bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibody affinity maturation in selectively bred high and low‐affinity mice
Authors: Steward Michael W. , Stanley Carolynne , Furlong Maria D. 
Published: February 2007

AbstractThe affinity of serum antibodies produced by selectively bred lines of mice [high affinity, low affinity, low nonmaturing (N/M)] injected with T‐dependent [human serum albumin (HSA), dinitrophenylated bovine γ‐globulin (DNP‐BGG)] and T‐independent (DNP‐Ficoll) antigens in saline and adjuvant has been determined. The lines of mice differ significantly in the affinity of antibody produced to T‐dependent antigens injected in saline but not to the T‐independent antigen. Unlike mice of the high and low‐affinity lines, low‐affinity N/M mice failed to show affinity maturation to HSA and DNP‐BGG injected in Freund's incomplete adjuvant. However, low‐N/M mice responded to DNP‐Ficoll injected in adjuvant by the production of antibody of affinity comparable to that produced in the other lines and with a similar maturation in affinity. Carrier priming resulted in the suppression of anti‐hapten antibody affinity in all lines but low‐N/M mice showed significantly greater suppression late in the response to challenge. Low doses of cyclophosphamide produced a significant increase in affinity in low‐N/M mice. These results suggest that the failure of low‐N/M mice to show affinity maturation results from increased suppressor T cell activity. The availability of the selectively bred mice provides a useful model for the detailed study of the cellular basis of the control of antibody affinity maturation.
Induction of rheumatoid factors in mice by immune complexes of bacterial lipopolysaccharide with mouse IgG antibody
Authors: Kanoh Makoto , Utsumi Sayaka , Hino Tomoo 
Published: February 2007

AbstractAdministration of 2,4,6‐trinitrophenylated E. coli lipopolysaccharide (TNP‐LPS) complexed with mouse IgG antibody to TNP specifically gave rise to a marked production of rheumatoid‐like factors (RF) in the recipient mice, in contrast to the low and nonspecific RF production via polyclonal B cell activation by the same dosage of LPS or TNP‐LPS alone. The RF activity induced by the LPS immune complexes was associated with both IgG and IgM and directed primarily to the Cγ2 region as judged by the heterophilic reactivity toward fragments of rabbit IgG. The results suggest that antibody molecules attached to LPS constitute novel epitopic groups on the mitogenic carrier and stimulate B cells in a specific manner to induce the autoantibodies.
A protective human monoclonal IgA antibody produced in vitro: Anti‐pneumococcal antibody engendered by Epstein‐Barr virus‐immortalized cell line
Authors: Steinitz Michael , Tamir Sara , Ferne Mina , Goldfarb Ada 
Published: February 2007

AbstractHuman lymphocytes that produce anti‐pneumococcal antibodies were separated and immortalized by Epstein‐Barr virus and then cloned. One clone (NAD‐Sel) produces an IgA, x antibody which is specific for the polysaccharides of type 8 pneumococcus, while not reactive with any of the polysaccharides derived from 24 other pneumococcal strains. The antibody, which is present in the cell supernatant as monomer and polymer, binds to protein A and does not fix complement. When incubated in vitro with type 8 pneumococci, it induces direct killing and increases the opsonization of these bacteria by mouse macrophages.
Defective membrane expression of the LFA‐1 complex may be secondary to the absence of the β chain in a child with recurrent bacterial infection
Authors: Lisowska‐Grospierre Barbara , Bohler Marie‐Christine , Fischer Alain , Mawas Claude , Sringer Thymothy A. , Giscelli Claude 
Published: February 2007

AbstractMembrane and intracellular processing of the LFA‐1 macromolecular complex, known to be involved in cytolytic function of T lymphocytes, was investigated in a child with recurrent bacterial infections, impaired natural killer activity, T cell‐mediated lymphocytolysis and absent adhesion and migration of phagocytic cells. Monoclonal antibodies to the LFA‐1 α and β subunits, able to precipitate the LFA‐1α, 180‐kDa chain, the p151 chain and β 94‐kDa chain (shared by both α chains), were used in immunoprecipitation studies of patient and control phytohemagglutinin‐blasts. Neither of the α chains nor the β chain were found in precipitates obtained from 125I‐surface‐labeled patient cells in contrast to controls. However, the precursor of the LFA‐1 α chain, a 170‐kDa polypeptide, was identified in lysates of biosynthetically labeled patients' cells. These results suggest that the defective membrane expression of the LFA‐1 complex may be secondary to the absence of the mature β chain.
Biochemical characterization of chicken secretory component
Authors: Peppard Jane V. , Hobbs Stephen M. , Jackson L. Elizabeth , Rose M. Elaine , Mockett Adrian P. A. 
Published: February 2007

AbstractHuman dimeric IgA was injected i.v. into chickens whose bile was then collected. The human IgA which had been transported across the hepatocytes of the chicken was subsequently purified from the bile and shown to be associated with a protein of 80 kDa and pI 4.6, which reacted with rabbit antisera to chicken bile proteins but not with an antiserum to human α chain. The chicken bile protein thus has functional and biochemical properties similar to those of mammalian secretory component.
Activation of resting T lymphocytes by a monoclonal antibody directed against an allotypic determinant on the T cell receptor
Authors: Staerz Uwe D. , Bevan Michael J. 
Published: February 2007

AbstractThe murine monoclonal antibody F23.1 reacts with an allotypic determinant on the β chain of the T cell receptor expressed by approximately 20% of T helper and cytotoxic T lymphocytes of most common mouse strains. This IgG2a antibody, either in soluble form or covalently coupled to Sepharose beads, can activate resting T cells from naive animals to proliferate. Interestingly, under all conditions of activation, the antibody can only induce proliferation if exogenous lymphokines in the form of Con A supernatant are provided. Thus, it is unlike most lectins and anti‐T3 antibodies in this regard. Furthermore, under all conditions of culture, F23.1 activates preferentially the Lyt‐2+ subset of T cells. This is the case even in the presence of accessory cells. Further evidence is provided that two soluble lymphokines, different from IL2, are required to initiate IL2‐dependent growth and to allow the expression of lytic activity.
Influence of carriers on the development and localization of anti‐trinitrophenyl antibody‐forming cells in the murine spleen
Authors: Claassen Eric , Kors Nel , Rooijen Nico Van 
Published: February 2007

AbstractMice were i.v. immunized with various 2,4,6‐trinitrophenyl (TNP)‐carrier conjugates, and the development and localization of specific (i.e. anti‐TNP) antibody‐forming cells (AFC) in the spleen was studied. The nature of the carrier used, thymus dependent (TD) or thymus independent type 1 or type 2 (TI‐1, TI‐2), had marked effects on the number and time of appearance of AFC. However, no influence of the different carriers on the localization of specific AFC in the spleen was observed. By using a double immunocytochemical technique we could simultaneously determine specificity (anti‐TNP) and isotype (class and subclass) of the AFC. The TNP‐carrier conjugates evoked (intracellular) immunoglobulins with carrier‐characteristic isotype distribution. No carrier‐dependent localization pattern, in the lymphoid compartments of the spleen, of these AFC was found. These results show for the first time the actual in situ effects of various TI and TD carriers on the development of specific AFC. Based on the present findings, no direct evidence for a special role of the marginal zone in the immune response against TI‐2 antigens could be demonstrated. We suggest that this new method for in vivo investigation, in combination with existing standard enzyme‐ and immunohistochemical techniques, can provide more insight into the precise role of lymphoid and nonlymphoid cells in TD and TI immune responses.
Conformational‐dependent recognition of influenza virus hemagglutinin by murine T helper clones
Authors: Mills Kingston H. G. , Skehel John J. , Thomas D. Brian 
Published: February 2007

AbstractA panel of H‐2k class II‐restricted T helper (Th) clones were established from individual CBA mice intranasally infected with A/X31 influenza virus. In a study of their fine specificity, it was revealed that recognition of hemagglutinin (HA) by certain Th clones was dependent on conformational features of the molecule. Five HA‐specific Th clones failed to recognize X31 mutant viruses R19 and R20 each with a His to Arg substitution at position 17 of HA1. This amino acid substitution affects the conformational stability of the molecule. Each of the 5 clones responded to purified HA but failed to recognize tryptic fragments of HA consisting of HA1 residues 28–328 (tops) and the remainder of the virus including residues 1–27 of HA1 (aggregate). A further 20 HA‐specific clones responded to R19 and R20 mutants and to HA1 tops. The R19 and R20 negative clones also showed diminished proliferative responses to pH 5‐treated X31. Low pH treatment results in an irreversable conformational change which affects the integrity of the globular head region of the HA trimer. In addition, four of the five clones failed to recognize variant virus Eng‐72 which has Arg to Gly substitution at position 208 in the interface antibody‐binding region. This region is antigenically and structurally altered in tops and pH 5‐treated X31. The results suggest that recognition of HA by certain Th clones is dependent on the three‐dimensional structure of the molecule and that Th cells may recognize conformational determinants in addition to primary structure.
The cellular basis of salivary immunity in the mouse: Incidence and distribution of B cells, T cells and macrophages in single‐cell suspensions of the major salivary glands
Authors: Oudghiri Mounia , Seguin Jacynthe , Deslauriers Noëlla 
Published: February 2007

AbstractA multiparametric analysis of the resident immune populations in the parotid, submandibular and sublingual salivary glands was done in single‐cell suspensions. The incidence of T and B cells and of macrophages was assessed using phenotypic markers in immunofluorescent staining and a functional assay was used to enumerate immunoglobulin (Ig)‐secreting cells. Characteristic frequencies and isotype distributions of cytoplasmic Ig+ B cells and surface Ig+ B lymphocytes were found in the three types of glands. Even though IgA was always found to be the predominant isotype in individual salivary secretions (90–93%) this was not directly correlated by an absolute predominance of IgA‐secreting cells in the glands (45–65%). Significant percentages of T cells (Thy‐1+ and Lyt‐1+ cells: 3–4%) and macrophages (Mac 1+ and esterase‐positive cells: 3–10%) were also recovered in our suspensions. It is therefore concluded that the murine salivary glands contain both effector and regulatory cells required for the development and expression of salivary immunity.
Internalization and processing of antibodies to surface antigens on human B cells. Monoclonal anti‐IgM antibodies are processed differently than monoclonal antibodies towards non‐Ig surface receptors
Authors: Ruud Erik , Blomhoff Heidi Kiil , Funderud Steinar , Godal Tore 
Published: February 2007

AbstractThe internalization and intracellular processing of monoclonal antibody to immunoglobulin μ heavy chain (Maμ) have been investigated in two human Burkitt lymphoma cell lines (Ramos and Raji), in a human B cell lymphoma and in normal human peripheral blood B cells. In addition to the degradation of 125I‐labeled Maμ to trichloroacetic acid (TCA) soluble material, a distinct pattern of larger 125I‐Map fragments was detected in all sources of B cells tested. The particular fragmentation pattern, as revealed by sodium dodecyl sulfate‐polyacrylamide gel electrophoretic analysis, involved the cleavage of both peptide bonds and disulfide bridges. This type of antibody fragmentation appeared to be a selective mechanism associated with sIgM, as no other degradation than that leading to TCA‐soluble material could be detected after the internalization and degradation of radiolabeled monoclonal antibodies towards a variety of non‐Ig B cell surface receptors. Three fragments of 125I‐Maμ degradation were also detected in the supernatant of Ramos cells, implying that the recycling and exocytosis of certain 125I‐Maμ fragments also took place.
Structural polymorphism of Vx21 E and Vx21 D gene products in laboratory mice
Authors: Primi Daniele , Barbier Eliane , Cazenave Pierre‐André 
Published: February 2007

AbstractThe aim of the present work was to study structural polymorphism of Vx genes products. To this end we isolated immunoglobulins expressing the Vx21 D and Vx21 E gene products from the normal sera of several inbred strains of mice using a monoclonal antibody that selectively recognizes Vx21 D and Vx21 E subgroups. Analysis of the isoelectric focusing pattern of the light chain of these immunoglobulins revealed the existence of 3 clearly different phenotypes. The first one is shared by most inbred strains of mice, the second one is expressed by C58/J, AKR and PL/J and the third one defines Vx21 D‐E light chains of SJL and SJA mice. Genetic analysis revealed that the locus controlling Vx21 D‐E chain structure is closely linked to the Ly2–3 and to the Igx‐Ef1 loci. Finally, using recombinant mouse strains, we could also order Vx21 D‐E genes with respect to the known loci affecting Vx polymorphism.Taken together our data argue against the possibility that the polymorphism observed results from strain‐specific expression of Vx genes common to all mice, but rather suggest that different allelic form of the same Vx gene subgroup exist in different strains.
Adsorption on B cell hybridomas removes suppressor cells from spleen cells of neonatally tolerized mice
Authors: Stockinger Brigitta , Darjes Heidi , Krammer Peter H. 
Published: February 2007

AbstractSpleen cells from CBA mice neonatally tolerized to Dd MHC (major histocompatibility complex) determinants were adsorbed on monolayers of Dd‐specific B cell hybridomas. Adsorption on 4 different Dd‐specific hybridomas but not on a Kd‐specific hybridoma removed suppressor cells and resulted in generation of cytotoxic T lymphocyte (CTL) effector cells against the tolerogen. Responses of normal CBA CTL against Dd as well as anti‐third party responses were not influenced by adsorption. Successful adsorption was also achieved on monolayers of fixed hybridoma cells. Monolayers of Dd‐specific hybridomas specifically removed suppressor cells from CBA mice tolerant to Dd; they failed to adsorb suppressor cells from AKR mice tolerant to H‐2b.Immunofluorescence analysis with antibodies specific for determinants on tolerizing cells showed the presence of donor‐derived F1 cells on the monolayer. Under the experimental circumstances described suppressor cells are most likely removed by recognition of their MHC determinants by the monolayer population.These data suggest that neonatal tolerance is actively maintained by donor‐derived suppressor cells.
Dissociation of interleukin 2‐dependent and ‐independent B cell proliferation with monoclonal anti‐interleukin 2 receptor antibody
Authors: Hashimoto Noboru , Nabholz Markus , MacDonald H. Robson , Zubler Rudolf H. 
Published: February 2007

AbstractIn a recent report from our laboratory (J. Exp. Med. 1984. 160: 1070), it has been shown that B cells which have been activated with lipopolysaccharide (LPS) plus anti‐Ig antibodies express interleukin 2 (IL2) receptors and proliferate in response to pure IL2. In the present study, we have investigated the role of IL2 during proliferative B cell responses supported by various T cell supernatants (SN) as well as by LPS itself. The following results were obtained: (a) B cells activated with LPS plus anti‐Ig were found to proliferate in response to either recombinant IL2, T cell SN or fresh LPS; (b) a monoclonal anti‐IL2 receptor antibody (PC61) could completely inhibit the effects of recombinant IL2 or various T cell SN (cloned T helper cell SN, EL4 SN, concanavalin A‐spleen cell SN or mixed leukocyte culture SN), but did not interfere with the effect of LPS; (c) B cells activated with LPS or LPS plus anti‐Ig were not found to secrete detectable amounts of IL2 by themselves.Thus, the data demonstrate that LPS‐stimulated B cell proliferation requires neither B cell autocrine nor T cell‐derived IL2. On the other hand, with regard to LPS plus anti‐Ig‐activated B cells, IL2 appeared to be the only growth‐promoting activity that could be detected in the supernatants obtained from total normal spleen cell populations.
Production and characterization of rabbit anti‐idiotypic antibodies specific to mouse monoclonal anti‐human IgE and reacting with IgE‐binding factors and lymphocyte receptors for IgE
Authors: Sarfati Marie , Duncan Douglas , Delespesse Guy 
Published: February 2007

AbstractA mouse monoclonal antibody specific to human IgE (mAb75) was employed to immunize a rabbit to obtain anti‐idiotypes (aId) bearing the internal image of human IgE determinants and reacting with IgE‐binding factors (IgE‐BF) and/or lymphocyte receptors for IgE (FcϵR). mAb75 was selected on the basis of inhibition assays where the binding of mAb 75 to radiolabeled IgE was blocked by IgE‐BF. The latter were produced by a lymphoblastoid cell line (RPMI 8866) expressing FcϵR. Sequential samples of rabbit serum, collected during the immunization period, were extensively absorbed on mouse and human Ig‐Sepharose 4B. The IgG fractions of the rabbit serum displayed the following activities: (a) they reacted with 125I‐labeled mAb 75 but not with other labeled mouse Ig including mAb‐aIgE, (b) this binding was inhibited in a dose‐dependent fashion by human IgE but not by other human Ig classes nor by heat‐inactivated IgE, (c) they reacted with a polyclonal rabbit anti‐human IgE and (d) they blocked the binding of 125I‐labeled IgE to mAb 75. It was concluded that the rabbit IgG contained aId (RaId) bearing the internal image of heat labile determinants of human IgE. The rosetting of IgE‐coated bovine erythrocytes with FcϵR‐bearing cells was inhibited by preincubating the receptor‐bearing cells with IgG RaId or its F(ab')2 but not with normal rabbit IgG. The ability of RaId to react with IgE‐BF as well as with FcϵR was also shown in inhibition experiments where IgE‐BF and solubilized FcϵR blocked the binding of mAb 75 to RaId. Finally, Western blot analysis of human colostrum, known to contain IgE‐BF, indicated that radioiodinated RaId and IgE identified the same 12‐16‐kDa molecules corresponding to IgE‐BF.It is concluded that RaId expresses the internal image of a heat‐labile determinant of IgE which is involved in the binding of IgE to IgE‐BF and FcϵR. An alternative interpretation is that RaId reacts with an idiotypic determinant of mAb 75 which is shared by IgE‐BF and FcϵR.
Inhibition of B cell growth factor (BCGF) by monoclonal antibodies directed against the C3d receptor (CR2)
Authors: Perri Robert T. , Wilson Barry S. , Kay Neil E. 
Published: February 2007

AbstractNormal human B cell proliferation is controlled by various immunoregulatory signals including the T cell‐derived lymphokine B cell growth factor (BCGF). Human BCGF provides the final proliferative signal to normal, activated B cells. We herein show that anti‐CR2 monoclonal antibodies inhibit human B cell responsiveness to purified BCGF. Addition of anti‐CR2 antibody, AB5, was capable of completely inhibiting BCGF‐mediated enhancement of either anti‐μ or staphylococcal protein A‐activated human B cells (191 ± 21 cpm vs. 3942 ± 622 cpm, mean ± SEM). Inhibition of B cell response to BCGF by AB5 occurred in a dose‐dependent manner. Monoclonal antibody anti‐B2, which recognizes the same 140‐kDa glycoprotein as AB5, in comparable concentrations also inhibited B cell responsiveness to BCGF. Monoclonal antibodies of the same subclass (IgG1) showed no inhibitory effect on BCGF enhancement of B cell proliferation. The F(ab')2 fragment of AB5 generated by pepsin digestion was similarly inhibitory as was the intact Ig. ABS‐mediated inhibition was independent of the target B cell state of activation. Both resting and activated B cells (anti‐μ or staphylococcal protein A activated) incubated with similar concentrations of AB5 were unresponsive to BCGF. The abilitv of anti‐CR2 antibodies to block BCGF‐dependent B cell proliferation suggests that occupancy of C3d membrane receptors may result in modulation of B cell proliferation in physiologic or clinical disease states.
Antigen presentation by human monocytes: Effects of modifying major histocompatibility complex class II antigen expression and interleukin 1 production by using recombinant interferons and corticosteroids
Authors: Rhodes John , Ivanyi Juraj , Cozens Peter 
Published: February 2007

AbstractLymphocyte proliferation in response to monocytes pulsed with an antigenic extract of Candida albicans was measured in vitro and the effects of modifying major histocompatibility complex (MHC) class II antigen expression at the surface of the antigen‐presenting cells was investigated. The study shows that no simple correlation exists between changes in MHC class II antigen expression and changes in the effectiveness of antigen presentation. Recombinant interferon‐αl (rIFN‐αl), rIFN‐γ and hydrocortisone were found to increase the expression of monocyte class II MHC antigens. In contrast, rIFN‐α2 did not increase class II antigen expression although it did increase MHC class I expression. Treatment of monocytes with rIFN‐αl, rIFN‐α2 or corticosteroids during antigen pulsing resulted in a reduction in the subsequent proliferative lymphocyte response. In all cases this inhibitory effect was restricted to antigen‐specific proliferative responses since the polyclonal lymphocyte response to pokeweed mitogen‐pulsed monocytes remained unaffected. Only rIFN‐γ treatment of antigen‐pulsed monocytes resulted in enhancement of the subsequent specific lymphocyte proliferative response. The suppressive effects of hydrocortisone could not be attributed to its well documented inhibitory effects on arachidonic acid metabolism. The effect of C. albicans antigen, IFN and corticosteroids on interleukin 1 (IL1) production by monocytes was also investigated. C. albicans antigen alone induced IL 1 production. So too did IFN‐αl and IFN‐γ IFN‐α2 did not induce IL 1 production. Addition of interferons together with C. albicans, however, resulted in the same level of IL1 productions as with C. albicans antigen alone. Neither antigen nor IFN had any effect on IL1 action in the thymocyte assay.Corticosteroids did not affect IL 1 production by monocytes but were potent antagonists of IL 1 in the thymocyte proliferation assay. Mitogen‐induced thymocyte proliferation was also inhibited by corticosteroids. Pretreatment of monocytes with hydrocortisone followed by washing did not markedly affect their subsequent ability to produce IL 1 neither was it possible to reverse the inhibitory effects of hydrocortisone on antigen presentation by addition of exogenous IL1. Thus, signals which alter class II MHC antigen expression influence the antigen‐presenting capacity of monocytes by a mechanism independent of IL 1. No simple correlation exists between class II expression and antigen‐presenting capacity.