bluuebunny/crossref_metadata_2025_split huggingface dataset:
The regulatory locus rλ1 affects the level of λl light chain synthesis in lipopolysaccharide‐activated lymphocytes but not the frequency of λl ‐positive B cell precursors
Authors: Sanchez Pierre , Primi Daniele , Levi‐Strauss Mathieu , Cazenave Pierre‐Andrë 
Published: February 2007

AbstractSeveral strains of mice, most notably the SJL strain, have a greatly reduced level of circulating λl immunoglobulins (rλ110 phenotype) compared with other mice. The locus responsible for this phenotype has been shown to be closely linked to the structural Cλl gene. Functionally this locus has been said to reduce the number of lymphocytes expressing surface λl molecules. In order to gain a better understanding of this phenomenon we compared the functional properties of activated B cells secreting λl immunoglobulins in the splenocytes of both BALB/c and SJL mice.Our results indicate that regulatory T cells, as well as regulatory ontogenetic processes, are not responsible for the rλ1lo phenotype. In addition, limiting dilution analyses revealed that the number of lipopolysaccharide‐sensitive precursors of λl‐secreting B cells was similar in the splenocytes of the two strains of mice tested. The quantity of λl molecules produced by a B cell clone, however, was found to be lower in SJL than in BALB/c mice. As the level of λl mRNA is greatly reduced in lipopoly‐saccharide blasts of SJL mice, as compared to the mRNA detected in BALB/c blasts, we conclude that the impairment responsible for the rλ110 phenotype is probably transcriptional. We tentatively propose that sequences 5′ to the Cλl region are defective in their capacity to enhance the λl transcripts in SJL mice.
Recombinant interferon‐γ can induce the expression of HLA‐DR and ‐DC on DR‐negative melanoma cells and enhance the expression of HLA‐ABC and tumor‐associated antigens
Authors: Carrel Stefan , Schmidt‐Kessen Andreas , Giuffrè Laura 
Published: February 2007

AbstractRecombinant interferon‐γ (IFN‐γ) induced the expression of HLA‐DR when added to the culture medium of HLA‐DR− melanoma cell lines. In addition, IFN‐γ induced the expression of another class II antigen, HLA‐DC, on a HLA‐DR+ and ‐DC− melanoma cell line and to a lower level on a ‐DR and ‐DC− melanoma line. IFN‐γ also enhanced the expression of HLA‐ABC and β2‐microglobulin, as well as HLA‐DR on DR+ melanoma cells. In contrast, IFN‐α gave no induction of expression of HLA‐DR and DC on two DR− melanoma lines, while it did enhance the expression of HLA‐ABC and of β2‐microglobulin. The expression of 3 out of 6 melanoma‐associated differentiation antigens was enhanced by IFN‐γ treatment. The modulation of antigens by IFN‐γ was both dose and time dependent. A minimum incubation time of 48 h was necessary for the appearance of HLA‐DR on the two HLA‐DR− melanoma lines, whereas HLA‐ABC and β2‐microglobulin were already increased after 24 h. A dose of 20 U/ml IFN‐γ started to induce the expression of HLA‐DR and DC on melanoma cells GLL‐19 and Me‐43 and a plateau of maximum antigen expression was reached with 100 U/ml. Analyses of IFN‐γ‐treated cells by flow micro‐fluorometry showed a homogeneous distribution of increased staining intensity rather than the appearance of two cell populations. Immunoprecipitation experiments using detergent‐solubilized 125I‐labeled membrane proteins of IFN‐γ‐treated melanoma cells and a monoclonal anti‐HLA‐DR antibody confirmed the presence of HLA‐DR antigens. When IFN‐γ‐treated cells were cultured without IFN the induced or enhanced expression of HLA antigens was reversible. Eight days after removal of IFN, the HLA‐DR level was reduced by more than 90% and the level of HLA‐ABC and β2‐microglobulin by more than 50%. The demonstration of the ability of HLA‐DR− melanoma cells to express HLA‐DR after IFN‐γ treatment was extended to cells from other types of tumor such as gliomas, colon carcinomas and one cervical carcinoma cell line.
Immediate hypersensitivity to drugs and simple chemicals: the efficacy of monovalent elicitors
Authors: Schneider Conrad H. , Guenin Raymond , Toffler Olga 
Published: February 2007

AbstractIntroduction of a reactive monohaptenic chemical into the sensitized organism will not normally result in elicitation of immediate reactions. Rather, the first products of chemical conjugation to suitable carriers in vivo are monohaptenic conjugates which are inhibitory according to the bridging concept, stating that the initiating event for mast cell and basophil activation is a cross‐linking of membrane‐bound antibody by dihaptenic or oligohaptenic antigen. Simple calculations and quantitative data are presented to show that built‐in inhibition is indeed a powerful barrier to any rapidly occurring allergenic manifestation which depends on the formation of divalent conjugates. If and when such a reaction does nevertheless occur, special requirements have to be invoked. One possibility is that the chemical or drug as such, i.e. without conjugation to a carrier, is an elicitor of anaphylaxis. Such compounds are known in a guinea pig passive cutaneous anaphylaxis model system, but there is evidence that they may also play a role in clinical situations. These monovalent elicitors possess in addition to the haptenic moiety an auxiliary group. The auxiliary group requirements were studied in the guinea pig passive cutaneous anaphylaxis system by using synthetic peptides with an N‐terminal 2‐carboxy‐4,6‐dinitrophenyl group as the hapten and phenylalanine and modified phenylalanine at the C‐terminus as auxiliary group. The conclusions are that effective auxiliary function depends on the benzene ring and neighboring carboxyl groups in selected positions. Anaphylactogenicity is high when the haptenic and auxiliary groups can act independently, i.e. when separated by a peptide chain of considerable length. Potent anaphylactogens with close linkage of the two groups have, however, also been found. It is unlikely that the passive cutaneous anaphylaxis elicitations observed here are mediated by some form of indirect bridging of membrane‐bound antibody.
Molecular and antigenic heterogeneity of the rat leukocyte‐common antigen from thymocytes and T and B lymphocytes
Authors: Woollett Gillian R. , Barclay A. Neil , Puklavec Michael , Williams Alan F. 
Published: February 2007

AbstractThe molecular forms and antigenic heterogeneity of the leukocyte‐common antigen (L‐CA) of rat lymphocytes have been analyzed. Thymocytes show one main band at 180 kDa, T cells four bands at 180,190, 200 and 220 kDa and B cells one broadband at about 240 kDa. T helper and T cytotoxic cell subsets show the same four bands with some differences in the proportion of each.Four mouse monoclonal antibodies (MRC OX‐1, 28, 29 and 30) reacted with all molecular forms of L‐CA and fell into two sets that were noncompetitive in binding to L‐CA (MRC OX‐1, 28, 29 vs. OX‐30). The antigenic determinants seen by all these antibodies were lost when L‐CA was reduced and alkylated. Three antibodies (MRC OX‐22, 31 and 32) reacted selectively with B cells, T cytotoxic cells and about 2/3 of T helper cells. OX‐22 and OX‐31 competed for binding but were noncompetitive with OX‐32. All these antibodies bound to a subfraction of the 190, 200 and 220‐kDa forms of T cell L‐CA but not at all to the 180‐kDa form of T cells or thymocytes. One antibody bound to B cells only (MRC OX‐33) and precipitated a subfraction of B cell L‐CA. With all the antibodies that did not label thymocytes the antigenic determinants survived reduction and alkylation. Subsequent proteolysis with trypsin then destroyed all determinants except the one reacting with MRC OX‐22 antibody, In this case tryptic peptides retained full antigenic activity which was, however, destroyed by further proteolysis with pronase.
Very large and isotypically atypical polyclonal plaque‐forming cell responses in mice infected with Trypanosoma cruzi
Authors: Lima Maria Regina D'Imperio , Joskowicz Mireille , Coutinho Antonio , Kip Tereza , Eisen Harvey 
Published: February 2007

AbstractNormal C3HIHeJ mice, acutely infected with T. cruzi, develop large numbers of splenic Ig‐secreting plaque‐forming cells (PFC). IgG2a, IgG2b and IgGl PFC account for over 90% of all PFC, while the numbers of IgG3‐ and IgA‐secreting PFC are lower than in normal animals. These effects appear to be due to both T helper‐dependent regulation and to a mitogenic activity associated with the parasites themselves.
A 3β‐cholestanyl‐containing mono‐benzylpenicilloyl oligoamide and peptide suppress anti‐benzylpenicilloyl antibody formation in mice
Authors: Lüscher Immanuel F. , De Weck Alain , Gitler Carlos 
Published: February 2007

AbstractA long‐chain linear mono‐benzylpenicilloyl (BPO) oligoamide and a succinoylated mono‐BPO decalysine were tested in BALB/c mice for suppression of IgE and IgG1 antibody formation. Both compounds were available with either a free C‐terminal end or were C‐terminally linked to a hydrophobic 3β‐cholestanyl residue. Only the sterol‐containing derivatives suppressed hapten‐specific IgE and IgG1 responses. Substantial suppression was obtained when the compountds were administered before primary or secondary, but not later immunizations.In an adoptive cell transfer experiment, spleen cells from tolerized animals actively suppressed anti‐BPO IgE antibody formation of immune spleen cells. This effect was reversed by pretreatment of the tolerized spleen cells with anti‐Lyt‐2.2 antibody plus complement.The requirement for macrophages in the induction of T suppressor cells was demonstrated by injecting antigen‐pulsed macrophages into naive recipients; upon immunization, only mice treated with tolerogen‐pulsed macrophages showed suppressed anti‐BPO IgE responses. It is suggested that lipid modification of antigens alters their processing and presentation by macrophages in a manner that leads to the induction of T suppressor cells.Injection of the cholestanyl derivatives into passively sensitized guinea pigs elicited anaphylactic reactions. By immune precipitation analysis and molecular weight estimation, these derivatives were shown to form micelles in aqueous solution. Therefore, the anaphylactic response appeared to be due to their behavior as multivalent antigens.
Abnormalities in autologous mixed lymphocyte reaction‐activated immunologic processes in systemic lupus erythematosus and their possible correction by interleukin 2
Authors: Takada Shinsuke , Ueda Yuji , Suzuki Noboru , Murakawa Yohko , Hoshino Takashi , Green Ira , Steinberg Alfred D. , Horwitz David A. , Sakane Tsuyoshi 
Published: February 2007

AbstractThe autologous mixed lymphocyte reaction (AMLR) represents the activation, proliferation and differentiation of T cells in response to signals from autologous non‐T cells. Upon stimulation by autologous non‐T cells, OKT4+ cells produce interleukin 2 (IL2); cells contained within both OKT4+ and OKT8+ cell populations can also be activated by autologous non‐T cells to become sensitive to IL2. Once these activated OKT4+ and OKT8+ cells are exposed to IL2 produced by OKT4+ cells, they will proliferate and go on to differentiate into effector cells.Patients with systemic lupus erythematosus (SLE) have a defect in the AMLR. The ability of OKT4+ cells to produce IL 2 in the AMLR is impaired. Upon triggering with autologous non‐T cells, their OKT8+ cells become sensitive to proliferative signals of IL2; however, their OKT4+ cells fail to express IL2 receptors. These defects are a consistent feature in patients with SLE. AMLR‐induced immunologic processes which require cell interactions between OKT4+ cell subpopulations are not correct‐ able even by the addition of normal IL2. However, the immunologic processes medi ated through OKT4+‐OKT8+ cell interactions can be corrected with normal 1L2. The latter finding suggests that the partial correction of the AMLR‐induced immunologic processes with IL 2 might lead to suppressed B cell hyperactivity of patients with SLE.
Various expressions of a unique anti‐human thyroglobulin antibody repertoire in normal state and autoimmune disease
Authors: Ruf Jean , Carayon Pierre , Lissitzky Serge 
Published: February 2007

AbstractPolyclonal anti‐human thyroglobulin (hTgb) antibodies (Ab) were purified from sera of rabbits immunized with human thyroglobulin, normal humans and patients suffering from Graves' disease, Hashimoto's thyroiditis and thyroid carcinoma. The avidity of the various Ab preparations for hTgb ranged from 0.3 × 1010−2.2 × 1010 M−1. By using well characterized mouse monoclonal antibodies (mAb) directed against hTgb, it was shown that the fine specificities of induced anti‐hTgb Ab in rabbits, natural Ab in normal subjects and autoantibodies in diseased patients were similar; however, they differed from that of rabbit anti‐bovine and anti‐porcine thyroglobulin Ab which were able to inhibit the hTgb binding of only a few of the mAb. Anti‐hTgb in rabbits and in patients with thyroid carcinoma varied from those in normal subjects only by uniformly elevated serum titers. In contrast, patients with Graves' disease and Hashimoto's thyroiditis showed an increased concentration essentially restricted to Ab reacting with few of the antigenic determinants recognized by the mAb. Our data suggest that the repertoire of anti‐hTgb Ab is similar in mouse, rabbit and human. Furthermore, the finding of identical fine specificities for anti‐hTgb Ab in normal and pathological conditions implies that autoantibodies are produced in normal subjects and held to a low level by regulatory processes which fail with respect to selected epitopes in autoimmune diseases.
Induction of an auto‐anti‐IgE response in rats. I. Effects on serum IgE concentrations
Authors: Marshall Jean S. , Bell Eric B. 
Published: February 2007

AbstractWith a view to specifically suppressing the IgE isotype, rats of high (BN) and low (PVG. RT1u) IgE‐responding phenotypes were immunized with a highly purified rat IgE myeloma (IR2) in an attempt to induce an anto‐anti‐IgE response. Rat IgE antibodies against ϵ determinants were detected in the serum of IR2‐immunized animals using a solid‐phase (plate) radioimmunoassay. The auto‐anti‐IgE antibodies detected were found to bind to IR2, to a second rat IgE myeloma (IR162) and to mouse monoclonal IgE but not rat IgG. The specificity of the anti‐ϵ binding was shown by inhibition studies. The raising of an auto‐anti‐IgE response in PVG. RT1u rats severely depleted the serum level of circulating IgE for at least 8 weeks. In BN rats, immunization with IR2 caused marked fluctuations in serum IgE levels. The rats in both strains remained healthy throughout the experiment. The rate and route of IgE break down was not altered in anti‐IgE‐producing rats. The relevance of the present model in understanding and possibly controlling allergic disorders is consid‐ ered.
Mapping cell surface antigens on mouse pre‐B cell lines
Authors: McKearn John P. , Rosenberg Naomi 
Published: February 2007

AbstractCharacterization of cell surface molecules expressed by B cell precursors has been hampered by the inability to routinely assay such cells from freshly explanted normal lymphoid tissues. However, a large number of transformed pre‐B cell clones have been isolated which presumably include those precursors recently entering the B cell lineage (obtained from fetal liver and more rarely from adult bone marrow) and extending to those clones which are poised to become surface Ig‐positive B cells. In this report, we have quantitated expression of 10 different cell surface molecules, 5 of which bear special interest as B cell differentiation antigens, among a large panel of pre‐B cell clones.
Polyclonal activation of the murine immune system by an antibody to IgD. VI. Influence of doses of goat anti‐mouse δ chain and normal goat IgG on B lymphocyte proliferation and differentiation
Authors: Finkelman Fred D. , Smith Joanne , Villacreses Nelly , Metcalf Eleanor S. 
Published: February 2007

AbstractThe injection of mice with 800 μg of an affinity‐purified goat antibody to mouse IgD (GaMδ) induces early, T‐independent polyclonal increases in the expression of B cell surface Ia, and B cell size and DNA synthesis, as well as later, T‐dependent polyclonal increases in spleen cell number and Ig secretion. We have now studied the effects of varying the doses of injected GaMδ on all phases of B cell activation, as well as the effects of supplementing GaMG with varying quantities of normal goat IgG (GIgG). We have found that while 12.5 μg of GaMδ modulates most of the IgD from the surface of splenic B lymphocytes, it fails to activate these cells. Increases in the expression of B cell surface Ia are first seen when 50 μg of GaMδ is injected, while increases in B cell DNA synthesis usually require the injection of 200 μg of GaMδ and peak with doses of approximately 800 μg. Increases in splenic B cell number and DNA synthesis during the T‐dependent phase of GaMδ‐induced B cell activation are seen only in those mice that were injected with sufficient quantities of GaMδ to induce DNA synthesis during the T‐independent phase. Supplementing the dose of GaMδ injected with additional GIgG has no significant effect on B cell DNA synthesis or B cell number but dramatically increases polyclonal IgGl secretion. Although mice which have been injected with 50 μg of GaMδ or with 800 pμ of GIgG alone have few polyclonal IgG1‐secreting cells, substantial increases in the number of IgG1,‐ secreting cells are seen in mice injected with 50 μg of GaMδ plus 750 μg of GIgG. GIgG and larger doses of GaMδ similarly act synergistically to increase polyclonal IgGl secretion. In contrast to the induction of polyclonal IgGl secretion, the stimulation of polyclonal IgM secretion requires the injection of mitogenic doses of GaMδ and is not enhanced by the injection of additional GIgG. These observations suggest that, in this model system, stimulatory signals that activate B cells through their surface Ig are limiting for the induction of polyclonal proliferation and IgM secretion, while the generation of T helper lymphokines that do not directly interact with B cells through their surface Ig may be more limiting for the stimulation of polyclonal IgGl secretion.
Constraints in T‐B cooperation related to epitope topology on E. coli β‐galactosidase. I. The fine specificity of T cells dictates the fine specificity of antibodies directed to conformation‐ dependent determinants
Authors: Manca Fabrizio , Kunkl Annalisa , Fenoglio Daniela , Fowler Andrée , Sercarz Eli , Celada Franco 
Published: February 2007

AbstractExperiments to test the relationship between the epitopes on a protein antigen recognized by T and B cells in their collaboration to produce antibody cannot rely solely on hapten‐carrier models. In the present work we used E. coli β‐galactosidase, a molecule whose tertiary and quaternary epitopes have been well characterized, as the model antigen. T helper cells were raised by stimulating mice with the intact or the denatured molecule or with any of several β‐galactosidase cyanogen bromide pep‐ tides. In a series of in vitro helper T cell assays we confronted the various T popula tions with B cells preimmunized with the native antigen, and we tested their capacity to help production of (a) binding antibodies and (b) antibodies directed to single conformational epitopes, characterized by their capacity to protect the enzyme from heat denaturation or to activate defective P‐galactosidase. According to our results, (a) equivalent T cell help can be provided by T helper cells primed with native or denatured antigen, even for the production of “conformational” antibodies; (b) one of the peptides (CB‐18) is most efficient in raising help for binding antibodies; and (c) two peptides (CB‐20 and CB‐21) rank highest in priming T helper cells for the even‐ tual production of protecting and activating antibodies, respectively. Thus, not every β‐galactosidase‐specific T helper cell is useful in providing help to B cells specific for any particular epitope on the molecule, but rather preferential pairings exist, possibly governed by a proximity rule.
Autoantibodies to anti‐DNA with anti‐allotypic and anti‐idiotypic specificities in (NZB × NZW)F1 mice
Authors: Eilat Dan , Fischel Ruth , Zlotnick Avinoam 
Published: February 2007

AbstractThe monoclonal A52 (IgG2b, x) anti‐DNA autoantibody represents a major cross‐ reactive idiotype in the murine and human autoimmune response to DNA. Examination of sera and purified IgG derived from (NZB × NZW)Fj mice showed that these mice develop an age‐dependent binding reactivity with the pure anti‐DNA IgG. Three monoclonal antibodies possessing this reactivity were prepared from unprimed female (NZB × NZW)F1 mice. One of these monoclonal antibodies appeared to be directed against allotypic determinants present in the NZB IgG2b the other two antibodies exhibited a marked preference for idiotypic determinants of the A52 IgG. The IgG anti‐allotype and anti‐idiotype activities in (NZB × NZW)Ft mice may, therefore, represent the products of a deregulated immune system and/or constitute the normal elements of a functional immune regulation system.
The respiratory burst is not required for killing of intracellular and extracellular parasites by a lymphokine‐activated macrophage cell line
Authors: Scott Phillip , James Stephanie , Sher Alan 
Published: February 2007

AbstractThe macrophage cell line, IC‐21, was found to be incapable of producing the oxygen products associated with the respiratory burst. However, IC‐21 cells were activated by lymphokine (LK) to kill intracellular (Leishmania donovani amastigotes) and extracellular (Schistosoma mansoni larvae) parasites, as well as tumor cells. In each case, the cytotoxicity exhibited by activated IC‐21 cells and activated peritoneal mac‐ rophages was indistinguishable. However, nonactivated IC‐21 cells were unable to kill L. donovani log‐growth phase promastigotes, while nonactivated peritoneal mac‐ rophages destroyed > 90% of the initial infection. These results indicate that amasti‐ gotes and schistosome larvae are susceptible to killing by nonoxidative cytotoxic mechanism induced by lymphokine activation but, on the other hand, support the concept that the killing of log‐growth phase promastigotes by nonactivated cells is dependent upon the respiratory burst. We propose that the IC‐21 cell line may be a useful model for studying nonoxidative killing functions of activated macrophages.
Partial biochemical characterization of IgG1‐inducing factor
Authors: Sideras Paschalis , Bergstedt‐Lindqvist Susanne , Severinson Eva 
Published: February 2007

AbstractIgG1, induction factor elevates the IgGl and suppresses the IgG3 and IgG2b responses in lipopolysaccharide‐stimulated murine spleen cell cultures. By the use of a quantitative assay, it was found that the three activities, induction of IgG1 and reduction of IgG3 and IgG2b synthesis, were found in the same fractions after different chromato‐graphic procedures, suggesting that the same molecule was responsible for the effects. The factor was precipitated by 60‐90% saturation of ammonium sulfate and was sensitive to proteolytic cleavage and to treatment with a buffer of pH 10. It had an apparent molecular mass of 20 kDa as judged by gel filtration chromatography and was separated into two peaks after isoelectric focusing, PI 7.4‐7.2 and 6.4‐6.2, respectively. Finally it was weakly hydrophobic and negatively charged at pH 7.55. These characteristics indicate that the factor is different from many previously characterized lymphokines and similar or identical to the B cell stimulating factor‐1 (BSF‐pl). The relevance of these findings to the mechanism of the immunoglobulin class switch is discussed.