bluuebunny/crossref_metadata_2025_split huggingface dataset:
Antibody 12‐15 cross‐reacts with mouse Feγ receptors and CD2: study of thymus expression, genetic polymorphism and biosynthesis of the CD2 protein
Authors: Altevogt Peter , Kohl Ulrike , Hoegen Paul Von , Lang Elke , Schirrmacher Volker 
Published: March 2007

AbstractPreviously we described a monoclonal antibody (mAb 12–15) that reacted with murine Fc receptor proteins (betal, beta2 and alpha) and an undefined molecule of 37 kDa (beta3) on certain types of cells. Here we present serological and biochemical evidence that the beta3 chain is expressed on mouse thymocytes and that it is identical to the CD2 antigen. By immunofluorescence staining and cytofluorographic analysis >95% of thymocytes were positive. Brightly staining cells coincided with cortison‐resistant thymocytes suggesting that mature thymocytes expressed higher levels of the antigen. Biosynthetic labeling of DBA/2 thymocytes with [35S]methionine showed that the size of the CD2 precursor molecule was 43 kDa which was processed to approximately 55–65 kDa in the mature molecule. mAb 12–15 was also reactive with the tunicamycin‐treated form of the CD2 antigen suggesting that the cross‐reactive epitope was of protein nature. Comparison of different mouse strains indicated that two molecular forms of CD2 exist. On BALB/c thymocytes, the relative mass of the native molecule was approximately 60–70 kDa (CD2.1) and slightly larger than in DBA/2 (CD2.2). Following endoglycosidase F treatment both proteins still showed a slight difference in electrophoretic mobility. Several inbred mouse strains were analyzed for expression of CD2 forms. When mAb 12–15 was used in cyotoxic T lymphocyte inhibition experiments using specific CTL and tumor target cells it was found that the antibody could specifically inhibit CTL‐mediated lysis presumably by interfering with CD2 function.
The epigenetic influences of bone marrow and fetal liver stroma cells on the developmental potential of Ly‐1pro‐B lymphocyte clones
Authors: Palacios Ronald , Stuber Susanne , Rolink Anthonius 
Published: March 2007

AbstractThe Ly‐1 Mac‐1 B‐220 CC11 progenitor clones LyD9 and LyB9 were previously shown to give rise to Ly‐1IgM B lymphocytes either in vivo or in vitro by coculture with nonlymphoid accessory cells from spleen and lipopolysaccharide. The clones did not generate T lymphocytes either in vivo or in vitro. We now find that both LyD9 and LyB9 progenitors are induced to differentiate in vitro by co‐culture with the RP.0.10 bone marrow stroma clone or with heterogeneous marrow‐adherent stroma cell populations obtained from adult mice into Ly‐1‐IgM B lymphocytes as well as myeloid GM1.2 Mac‐1 cells. We could obtain evidence that a high proportion of LyD9 and LyB9 cells already switched off expression of Ly‐1 and CC11 (interleukin 3 receptor) surface molecules 2 days after initiation of the cultures, and by days 8–10 of culture no detectable Ly‐1 cells and only about 20% CC11 cells were observed. Ly‐1 surface expression could not be re‐induced on the progeny of LyD9 and LyB9 progenitors generated under the influence of marrow stroma cells. Remarkably, the LyD9 and LyB9 progenitors gave rise to both Ly‐1IgM and Ly‐1‐IgM B cells upon culture with heterogeneous stroma monolayers obtained from 18‐day fetal liver. Finally, the differentiating property of the stroma cells for the LyD9 and LyB9 progenitors could not be replaced with soluble factors produced either spontaneously or after stimulation by the marrow stroma cells. Our results show the importance of epigenetic influences provided by a given microenvironment on the developmental potential of B cell progenitors. They provide direct evidence that the same pro‐B lymphocyte can give rise to both Ly‐1 and Ly‐1‐IgM B cells depending on both the time of development and the tissue of origin of stroma cells with which the B cell progenitor interacts. Also, the results strongly suggest that cell contact between the stroma cell and the B cell progenitor is essential to induce rearrangement and expression of the Ig genes in pro‐B lymphocytes.
Characterization and growth factor requirements of SJL lymphomas. II. Interleukin 5 dependence of the in vitro cell line, cRCS‐X, and influence of other cytokines
Authors: Lasky Jennifer L. , Jeanette Thorbecke G. 
Published: March 2007

AbstractFollicular B cell lymphomas of SJL mice [reticulum cell sarcoma (RCS)] are dependent on syngeneic Ly‐1,2‐ T cells for their growth. These T cells produce a number of lymphokines in response to stimulation with γ‐irradiated RCS cells including interleukin (IL) 2, interferon‐γ (IFN‐γ), IL 4 and IL 5, some of which may be required for growth of the tumor. Previous studies have shown that an RCS cell line, cRCS‐X, can be maintained in vitro indefinitely, if the cultures are supplemented with Y‐irradiated lymph node (LN) cells or with a preparation of human B cell growth factor (BCGF). In the present studies, the growth requirements of this cell line were analyzed in more detail in short‐term assays of both [3H]thymidine incorporation and colony formation in agarose. Recombinant murine IL 5 caused dose‐dependent proliferation of cRCS‐X cells similar to that induced with BCGF. The level of colony formation by cRCS‐X cells induced by optimal concentrations of BCGF was not increased further by the addition of IL 5, suggesting that the two factors act via a common mechanism. IL 1 and IFN‐y each enhanced cRCS‐X proliferation induced by BCGF or IL 5 in both assays. The effects of IL 1 plus BCGF, IFN‐γ plus BCGF, and IL 1 plus IL 5 were clearly synergistic. Preincubation of cRCS‐X cells with IL 1 enhanced their ability to proliferate in response to BCGF or IL 5 in [3H]thymidine incorporation assays, but the reverse sequence of cytokine addition showed no effect of IL 1. No such effect was seen with IFN‐gM. Indeed, IL 1 and IFN‐gM appeared to affect BCGF‐induced cRCS‐X growth by different mechanisms and their combined effects were greater than that of IL 1 or IFN‐gM added separately. None of the other cytokines studied, including IL 2, IL 3, IL 4, IL 6, tumor necrosis factor‐γ, granulocyte monocyte‐colony‐stimulating factor or transforming growth factor‐β, had any detectable effect on cRCS‐X cells, either alone or in combination with BCGF or IL 5.Like IL 5, SJL γ‐irradiated LN cells induced cRCS‐X colony‐forming units (CPU) in a dose‐dependent manner. IL 1, or the combination of IL 1 plus IFN‐γ, clearly synergized with LN cells in the induction of cRCS‐X CFU, suggesting that LN cells contribute IL 5. The level of CFU induced by an optimal dose of BCGF was enhanced further in the presence of LN cells and IL 1. However, this was not observed when both IL 1 and IFN‐γ were added to the medium, in which case the level of CFU induced by an optimal dose of BCGF was not further enhanced by the addition of an optimal dose of γ‐irradiated LN cells. In combination with previous observations, these data support the hypothesis that RCS growth in vivo and in vitro is dependent on and promoted by IL 5 and IFN‐γ produced by syngeneic RCS‐specific helper T cells, and IL 1 produced by macrophages.
Resistance to experimental autoimmune encephalomyelitis induced by neonatal tolerization to myelin basic protein: clonal elimination vs. regulation of autoaggressive lymphocytes
Authors: Qin Yufen , Sun Deming , Goto Masamichi , Meyermann Richard , Wekerle Hartmut 
Published: March 2007

AbstractThe target autoantigen of experimental autoimmune encephalomyelitis (EAE), myelin basic protein (MBP), appears late in ontogeny. In the rat MBP is expressed first on days 2–3 post partum, at a development stage, when self tolerance to most other autoantigens has already developed.To shed light on the cellular mechanisms that lead to immunological self tolerance to MBP, we treated neonatal rats with high doses of MBP before ontogenetic appearance of this autoantigen. We found that high doses are required to confer MBP‐specific tolerance lasting until the adult life. Neonatally tolerized, adult rats are completely resistant to induction of EAE by injection of MBP in complete Freund's adjuvant (CFA). Upon MBP CFA challenge, these animals develop a limited humoral response to MBP, but are completely unreactive to MBP on the T cell level. The function of antigen‐presenting cells is unchanged by neonatal tolerization, and there is no evidence for the induction of suppressive mechanisms. Transfers of large numbers of tolerized lymphocytes to normal hosts fails to interfere with EAE inducibility. Moreover, neonatally tolerized lymphocytes do not reduce MBP reactivity of primed lymph node cells or T line cells in vitro. Finally, neonatally tolerized rats are susceptible to EAE transferred by activated primed lymphocytes or by in vitro‐activated MBP‐specific T line cells.The apparent deletion of MBP‐specific T lymphocytes in neonatally tolerized rats is in striking contrast to the physiological self tolerance to MBP, which is characterized by the presence of MBP‐specific clones in the normal immune repertoire.
Tolerance to class I major histocompatibility complex antigens in chicken B cell chimeras. Effect of B cell depletion on transferability of tolerance
Authors: Lehtonen Lasse , Vainio Olli , Veromaa Time , Toivanen Paavo 
Published: March 2007

AbstractB cells from bursa of Fabricius of newly hatched chickens are able to reconstitute the B cell compartment of chemically bursectomized chickens. The resulting B cell chimerism can be detected with monoclonal antibodies against donor B cell alloantigen. Chimeric chickens accept donor‐type skin grafts and are unresponsive to donor major histocompatibility complex (MHC) antigens in graft‐vs.‐host splenomegaly assay and mixed lymphocyte reaction. To study the capability of B cells to induce tolerance to selected MHC antigens, we transplanted class I or total MHC‐incompatible bursa cells into cyclophosphamide‐treated recipients. The recipients of class I or total MHC‐incompatible bursa cells were equally tolerant of donor‐MHC antigens. To further analyze the mechanisms of tolerance to class I antigens vs. total MHC, spleen cells from tolerant chickens were transferred to irradiated, histocompatible secondary hosts. The secondary recipients were also unresponsive to bursa cell donor‐strain MHC antigens. However, if the chimeric B cells were depleted before the spleen cell transfer, the transfer of tolerance to total MHC was severely inhibited. Instead, most recipients of B cell‐depleted spleen cells tolerant of class I antigens were still tolerant of bursa cell donor MHC. Our results indicate differences in the transferability of tolerance to class I antigens vs. entire MHC, although in primary recipients of bursa cells the tolerance is similar. These data suggest that a mechanism that is not dependent on the presence of donor cell chimerism contributes to the maintenance of tolerance to donor class I antigens. The transfer of tolerance to total MHC disparity requires the presence of chimeric cells indicating that donor alloantigen expression is needed for induction of tolerance in the secondary hosts.
Molecular characterization of the VH region of murine autoantibodies from neonatal and adult BALB/c mice
Authors: Sollazzo Maurizio , Hasemann Charles A. , Meek Kateryn D. , Glotz Denis , Donald Capra J. , Zanetti Maurizio 
Published: March 2007

AbstractWe report on the molecular characterization of the heavy (H) chain variable (V) region of two murine autoantibodies reacting with a conventional self antigen, thyro‐globulin (Tg), originated from unimmunized/unstimulated neonatal mice (clone B10H2) and from an adult hyperimmunized mouse (clone 62), respectively. Serologically, both hybridoma antibodies express the same idiotype (Id). By cloning and sequencing we demonstrated that their VH regions are encoded by identical VDJ gene elements including the VD and DJ joints. This VH belongs to the VH 7183 gene family, the most 3′‐end proximal family in the murine genome. The D segment is unique and only 50% similar to any murine D segment. The J segment utilized is germ‐line JH4. The cloned DNA rearrangement was transfected into the J558L myeloma cells and the secreted antibody was found to express the reference Id on the H chain, hence proving that the productive VDJ rearrangement had been identified. These results show that a spontaneously arising and an antigen‐induced autoantibody use an identical VDJ gene rearrangement and that after hyperimmunization somatic mutation did not occur. The significance of this finding with respect to ontogeny of the B cell repertoire is discussed.
The mucosa of the male genital tract; part of the common mucosal secretory immune system?
Authors: Fritz Franz Joachim , Westermann JÜRgen , Pabst Reinhard 
Published: March 2007

AbstractThe selective migration of mucosal‐derived lymphoid blasts to other mucosal organs is taken to be an essential part of the common secretory immune system. In rats, proliferating lymphoid cells from mesenteric lymph nodes (mLN) and peripheral lymph nodes (pLN) were labeled in vitro using two different techniques, in order to test the hypothesis that the mucosa of the male genital tract is a preferential site for mLN lymphoid blasts to home to. A low but significant migration to male genital organs was found, but with no difference between blasts from pLN and mLN. Thus there is no evidence to include the male genital tract in the common mucosal secretory immune system.Recirculating lymphocytes from the thoracic duct entered the male genital organs with a similar distribution to the pattern of lymphoid blasts. There is probably an exchange between these immigrating lymphocytes and the different subsets, which are localized in the epithelium (T suppressor) and interstitial tissue (T helper) in male genital organs. The lymphoid cells in the male genital tract might play an important role in the immune function of seminal fluid and in sexually transmissible diseases.
Co‐cross‐linking of surface immunoglobulin Fcγ receptors on B lymphocytes uncouples the antigen receptors from their associated G protein
Authors: Rigley Kevin P. , Harnett Margaret M. , Klaus G. B. 
Published: March 2007

AbstractCross‐linking of surface Ig receptors (sIg) by mitogenic forms of anti‐Ig antibodies (e.g. F(ab′)2 fragments of rabbit anti‐Ig) causes the rapid, and prolonged breakdown of phosphatidylinositol 4,5‐bisphosphate. This response involves an unidentified guanine nucleotide regulatory protein (termed Gp), which couples sIg to the polyphosphoinositide‐specific phosphodiesterase. Intact (IgG) rabbit anti‐Ig antibodies, which co‐cross‐link sIg and Fcγ receptors on B cells, only induce short‐lived inositol phospholipid breakdown and abortive B cell activation. We show here that in permeabilized B cells intact anti‐Ig inhibits the reconstituted breakdown of inositol phospholipids given by a combination of F(ab′)2 anti‐Ig and the non‐hydrolyzable GTP analogue guanosine‐5′‐O‐(3‐thiotriphosphate) (GTPγS), but not the basal stimulation of Gp induced by GTPγS alone. These results therefore indicate that cocross‐linkage of sIg and Fcγ receptors on B cells uncouples the antigen receptors from the associated G protein, but does not affect coupling between Gp and the phosphodiesterase. These observations therefore provide further insight into the mechanisms whereby engaging Fc receptors on B cells, by antigen‐antibody complexes for example, could modulate antigen‐induced B cell activation.
Permanent alteration of the murine Ly‐1 B repertoire due to selective depletion of Ly‐1 B cells in neonatal animals
Authors: Lalor Paul A. , Stall Alan M. , Adams Sharon , Herzenberg Leonore A. 
Published: March 2007

AbstractStudies presented here demonstrate that paternal allotype Ly‐1 B cells are permanently depleted following neonatal treatment with antibodies to the paternal IgM allotype. Paternal allotype conventional B cells, in contrast, are temporarily depleted by treatment with either anti‐IgM or anti‐IgD allotype antibodies and return rapidly to normal frequencies once the antibody treatment disappears. These differences are explained by basic developmental differences between Ly‐1 B and conventional lineage B cells. That is, the conventional B cell population is replenished from Ig‐ precursors throughout life and, therefore, is only temporarily affected when depleted in neonates. The Ly‐1 B cell population, in contrast, develops from Ig‐ progenitors during the prenatal and neonatal life but survives because it is exclusively self‐replenishing in adults. Therefore, elimination of a population of Ly‐1 B cells from neonates is tantamount to removing it forever.These findings suggest that while conventional B cells turn over rapidly and have an effectively unlimited repertoire, Ly‐1 B cells express a repertoire whose composition is strongly influenced by neonatal conditions that favor or select against the retention of cells producing certain antibody molecules. Thus, Ly‐1 B cells play a unique role in the immune system in that they retain indefinitely the history of the neonatal animal's immunological experience.
The immune response of BALB/c mice to influenza hemagglutinin: commonality of the B cell and T cell repertoires and their relevance to antigenic drift
Authors: Barnett Barbara C. , Graham Christine M. , Burt David S. , Skehel John J. , Brian Thomas D. 
Published: March 2007

AbstractAn extensive analysis of the class II (I‐Ad)‐restricted T cell repertoire for influenza hemagglutinin (HA) of the H3 subtype, elicited by natural infection, has shown that a majority of CD4 memory T cell clones focus on antibody‐binding regions of HA, sites B and E, and are sensitive to the residue substitutions that have occurred in these regions during antigenic drift. The proliferative responses of CD4 clones to synthetic peptides have identified T cell epitopes within site B, HA1 177–199 and HA1 182–199, and site E, HA1 56–76. The recognition specificity of T cell clones for antibody‐selected mutant viruses, with single amino acid substitutions within these recognition sites identified residues 63, 189, 193 and 198 as being important for T cell recognition and thus established that BALB/c, CD4 T cell clones were sensitive to the same substitutions known to abrogate BALB/c antibody recognition of the native HA. Our findings indicate extensive commonality of the B cell and T cell repertoires for HA, which may be relevant to an understanding of the immune pressures for antigenic drift, and, moreover, suggest that the antigen‐specific B memory cell may be instrumental in selection of the peripheral T cell repertoire.
The structural requirements for class II (I‐Ad)‐restricted T cell recognition of influenza hemagglutinin: B cell epitopes define T cell epitopes
Authors: Graham Christine M. , Barnett Barbara C. , Hartlmayr Irene , Burt David S. , Faulkes Ralph , Skehel John J. , Brian Thomas D. 
Published: March 2007

AbstractA majority of I‐Ad‐restricted CD4 clones elicited by influenza X31 (H3N2) virus infection, recognize a synthetic peptide of hemagglutinin (HA) corresponding to an antibody binding region of the HA1 subunit (site B: HA1 177–199). The structural requirements for class II‐restricted T cell recognition were investigated by determining the proliferative responses of representative CD4 clones to truncated HA1 peptides and synthetic peptide analogues. Two distinct T cell epitopes were identified and CD4 clones, specific for either determinant, were sensitive to the same single amino acid substitutions in synthetic peptides at HA1 193 S→N or HA1 198→E, that had featured in antigenic drift and abrogated antibody binding to native HA. Competitive inhibition studies, between stimulatory HA1 peptides and non‐stimulatory analogue peptides, for antigen presentation to CD4 clones established that the 193 S → N and 198 A → E substitutions could affect either interaction with the T cell receptor or class II molecule, according to the specificity of the CD4 clone examined. The structural requirements for class II‐restricted T cell recognition of the linear sequence determinants of HA are, therefore, integrally linked to conformationdependent antibody recognition of the native molecule.
Regulation of human B cell activation and antibody production by non‐major histocompatibility complex‐restricted cytotoxic T lymphocytes
Authors: Boué François , Goujard Cécile , Delfraissy Jean‐françois , Galanaud Pierre , Hercend Thierry 
Published: March 2007

AbstractTo determine whether non‐major histocompatibility complex‐restricted cytotoxic human T lymphocytes (NrCTL) are involved in the regulation of antibody response, we studied the effect of a CD3, T cell receptor (TcR)‐α/β, NKH1 clone named JT9 on B cell proliferation and differentiation. It was found that low amounts of JT9 clone (5%) profoundly inhibited (> 80%) in vitro specific anti‐trinitrophenyl primary antibody response. This inhibition did not need the presence of autologous T cells and took place at the induction phase of the antibody response. JT9 clone had no effect on resting B cells but enhanced proliferation of anti‐μ‐stimulated B cells. Respective involvements of cell to cell interaction, cytotoxicity and lymphokines were investigated. (a) The effect of monoclonal antibodies (mAb) inhibiting cytotoxic properties of JT9 clone, i.e. an anti‐clonotypic structure mAb and a mAb directed against a target cell antigen similar to 4F2, were studied. These mAb did not reverse the effects of JT9 on B cell activation and differentiation. Thus, these contrasting effects of JT9 clone on B cell response did not seem to involve an interaction of JT9 clone TcR with its target or, further, cytotoxic properties for which this clone had been characterized. (b) Supernatant of JT9 clone stimulated by cross‐linking of TcR complex, in the absence of interleukin 2, exerted a proliferative effect on anti‐μ‐stimulated B cells but not on resting B cells. These findings suggest that JT9 clone could secrete a B cell growth factor – like activity and that NrCTL cells may play an important role in the regulation of antibody response.
Production of macrophage‐, granulocyte‐, granulocyte‐macrophage‐ and multi‐colony‐stimulating factor by peripheral blood cells
Authors: Oster Wolfgang , Lindemann Albrecht , Mertelsmann Roland , Herrmann Friedhelm 
Published: March 2007

AbstractThe specific cell sources and signals for induction of various colony‐stimulating factors (CSF) in peripheral blood mononuclear cells (PBMC), purified T lymphocyte and monocyte (Mo) populations have been investigated. In the absence of exogenous activating stimuli, human PBMC, T cells and Mo failed to produce stable cytoplasmic mRNA for CSF for macrophages (M‐CSF or CSF‐1), for granulocytes (G‐CSF), for granulocytes and macrophages (GM‐CSF) and for multilineage CSF [multi‐CSF, interleukin (IL) 3] and thus failed to release CSF proteins. However, after stimulation with phorbol myristate acetate and phytohemagglutinin, M‐, G‐, GM‐ and multi‐CSF mRNA became detectable in PBMC, resulting in the secretion of the respective proteins. Identical culture conditions resulted in synthesis of only G‐ and M‐CSF by purified Mo, whereas purified T lymphocytes produced GM‐CSF and multi‐CSF only. When Mo or T lymphocytes were exposed to recombinant human interferon‐γ or were stimulated by triggering the epitopes recognized by the monoclonal antibodies anti‐T112 and T113, respectively, again disparate CSF expression patterns were found to be associated with both cell species. Moreover, IL2‐receptive T lymphocytes showed the same distinct pattern of CSF secretion when activated by recombinant human IL2.