Graham Christine M. , Thomas D. Brian 
Published: February 2007

AbstractNIMF4‐31.7 is a monoclonal IgM antibody with affinity for terminal galactose residues of membrane glycoproteins, Sepharose and agarose. It is cytotoxic for a subpopulation of murine thymocytes and peripheral lymphocytes, corresponding to the peanut agglutinin‐positive population, but reacts with a majority of cells after neuraminidase treatment. It has revealed a genetic linkage between the Thy‐1 locus and quantitative expression of carbohydrate determinants on the thymocyte membrane.
Immunoregulation of lysozyme‐specific suppression. II. Hen egg‐white lysozyme‐specific monoclonal suppressor T cell factor suppresses the afferent phase of delayed‐type hypersensitivity and induces second‐order suppressor T cells
Authors: Adorini Luciano , Colizzi Vittorio , Doria Gino , Ricciardi‐Castagnoli Paola 
Published: February 2007

AbstractCulture supernatant from a monoclonal T cell lymphoma line (LH8‐105) obtained by radiation leukemia virus‐induced transformation of hen egg‐white lysozyme (HEL)‐specific suppressor T lymphocytes is able, when injected into mice, to specifically suppress the delayed‐type hypersensitivity (DTH) reaction induced by HEL. The suppressor T cell factor (TsF) exhibits fine antigenic specificity since it suppresses the DTH response induced by HEL without affecting the DTH response induced by ring‐necked pheasant egg‐white lysozyme (REL), a lysozyme closely related to HEL. Conversely, LH8‐105 TsF is able to suppress the DTH response induced by human lysozyme, distantly related to HEL but sharing a common epitope critical for induction of suppressive activity. The fine antigenic specificity of LH8‐105 TsF for a restricted epitope on the HEL molecule is confirmed by binding to HEL but not to REL immunosorbents. This TsF also bears I‐J determinants, as demonstrated by binding to monoclonal anti‐I‐J immunosorbents, and it suppresses the afferent but not the efferent phase of the DTH response to HEL. The afferent suppression is controlled by genes apparently mapping in the I‐J subregion of the H‐2 complex since I‐J‐incompatible mice are not suppressed by LH8‐105 TsF injection. This inducer‐type TsF induces second‐order effector suppressor T cells only in HEL‐primed mice indicating the primary role of antigen, in association with H‐2 (I‐J) products, in the afferent portion of this suppressive circuit.