bluuebunny/crossref_metadata_2025_split huggingface dataset:
Gut mucosal mast cells in Nippostrongylus‐primed rats are the major source of secreted rat mast cell protease II following systemic anaphylaxis
Authors: King Stephen J. , Miller Hugh R. P. , Woodbury Richard G. , Newlands George F. J. 
Published: February 2007

AbstractThe distribution of the predominant chymotrypsin‐like enzyme of mucosal mast cells (rat mast cell protease 11: RMCP II) was examined in naive and Nippostrongylus‐primed rats both before and after the induction of systemic anaphylaxis. Anaphylactic secretion of RMCP II following i.v. challenge of primed rats with worm antigen was accompanied by significant depletion of this enzyme from the jejunal and gastric mucosae; the concentrations were not altered in the ileum and colon. Despite significant increases in the levels of RMCP II in lung and mesenteric lymph node following infection with N. brasiliensis there was no anaphylactic depletion of this enzyme from these sites. No RMCP II was detected in liver, spleen, kidney or bone marrow either before or after systemic anaphylaxis. Mucosal mast cells were depleted from the jejunal, gastric and colonic mucosae following antigen challenge of primed rats. These data provide further evidence that gastrointestinal mucosal mast cells are the major source of secreted RMCP II following systemic anaphylaxis in the rat.
Human B cell activation: Selective sensitivity of the early stages to calcium channel‐blocking drugs
Authors: Dugas Bernard , Vazquez Aimé , Delfraissy Jean‐François , Gérard Jean‐Philippe , Rannou Marie‐Thérèse , Galanaud Pierre 
Published: February 2007

AbstractThe importance of Ca2+ in the early events of lymphocyte activation has been suggested by several studies. We examined the effect of calcium channel‐blocking drugs (verapamil and nitrendipine) on the progression of human B cells through their activation cycle. Our results show that these drugs suppress the anti‐μ‐induced human B cell proliferation and interfere with the early events of the B cell activation in a dose‐dependent fashion. This suppression correlates with a marked decrease in anti‐μ‐induced 45Ca2+ uptake. Calcium channel‐blocking drugs inhibit the anti‐μ‐induced uridine incorporation and the appearance of the activation marker defined by the 4F2 monoclonal antibody. Calcium channel‐blocking drugs also inhibit B cell proliferation induced by the costimulation with anti‐μ antibody and B cell growth factor (BCGF). However, this inhibition takes place at the early (anti‐μ‐dependent) stage of B cell activation: the BCGF‐dependent proliferation of in vitro anti‐μ‐activated B cells is only marginally inhibited. Finally the proliferation of Epstein‐Barr virus‐infected B cell lines is resistant to the effect of calcium channel‐blocking drugs.
Mouse B cells do not proliferate in human interleukin 2
Authors: Leanderson Tomas , Julius Michael H. 
Published: February 2007

AbstractBy pre‐activation with a monoclonal anti‐IgM antibody coupled to Sepharose, either in the absence or presence of low doses of lipopolysaccharide, mouse B cell populations were rendered responsive to recombinant DNA derived human interleukin 2 (IL2). However, if the B cell populations were subjected to separation based on their buoyant density before pre‐activation, only low but not high buoyant density cells became responsive to IL2. Both cell populations subscquent to anti‐IgM pre‐activation were equally responsive to a Sephadex G‐100 fraction of supernatants from rat spleen cells stimulated with concanavalin A. Furthermore, the differences in the IL2 titration curves on T and B cell populations indicate that only a subpopulation of cells are responding to IL2 in the B cell populations. In B cell populations that did respond to IL2, a population of Thy‐1.2‐positive cells appeared. The proportion of IL2‐responsive T cells needed to give a significant signal when admixed with nonresponding B cell populations was quantitated to be less than 1 %.
Recombinant interleukin 2 enhances spontaneous insulin‐dependent diabetes in BB rats
Authors: Kolb Hubert , Zielasek Jürgen , Treichel Ulrich , Freytag Götz , Wrann Michael , Kiesel Ulrich 
Published: February 2007

AbstractTreatment of BB rats with recombinant interleukin 2 (IL 2) enhanced the development of spontaneous diabetes in these animals. A dose of 20 μg IL 2/kg body weight was administered twice daily for 80 days starting at 42 days of age. The rate of diabetes was doubled after IL2 administration (53% vs. 23%) and the onset of diabetes was found to be accelerated by a mean of 18 days. Histological analysis showed enhanced inflammation of islets and in addition interstitial pancreatis. It is concluded that IL2 has a regulatory effect on spontaneous organ‐specific autoimmunity.
Cloned helper T lymphocytes exposed to interleukin 2 become unresponsive to antigen and concanavalin A but not to calcium ionophore and phorbol ester
Authors: Otten Gillis , Wilde David B. , Prystowsky Michael B. , Olshan Jerrold S. , Rabin Harvey , Henderson Louis E. , Fitch Frank W. 
Published: February 2007

AbstractTwo cloned murine helper T lymphocyte (HTL) lines were used to investigate the immunoregulatory properties of highly purified interleukin 2 (IL2). The clone, designated J6.19, secretes lymphokines, including IL2, and proliferates when stimulated with ovalbumin in the presence of I‐Ak‐bearing spleen cells, while the alloreactive clone, L2, secretes lymphokines, including IL2, and proliferates when stimulated with Mlsa,d‐bearing spleen cells. When either clone was exposed to a high concentration of pure IL2 for 1 to 2 days in the absence of either antigen or spleen cells, the HTL became unresponsive to rechallenge with antigen. Unresponsiveness to antigen was indicated by an inability of HTL to proliferate or secrete usual amounts of IL 2 or colony‐stimulating factor. Within 5–7 days after exposure to IL2, the cloned HTL again responded to antigen. Thus, in addition to being a growth factor for HTL, IL2 can limit the magnitude of the HTL response to antigen. L2 or J6.19 cells could also be induced to secrete lymphokines by the lectin, concanavalin A (Con A) or by a combination of the calcium ionophore, A23187, and phorbol myristate acetate (PMA). After exposure of L2 or J6.19 cells to sufficient IL2 to induce unresponsiveness to antigen, cells were also unresponsive to Con A, as indicated by a reduction in the level of lymphokines secreted. In contrast, lymphokine levels stimulated by A23187/PMA were comparable to those produced by cells not exposed to IL2. The failure of antigen to stimulate lymphokine release and proliferation by HTL previously exposed to IL2 therefore may result from an inability of HTL to recognize antigen or to transduce effectively the antigen recognition signal. Several T cell surface molecules are known to be involved in antigen activation of HTL; these include the antigen receptor and the “associative recognition” structures L3T4 and LFA‐1. We observed that L2 cells, rendered unresponsive to antigen by exposure to IL2, expressed normal levels of antigen receptor, as identified by the monoclonal antibody, KJ16–133.18. Furthermore, expression of L3T4 and LFA‐1 was not decreased. Unresponsiveness to antigen induced by IL2 thus could not be correlated with decreases in the expression of antigen receptors, L3T4, or LFA‐1. Unresponsive HTL may therefore be capable of recognizing antigen but the signal generated by antigen binding may be attenuated during its transduction, resulting in the failure of cloned HTL to proliferate or secrete lymphokines at the usual levels.
Differential expression of T cell differentiation antigens and major histocompatibility antigens on activated T cells during the cell cycle
Authors: Matsui Yoshiki , Shapiro Howard M. , Sheehy Michael J. , Christenson Lisa , Staunton Donald E. , Eynon Elizabeth E. , Yunis Edmond J. 
Published: February 2007

AbstractIn this report we have analyzed cell cycle‐related fluctuations of both quantity and density of the T cell differentiation antigens, CD3 (T3), CD4 (T4) and CD8 (T8), as well as the major histocompatibility complex (MHC) antigens on the cell surface of activated T cells. Phytohemagglutinin‐activated T cells cultured for 3 days with or without conditioned medium or for 10 days with conditioned medium and mixed lymphocyte culture‐derived T cell clones were used for the analysis. Correlated measurements of the surface antigen quantity (immunofluorescence), DNA content (dye Hoechst 33342), and cell size (light scatter), not influenced by synchrony induction methods and cell fixation, were performed by dual‐beam flow cytometry. Our results demonstrate that the T cell differentiation antigens, CD3, CD4 and CD8, and class I MHC antigens are increased in density in the G1 phase for all activated T cells tested. In contrast, class II MHC antigens are increased in density in the G2 phase of activated T cells maintained with conditioned medium. Since it is known that the T cell differentiation antigens and class I MHC antigens on activated T cells are necessary for proliferation of T cells, our study suggests that this effect is more significant in the G1 phase. The cell cycle changes in expression of class I and class II MHC antigens, but not of the T cell differentiation antigens, appear to be mediated by soluble factors, probably including interferon‐γ, which could produce a differential increase of class I and class II MHC antigens on G2 phase cells.
Antigen‐presenting cell function of dendritic cells and macrophages in proliferative T cell responses to soluble and particulate antigens
Authors: Kapsenberg Martien L. , Teunissen Marcel B. M. , Stiekema Frank E. M. , Keizer Hiskias G. 
Published: February 2007

AbstractThe capacity of dendritic cells (DC) and macrophages (MΦ) to present soluble and particulate antigen was tested in an ovalbumin (OVA)‐specific T cell proliferation assay. In a comparative investigation we found that both DC and MΦ, were able to present soluble OVA, but that only MΦ, could present insolubilized OVA to T cells. DC were found to be able to present OVA in collaboration with MΦ. The failure of DC to present insolubilized OVA is probably caused by their inability to endocytose these antigens.DC appeared not to endocytose substantial amounts of soluble OVA either. In contrast to MΦ, antigen presentation by DC is not blocked by lysosomotropic drugs. Taken together, these observations suggest that DC can present soluble protein antigens without intracellular degradation.
The role of self‐Ia antigens in the murine mixed lymphocyte response
Authors: Baxevanis Constantin N. , Ioannides Constantin‐Demosthenes G. , Papamichail Michail 
Published: February 2007

AbstractMouse splenic macrophages (MΦ) were tested for their ability to potentiate in vitro allogeneic mixed lymphocyte response (MLR) of highly purified syngeneic responder T cells against allogeneic MΦ. It was shown that even extremely low numbers of MΦ, syngeneic to the responder T cells were able to induce significantly stronger MLR. This potentiating effect was demonstrated to be expressed via the self‐Ia antigens present on the surface of syngeneic MΦ., The functional involvement of self‐Ia antigens was substantiated by two approaches: (a) by using monoclonal antibodies specific for I‐region determinants of the responder haplotype MΦ, and (b) by setting up MLR cultures with stimulator MΦ of (responder X stimulator) F1 origin which express both self‐ and allo‐Ia antigens. The results obtained in this study demonstrate that the presentation of self‐Ia antigens, in conjunction with the recognition of allomajor histocompatibility complex antigens, are required for in vitro primary MLR.
Lack of correlation between hypomethylation and expression of the HLA‐DRα gene
Authors: Gambari Roberto , Senno Laura Del , Barbieri Raffaella , Buzzoni Daniele , Gustafsson Kenth , Giacomini Patrizio , Natali Pier Giorgio 
Published: February 2007

AbstractDNA methylation at the 5′‐CCGG‐3′ sites of the HLA‐DRα gene and relative flanking regions has been analyzed by Msp I and Hpa II enzymatic digestion in order to determine whether a correlation exists between DNA methylation and transcription of the HLA‐DRα gene.Unexpectedly, and in contrast to the behavior of most eukaryotic genes, no positive correlation was found between hypomethylation and expression. In fact, HLA‐DRα appears to be fully unmethylated at Msp I/Hpa II sites in K562 cells, not expressing DR molecules, and to exhibit a high degree of methylation in Colo 38 cells, which actively transcribe the gene.The unorthodox behavior of HLA‐DRα is not unique to melanoma or erythroid cells since a similar, positive correlation between methylation and expression also exists when this analysis is extended to cell lines belonging to other histotypes.
The basis for major histocompatibility complex (MHC) and immunoglobulin gene control of helper T cell idiotopes
Authors: Martinez‐A. Carlos , Pereira Pablo , De La Hera António , Bandeira Antóio , Marquez Carlos , Coutinho António 
Published: February 2007

AbstractBALB/c helper T cells, prepared against 2,4,6‐trinitrophenyl (TNP)‐derivatized syngeneic spleen cells, fail to recognize other hapten modifications [(4‐hydroxy‐3‐nitrophenyl)acetyl, fluorescein isothiocyanate] of syngeneic cells, as well as TNP‐derivatized cells from major histocompatibility complex‐congenic donors. T helper cell interactions with “presenting” cells and “target” B lymphocytes are inhibited by monoclonal antibodies directed either to the hapten or to I‐A molecules on target cells. Helper activity is also inhibited by monoclonal anti‐idiotypic antibodies directed to an idiotope expressed by the TNP‐binding myeloma protein MOPC 460, but not by soluble TNP‐protein conjugates. The study of congenic mouse strains revealed that while the fine specificity of TNP recognition and the quantitative levels of M460 idiotope expression are I‐A linked, the expression of the M 460 idiotope by helper cells is controlled by IgCh‐linked genes. Absence of anti‐idiotope inhibition of helper cells prepared in anti‐μ‐suppressed mice suggests, however, that immunoglobulin idiotype expression by T cells results from network interactions selecting available lymphocyte repertoires which operate before antigenic stimulation.
The roles of interdigitating cells and natural killer cells in the rapid rejection of allogeneic lymphocytes
Authors: Fossum Sigbjørn , Rolstad Bent 
Published: February 2007

AbstractThe fate of radiolabeled allogeneic thoracic duct lymphocytes injected into congenitally athymic, nude rats was followed by autoradiography and electron microscopy. The allogeneic cells entered the host lymphoid organs at a normal rate, but once inside the lymphoid tissue they were rapidly phagocytozed by interdigitating cells (IDC) situated in the lymph node paracortex and the splenic periarteriolar lymphoid sheaths. Neither host nor donor T cells were required to initiate phagocytosis, as purified donor B cells were also avidly ingested by the athymic host IDC. Compared with fully allogeneic cells phagocytosis of semiallogeneic donor cells was much less efficient. When natural killer cell activity was blocked by preinjecting the recipients with antibodies against natural killer cells (anti‐asialo GM1 or MRC OX‐8) phagocytosis of the allogeneic cells was strongly reduced. As IDC did not bind these antibodies, the finding indicates that natural killer cells were needed to discriminate between own and foreign lymphocytes and to kill the allogeneic cells, which were then ingested by surrounding IDC. This was further supported by the observation that dendritic, constitutively Ia+ cells from peripheral lymph, phenotypically identical to IDC, did not lyse or phagocytoze allogeneic lymphocytes in vitro.
Peritoneal Ly‐1 B cells: Genetic control, autoantibody production, increased lambda light chain expression
Authors: Hayakawa Kyoko , Hardy Richard R. , Herzenberg Leonore A. 
Published: February 2007

AbstractPrevious studies demonstrate that Ly‐1 B cells and their progenitors are clearly detectable in peritoneum in normal mice. In this publication, we show (a) that peritoneal Ly‐1 B cells resemble splenic Ly‐1 B cells with respect to surface marker expression and functional activity (autoantibody production); (b) that Ly‐1 B frequencies in peritoneum are considerably higher than in spleen; and (c) that genetic mechanisms reduce peritoneal Ly‐1 B frequencies to minimal levels in SJL‐related mice and to below detectability in CBA/N and other mice with the X‐linked immunodeficiency (Xid). In addition, we show that that peritoneal (and perhaps splenic) Ly‐1 B populations demonstrate an unique bias in immunoglobulin commitment. That is, they are selectively enriched for cells that express IgM heavy chains in association with lambda light chains. Thus, as a whole, evidence presented here defines the peritoneum as a tightly regulated lymphocyte compartment that normally houses a large population of mature Ly‐1 B cells with distinctive functional properties.
Interleukin 2 receptors are released by cells in vitro and in viva. I. Detection of soluble IL 2 receptors in cell culture supernatants and in the serum of mice by an immunoradiometric assay
Authors: Osawa Hisao , Josimovic‐Alasevic Olivera , Diamantstein Tibor 
Published: February 2007

AbstractAn immunoradiometric assay (IRMA) detecting nanogram amounts of soluble mouse interleukin 2 receptors (IL 2R) is described. The IRMA is based on the finding that the two monoclonal antibodies AMT‐13 and 7D4 react with two different epitopes of the mouse IL2R molecule. As detected by IRMA, T lymphoblasts and IL2R+ leukemic cells when incubated release IL2R in soluble form into the culture medium. In the serum of mice inoculated with syngeneic IL2R+ leukemic cells, growing as a solid tumor, IL2R were detectable. The results raise the question whether circulating IL2R are involved in down‐regulation of immune responses.
T cell activation by anti‐T3 antibodies: Comparison of IgG1 and IgG2b switch variants and direct evidence for accessory function of macrophage Fc receptors
Authors: Smith Kenneth G. C. , Austyn Jonathan M. , Hariri Gita , Beverley Peter C. L. , Morris Peter J. 
Published: February 2007

AbstractThe human T3 antigen is closely associated with the T cell receptor. Some anti‐T3 antibodies cause T cell proliferation in the presence of monocytes which have Fc receptors (FcR) that bind particular antibody subclasses. Such an interaction is thought to determine whether or not an anti‐T3 antibody is mitogenic. We examined the mitogenicity of an IgG1 antibody, UCHT1, and an IgG2b switch variant of identical specificity, UCHT1B. With autologous monocytes, 76% of individuals responded to UCHT1 and 9% to UCHT1B, falling into three patterns of responsiveness. Both antibodies in the absence of monocytes induced responsiveness to recombinant interleukin 2, even for UCHT1B nonresponder T cells. The proliferation induced by UCHT1B, however, was always less than that induced by UCHT1. These findings demonstrate the critical role played by the Fc region for mitogenesis, and suggest a possible role for the hinge region.We then obtained direct evidence that mitogenicity can be mediated exclusively via FcR. Mouse macrophages have distinct FcR: FcRI binds IgG2a but FcRII binds IgG1 and IgG2b and its function can be inhibited by the specific antibody 2.4G2. Because UCHT1 and UCHT1B were of the correct subclass to interact with FcRII we examined the accessory function of mouse peritoneal macrophages. Without exception, human T cells now responded to both antibodies. Proliferation was drastically inhibited by 2.4G2 but not by an irrelevant anti‐macrophage antibody, F4/80, nor by an anti‐human neutrophil FcR antibody, 3G8. Furthermore, 2.4G2 did not inhibit the accessory function of mouse macrophages for OKT3, an IgG2a antibody that presumably interacts with FcRI, and did not inhibit the function of human monocytes for UCHT1 and UCHT1B.Mouse B cells, in contrast to macrophages, have an FcR which binds all three subclasses, but which can be inhibited by 2.462. B cells, however, were not accessory cells for mitogenesis with UCHT1, UCHT1B or OKT3. These findings are discussed in relation to other requirements for T cell activation by anti‐T3 antibodies.
Ir gene expression on T cells: Effect of a monoclonal antibody directed against I region‐controlled determinants on T cells
Authors: Yagi Junji , Nonaka Makoto , Abe Ryo , Tada Tomio 
Published: February 2007

AbstractA monoclonal antibody directed at an I region‐controlled epitope uniquely expressed on T cells (Iat) was studied for its in vivo effect on the antibody response under the control of an Ir gene. The antibody was produced by a hybridoma made from A.TH spleen cells immune to A.TL (anti‐Ik), that was selected for its reactivity with T but not B cells and macrophages, and thus was designated as anti‐Iatk. The injection of this anti‐Iatk into H‐2k, H‐2b and H‐2k×bF1 mice resulted in the suppression of antibody response to poly‐L‐(His,Glu)‐poly‐D,L‐Ala–poly‐L‐Lys [(H,G)‐A–L] in H‐2k and F1 mice but not that to poly‐L‐(Tyr,Glu)‐poly‐D,L‐Ala–poly‐L‐Lys [(T,G)‐A–L] both in H‐2b and F1 mice. The adoptive cell transfer of the combinations of anti‐Iatk‐or normal mouse serum‐treated T and B cells into irradiated hosts demonstrated that anti‐Iatk primarily affected (H,G)‐A–L‐specific helper T cells but not B cells and macrophages, resulting in the specific elimination of the antibody response. Suppressor T cells were not induced by the treatment with anti‐Iatk. The antibody specifically eliminated the (H,G)‐A–L‐specific but not (T,G)‐A–L‐specific helper T cells in F1 spleen cells that had been primed with both (H,G)‐A–L and (T,G)‐A–L. The results indicated that anti‐Iatk affected the H‐2k‐associated Ir gene function born by T cells but not by antigen‐presenting cells, which was expressed on F1 helper T cells with apparent exclusion of the other allele, and implied that the Iat antigen on helper T cells is one of the sites of expression of Ir genes.
In the murine syngeneic mixed lymphocyte reaction, one T cell subset replicates in the presence of B cells or macrophages and replication is inhibited by simultaneous presence of both stimulator cells
Authors: Stevenson J. Ross , Battisto Jack R. 
Published: February 2007

AbstractThe murine T‐non‐T cell syngeneic mixed lymphocyte reaction has been examined to determine whether B cells and macrophages stimulate the same or different subpopulations of T cells. By using experiments in which replicating T cells were suicided, we found that the two different stimulators caused replication of what appears to be the same subset(s) ot T cells. Since B cells and macrophages carry the same stimulating antigens (class II plus mls or others), one would expect them to stimulate the same T cell subpopulations were it not that they have been reported to stimulate two different subpopulations in humans. When B cells and macrophages were simultaneously used as stimulators, diminished T cell replication occurred. We have found the reduced response is not attributable to exhaustion of culture nutrients or to displacement of the response peak. Other possibilities to account for this marked reduction have been discussed from the viewpoint of suppression emanating from macrophages and/or T cells.