bluuebunny/crossref_metadata_2025_split huggingface dataset:
Helix pomatia A hemagglutinin: selectivity of binding to lymphocyte surface glycoproteins on T cells and certain B cells
Authors: Axelsson B. , Kimura A. , Hammarström S. , Wigzell H. , Nilsson K. , Mellstedt H. 
Published: February 2007

AbstractHuman and mouse lymphocytes were surface‐labeled by lactoperoxidasecatalyzed iodination, or by galactose oxidase oxidation followed by reduction with tritiated sodium borohydride. The labeled cells were lysed with Nonidet P‐40. Proteins binding to Helix pomatia A hemagglutinin (HP) were isolated by affinity chromatography on HP‐Sepharose and analyzed by sodium dodecyl sulfate polyacrylamide gel electrophoresis and autoradiography.A major cell surface glycoprotein (apparent mol. wt. 150000, using reducing conditions) on human lymphocytes was responsible for almost all binding of HP. This protein was present on normal and malignant thymus‐derived lymphocytes, e.g. thymocytes, blood T cells and T leukemia cell lines. It was also found on chronic lymphocytic leukemia cells, one null cell leukemia line, one unidentified leukemia line, one lymphoblastoid cell line of B origin and on one stem cell lymphoma line. In contrast, this protein was not found on various B cells at different steps of differentiation, e.g. four B lymphoma lines or one myeloma line. It was also absent from a histiocytic leukemia line. However, two of the four B lymphoma lines and the myeloma line had another HP‐binding surface glycoprotein (mol. wt. 200000) instead of the 150000 protein.Studies of mouse lymphocytes similarly showed that thymus‐derived lymphocytes (normal and malignant) but not normal adult B cells expressed a major HP‐binding surface glycoprotein of apparent mol. wt. 130000 (reducing conditions).
Nature of T cell‐macrophage interaction in helper cell induction in vitro I. Evidence for genetic restriction of T cell‐macrophage interactions prior to T cell priming
Authors: Erb P. , Meier Barbara , Kraus Daniele , Von Boehmer H. , Feldmann M. 
Published: February 2007

AbstractThe nature of the genetic restriction of T cell‐macrophage interaction in helper cell induction has been investigated. By incubating F1 hybrid T cells with keyhole limpet hemocyanin and macrophages of one parental haplotype, helper cells were generated that cooperated with B cells of either parental haplotype, provided macrophages of the haplotype used for the initial priming were present in the cooperative culture. The experiment is in line with the view that F1 T cells reactive to a given antigen contain at least two independent clones, each responsive to antigen recognized in conjunction with macrophages of one parental strain, and moreover, indicates that genetic restriction of T cell‐macrophage interaction may be induced by priming. However, by using F1 T cells it is not possible to exclude that restriction is already manifest prior to priming. Thus, experiments were performed using T cells from chimeric mice instead of F1 mice. Chimeric mice, prepared by injecting lethally irradiated F1 mice with anti‐θ‐treated bone marrow cells of both parental types, have two histoincompatible lymphoid pools which are mutually tolerant. T cells of one type, prepared by treatment with anti H‐2 serum and complement, were not able to interact with macrophages of the other histoincompatible parental type indicating that genetic restrictions in interaction may be expressed prior to antigenic stimulation.The possibility that suppression is the mechanism of the restriction of T cell‐macrophage interaction in helper cell induction has been investigated and excluded, based on several lines of evidence. First, genetic restriction is not broken by treatment of helper cells induced by allogeneic genetically related macrophage factors (GRF) (or mixtures of syngeneic and allogeneic GRF) with antisera which kill suppressor cells, which may have masked the help induced with allogeneic GRF. Second, chimeric mice, which have not been shown to have suppressor cells, still show the same genetic restriction. The implication of these findings for patterns of T cell recognition is discussed.
Preparation and characterization of anti‐framework antibodies to the heavy chain variable region (VH) of mouse immunoglobulins
Authors: Ben‐Neriah Y. , Wuilmart C. , Lonai P. , Givol D. 
Published: February 2007

AbstractThe heavy chain variable portion of mouse myeloma protein MOPC‐315 (α, λ2) was obtained from its Fv fragment (J. Hochman, D. Inbar and D. Givol, Biochemistry 1973. 12: 1130.) and was used to immunize rabbits. Rabbit anti‐VH antibodies precipitated VH, Fv and the intact protein 315. The VH region specificity of these antibodies was evident from the line of identity in agar gel diffusion between Fv and M315, and from the lack of precipitation with another a chain of XRPC‐25 or with light (L) chains. Radioimmunoassay binding and inhibition studies demonstrated that anti‐VH 315 antibodies cross‐react with heavy (H) chains derived from various mouse myeloma proteins (MOPC‐460, XRPC‐25, MOPC‐104E, UPC‐10, TEPC‐15, HOPC‐8, MOPC‐167) as well as with H chains derived from mouse IgG. These H chains can inhibit 90–100% of the binding of VH 315 by anti‐VH indicating extensive sharing of antigenic determinants by various VH regions. The relative affinity of anti‐VH for various H chains was 20–1000‐fold weaker than its affinity for the MOPC‐315 H chain. The cross‐reaction of the various H chains was independent of antibody specificity, subclass, subgroup or CH allotype. This suggests that anti‐VH may be considered as anti‐V framework antibody.Anti‐VH 315 cross‐reacts with isolated H chains but not with intact molecules and can therefore be used to detect VH determinants only in the absence of chains.
Idiotype suppression. III. Induction of unresponsiveness to sensitization with anti‐idiotypic antibody: identification of the cell types tolerized in high zone and in low zone, suppressor cellmediated, idiotype suppression
Authors: Hetzelberger Doris , Eichmann K. 
Published: February 2007

AbstractUnresponsiveness of strain A/J mice to sensitization with guinea pig IgG anti‐A5A idiotypic antibody is induced by prior injection of guinea pig IgG2 anti‐A5A idiotypic antibody or unfractionated anti‐A5A antiserum. Two different forms of unresponsiveness could be induced depending on the dose of IgG2 anti‐A5A: high‐zone suppression was maximal one week after injection, could not be transferred by lymphocytes and disappeared within 3 to 4 weeks. Low‐zone suppression took 7 weeks to fully develop and could be transferred by splenic and lymph node T cells.High‐zone suppression is expressed as transient unresponsiveness in both the A5A‐idiotype‐positive T helper as well as B precursor cell compartments. Low‐zone, suppressor cell‐mediated suppression is expressed as chronic unresponsiveness in the A5A‐idiotype‐positive T helper cell compartment only, whereas the A5A‐idiotype‐positive B precursor cells remain fully responsive as revealed by addition of nonsuppressed T helper cells. These data satisfactorily explain that suppression of T helper cell‐independent idiotypes does not involve T suppressor cells. However, since the presence of suppressor T cells is accompanied by selective unresponsiveness of A5A‐positive B cells, the data imply that idiotypic restrictions exist for T‐B cooperation.
Recognition of idiotypes in lymphocyte interactions II. Antigen‐independent cooperation between T and B lymphocytes that possess similar and complementary idiotypes
Authors: Eichmann K. , Falk I. , Rajewsky K. 
Published: February 2007

AbstractAntigen‐independent cooperation between T and B lymphocytes is demonstrated in vitro in two different experimental protocols: (a) B cells from A/J mice immunized in vivo either with Group A streptococcal vaccine (Strep.A) or with the IgG1 fraction of guinea pig anti‐idiotypic antibody to the A5A idiotype, mature into plaque‐forming cells (PFC) with specificity for Group A streptococcal carbohydrate (A‐CHO) during a 4‐day culture together with T cells from A/J mice immunized in vivo with A5A idiotypic antibody. (b) B cells from A/J mice immunized in vivo with Strep.A generate PFC specific for A‐CHO when cultured in the presence of small concentrations of anti‐A5A idiotypic antibody and of T cells primed with Strep.A. In both cases, antigenindependent cooperation is idiotypically selective, such that only those B cells respond that secrete antibody with the A5A idiotype.The data are interpreted to suggest that, in addition to antigen‐specific helper cells, idiotype‐specific may participate in antibody responses, and that the latter type of help may be responsible for the idiotypic selectivity in T‐B cooperation observed previously. Furthermore, idiotype‐specific cooperation may be a means to generate and maintain B cell diversity during the evolution and ontogeny of the immune system.
Cytological and functional analysis of inflammatory infiltrates in human malignant tumors II. Functional investigations of the infiltrating inflammatory cells
Authors: Tötterman T. H. , Häyry P. , Saksela E. , Timonen T. , Eklund B. 
Published: February 2007

AbstractSix individual human carcinomas displaying an unusually strong inflammatory reaction were dispersed by a mixture of collagenase and deoxyribonuclease and fractionated in 1 × g velocity sedimentation. This method gave an excellent separation of cancer cells from infiltrating inflammatory cells. The viability in both cell populations exceeded 95%. Blood mononuclear leukocytes and tumor‐infiltrating inflammatory cells from the cancer‐bearing patients were then tested in the short‐term 51Cr release test for in vitro cytotoxicity to their autochtonous tumor cells and to target cells known to be sensitive to the socalled “natural killer” (NK) lytic effects. In two patients with testicular seminoma, the blood leukocytes were strongly cytotoxic to the patients' own tumor cells; in one case of thyroid carcinoma, the patient's blood leukocytes also exhibited a distinct albeit slight cytotoxic activity towards his autochtonous tumor. Blood mononuclear leukocytes of all these cancer patients were strongly cytotoxic to the NK targets MOLT‐4, K‐562, chicken red cells and human embryonic fibroblasts (Ef). In striking contrast, the tumor‐infiltrating inflammatory cells were entirely unable to lyse the autologous tumor cells. Neither, with the exception of the Ef targets, did the tumor‐infiltrating cells display any cytotoxic activity towards the NK targets. The findings demonstrate a widespread functional paralysis (or absence) of effector cells directed to the patients' own autologous tumor cells and to NK target cells in the tumor‐infiltrating inflammatory cell population.
Induction in vitro of reversible immunosuppression and inhibition of B cell receptor regeneration by defined metabolites of cyclophosphamide
Authors: Shand F. L. , Howard J. G. 
Published: February 2007

AbstractA number of defined metabolites and derivatives of cyclophosphamide (CY) were compared with the parent compound for their capacity to induce suppression of humoral antibody responses in vivo and in vitro and to inhibit the regeneration of surface immunoglobulin (sIg) receptors on B cells subsequent to capping with anti‐Ig serum. Both functions were inhibited by exposing spleen cells in vitro to the most active compounds (4‐hydroperoxycyclophosphamide and phosphoramide mustard) in concentrations of 10 μg/ml or less. Although these inhibitory activities were found to be restricted to those molecules with demonstrable alkylating activity, they are nevertheless reversible and not dependent on events leading to cell death.Inhibition with microsomally activated CY in vitro rendered splenic B cells hyper‐susceptible to tolerance induction by levan, although in the absence of this antigen they recovered full responsiveness to it within 7–10 days. Since lethally irradiated mice repopulated with adult bone marrow cells do not regenerate normal responsiveness to polysaccharide antigens in less than 50–100 days (Howard, Moreno, Hale and Vicari, Eur. J. Immunol. 1977. 7: 431.), it is considered that the rapid recovery by CY‐treated spleen cells involves reversal of suppression in B cells and not renewal from stem cells. Our previous proposal (Shand and Howard, Nature 1978. 271: 255.) that impairment of B cell receptor regeneration by CY is causally related to its capacity to promote B cell tolerance induction by thymus‐independent antigens is supported by the present data.
Detection and partial characterization of a new murine T‐lineage antigen: evidence for its enzymatic modulation
Authors: Thiele Heinz‐Günter , Arndt Rüdiger , Hamann Alf , Stark Rosemarie 
Published: February 2007

AbstractA molecule with an apparent molecular weight of 21000 daltons was found to be a predominating differentiation antigen of peripheral rat T lymphocytes. This antigen is also expressed on the cell surface of thymus lymphocytes though partially in masked form. The observation that these determinants could be unmasked by neuraminidase treatmentin vitrosuggests that enzymatic processes may play an important role in antigenic transformation along the differentiation pathway of T axis lymphocytes. Since this structure was found to be displayed also by peritoneal exudate macro‐ phages, it is referred to as T lymphocyte‐macrophage antigen. The finding that an identical antigen could be identified in the mouse suggests its more common biological significance.
Immune depression in trypanosome‐infected mice. III. Suppressor cells
Authors: Pearson Terry W. , Roelants Georges E. , Pinder Margaret , Lundin Lena B. , Mayor‐Withey Kathleen S. 
Published: February 2007

AbstractSpleen cells from trypanosome‐infected mice strongly suppressed lymphocyte stimulation induced in normal spleen cell populations by lipopolysaccharide, concanavalin A or allogeneic (H‐2‐different) stimulator cells. This suppression was not H‐2‐restricted, as responses of spleen lymphocytes both allogeneic and syngeneic to the suppressors were inhibited. Irradiation or mitomycin C treatment of suppressor populations markedly reduced but did not eliminate suppressor activity. Suppressor populations were effective when present in very low numbers. Addition of suppressor cells to mixed lymphocyte cultures at various intervals after initiation of the cultures showed that the suppressors require 48 h to manifest their activity. Cell depletion or enrichment experiments indicate that the mechanism of suppression is complex and involves more than one cell type.
T cell‐produced immunoglobulin binding factor (IBF) bears determinants coded for by the I region of the major histocompatibility complex and lacks allogeneic restriction
Authors: Rabourdin‐Combe Chantal , Fridman Wolf H. , Dorf Martin E. , Guimezanes Annick 
Published: February 2007

AbstractAn immunoglobulin binding factor (IBF) produced by in vivo alloantigen‐activated T cells suppresses in vitro antibody production to sheep red blood cells (SRBC) and probably represents the soluble form of the T cell Fc receptor. To study the relationship between IBF and the major histocompatibility complex (MHC), two types of experiments were undertaken. First, different IBF were prepared by injecting thymocytes from mice of H‐2k, H‐2b and H‐2d haplotypes into irradiated, allogeneic recipient mice. Cells recovered in the spleens five days later were incubated for 2 h at 37 °C, and IBF was purified by affinity chromatography on insolubilized IgG. Purified IBF was then applied to immunosorbents prepared with anti‐H‐2 and anti‐Ia anti sera. Acid eluates were then tested for their suppressive activity on in vitro antibody production to SRBC. Under these conditions, IBF was found to react with anti‐sera raised against products of the whole MHC and of the I region of the MHC, but not with anti‐H‐2 D antisera. These data indicate that IBF bears, or is associated with Ia determinants. Second, IBF preparations from mice of H‐2k, H‐2b, H‐2d haplotypes were tested for their capacity to suppress the in vitro antibody production to SRBC by spleen cells of a series of mouse strains. The data indicate that IBF is not genetically restricted in its function.
The migration of lymphocytes in the fetal lamb
Authors: Paper Short , Cahill Ross N. P. , Poskitt David C. , Hay John B. , Heron Iver , Trnka Zdenek 
Published: February 2007

AbstractThe migration of 51Cr‐labeled autologous lymphocytes from intestinal or prescapular lymph was compared in fetal lambs and adult sheep. A subpopulation of lymphocytes present in intestinal lymph of adults which migrated to the small intestine was not found in fetal intestinal lymph. There were marked differences in the migration of fetal and adult lymphocytes to the lungs and liver. In spite of the absence of circulating antibodies or immunoglobulins and of extrinsic antigen in the immunologically virgin sheep fetus, the circulation of lymphocytes through the spleen and lymph nodes of fetal lambs was more intense than in the adult.
Expression of Ly‐6 alloantigen during differentiation of cytotoxic T cells
Authors: Horton Michael A. , Beverley Peter C. L. , Simpson Elizabeth 
Published: February 2007

AbstractWe have prepared anti‐Ly‐6.2 by immunization of (CBA/Ca × A‐Thy‐la)F1 with AKR/Crc lymphocytes and used the antiserum to study heterogeneity of peripheral T lymphocytes. The Ly‐6 alloantigen is found on all activated cytotoxic T cells studied, directed to a variety of different target antigens. The antiserum reveals heterogeneity among the precursors of T killer cells, i.e. allogeneic precursors are Ly‐6−, whereas the generation of cytotoxic cells to hapten‐modified syngeneic cells and xenogeneic cells is partially abrogated by serum pretreatment. Precursors of some in vivo primed responses are also Ly‐6+. These findings indicate that the expression of Ly‐6 antigen is, at least, partially related to the stage of T cell activation. The in vitro proliferative response of T cells to allogeneic Ia antigens is substantially reduced by pretreatment with anti‐Ly‐6.2 serum suggesting that this antiserum may be a useful tool for the study of heterogeneity in the Ly‐l+ pool of T cells.
Identification of Ia glycoproteins in rat thymus and purification from rat spleen
Authors: McMaster W. Robert , Williams Alan F. 
Published: February 2007

AbstractA fraction of la‐like glycoproteins was prepared from rat thymocytes by lentil lectin affinity chromatography and gel filtration in deoxycholate. Spleen cells from mice immunized with this preparation were fused with myeloma cells to produce antibody‐secreting hybrid cell lines. Antibody from four lines called MRC OX, 3, 4, 5, 6 reacted with the la‐like glycoproteins, and MRC OX 3 antibody recognized an antigenie determinant polymorphic in the rat. All four antibodies also bound to mouse spleen cells and all detected polymorphisms. Studies on recombinant mouse strains suggest that the determinants are coded by the I‐A subregion of the H‐2 complex. MRC OX 3 correlates with Ia specificity 9, while MRC OX 4, 5, 6 correlate with specificity 17 or 18. MRC OX 4 monoclonal antibody was used for affinity chromatography to purify Ia glycoproteins from rat spleen. The rat Ia glycoprotein complex was composed of two noncovalently linked polypeptide chains of apparent mol. wt. (unreduced) 30 000 and 24 000 as determined by polyacrylamide gel electrophoresis in sodium dodecyl sulfate. The purified Ia glycoprotein partially inhibited the binding to thoracic duct lymphocytes of an alloantiserum which detects Ia antigens linked to the major histocompatibility complex. The monoclonal anti‐la antibodies bound to the majority of peripheral B lymphocytes and 18% of thymocytes, but did not significantly bind to peripheral T lymphocytes. There were on average 150000 molecules of Ia glycoprotein per la‐positive B lymphocyte, and 45 000 molecules per la‐positive thymocyte.From the same fusion, another cell line was prepared called MRC OX 2 which secretes monoclonal antibody to a previously undefined thymus glycoprotein of apparent mol. wt. 60000. Preliminary studies showed that the antigen was expressed on all thymocytes and on peripheral B lymphocytes in smaller amounts. It was also present in brain, but not liver or kidney homogenate.
Lysis of enucleated tumor cells with allogeneic and syngeneic cytotoxic thymus‐derived lymphocytes
Authors: Hale Arthur H. , Paulus Leslie K. 
Published: February 2007

AbstractThese studies were initiated to understand the minimal requirements for lysis of target cells by cytotoxic thymus‐derived lymphocytes (CTL). In particular, the significance of the nucleus to the susceptibility of the target cell to be lysed by CTL have been studied. P815 mastocytoma cells and EL4 lymphoma cells were enucleated by cen‐ trifugation through a discontinuous Ficoll gradient containing 10 μg/ml of cytochalasin B. The resultant vesicles were then analyzed for susceptibility to lysis by different CTL specific for the H‐2K and H‐2D gene products, minor histocompatibility antigens, trinitrophenyl groups, and Sendai virus‐specific antigens. The results indicate that enucleated vesicles obtained from both EL 4 and P 815 cells are susceptible to lysis by these CTL. The lysis of EL 4‐enucleated vesicles (unlike P 815‐enucleated vesicles), however, required 2–4 times more effector cells than were required for equivalent lysis of intact EL 4 cells. This reduced susceptibility to lysis of enucleated EL 4 vesicles was not the result of an inability of the CTL to recognize and bind the vesicles. This conclusion was suggested by the fact that both enucleated EL 4 vesicles and intact cells inhibited equally well the lysis of 51Cr‐labeled concanavalin A‐stimulated BALB. B spleen cells by anti‐H‐2b CTL. Although enucleated vesicles obtained from both P 815 and EL 4 cells were susceptible to lysis by CTL, they exhibited a reduced capacity to “cap” their serologically defined H‐2 antigens.Lysis of these enucleated vesicles by CTL has the same requirements as lysis of intact cells. This conclusion was based upon the requirement for Ca++ and Mg++ and also because lysis of the modified vesicles (trinitrophenyl or viral antigens) occurred in an H‐2‐restricted fashion. Moreover, the enucleated vesicles were susceptible to antibody and complement‐mediated lysis and also lectin‐dependent cell‐mediated cytotoxicity.
Specific binding of radiolabeled membrane vesicles by T cells activated in the mixed lymphocyte reaction
Authors: Elliott Bruce E. , Takács Béla , Nagy Zoltan 
Published: February 2007

AbstractAn assay was developed to quantitate binding of radiolabeled membrane vesicles by T cells activated in the primary mixed lymphocyte reaction (MLR). T blasts generated in unidirectional, reciprocal MLR combinations were found to bind much more effectively membrane vesicles prepared by nitrogen cavitation from allogeneic stimulator cells than from syngeneic spleen and lymph node cells which had been previously labeled biosynthetically with [3H]leucine. Specific inhibition of binding with cold vesicles prepared from stimulator cells but not from responder cells was observed. The number of specific antigen‐binding cells is proportional to the concentration of membrane vesicles used. The proportion of labeled cells increases between 15 and 60 min of incubation with membrane vesicles, but thereafter remains constant. The binding of stimulator material is H‐2‐specific: cells bind membrane vesicles from congeneic mouse strains only if they share the H‐2 antigens of the original stimulator strain. Responder blasts bind labeled stimulator membrane fragments after as early as 2 days of primary MLR culture; no binding of membrane vesicles by small lymphocytes was detected between 2 and 5 days of culture. However, between 8 and 12 days of culture, a significant proportion of small lymphocytes bind specifically stimulator membrane vesicles. The recognition function is sensitive to trypsin treatment but is regenerated within 5 to 6 h.