bluuebunny/crossref_metadata_2025_split huggingface dataset:
Low‐molecular weight B cell growth factor (BCGF‐12KD) as an autocrine growth factor in B cell chronic lymphocytic leukemia
Authors: Fournier Sylvie , Biron Guy , Rubio Manuel , Delespesse Guy , Sarfati Marika , Jackson James , Kumar Ashok , King Thomas , Sharma Surendra 
Published: March 2007

AbstractThe role of cytokines in the growth and spreading of human hematologic malignancies has been underlined in recent years. Here we report evidence that a human 12‐kDa B cell growth factor (BCGF‐12KD) may function as a growth stimulatory factor in B cell chronic lymphocytic leukemia (B‐CLL). First, recombinant BCGF‐12KD induced dose‐dependent DNA synthesis in neoplastic B cells of four B‐CLL patients tested. Second, seven different B‐CLL clones secreted a BCGF‐12KD‐like product that accounted for their proliferation. A neutralizing monoclonal antibody (mAb; Ac8) directed against a BCGF‐12KD synthetic peptide inhibited the spontaneous growth of the leukemic B cells. The same mAb blocked DNA synthesis in normal tonsillar B lymphocytes induced by the culture supernatant of spontaneously proliferating B‐CLL cells. Finally, BCGF‐12KD mRNA was expressed in freshly isolated (two of three patients) as well as in vitro proliferating B‐CLL cells (three of three patients). These findings strongly suggest that BCGF‐12KD can modulate the growth of B‐CLL cells in vivo as well as in vitro. They may offer significant insights into the biology of this frequent B lymphoproliferative disorder.
Specificity of rat T cell receptor Vβ chain usage in proliferative responses to staphylococcal enterotoxin B
Authors: Sellins Karen S. , Bellgrau Donald , Gold Daniel P. 
Published: March 2007

AbstractThe staphylococcal enterotoxins (SE) are potent stimulators of T cell proliferative responses in humans and in mice. In these systems, the toxins function as superantigens and stimulate T cells bearing particular Vβ. Although homology between the Vβ of mice and humans is limited, related Vβ families may respond to certain SE in a similar fashion. In this report, we have characterized the rat T cell response to staphylococcal enterotoxin B (SEB). Rat T cells from several lymphoid organs proliferated strongly in response to both commercially available and recombinant SEB. Using a polymerase chain reaction assay, we identified the predominant Vβ families stimulated by this enterotoxin. The T cell receptor Vβ elements used by rat T cells were similar to but not completely identical with those used by mice. The Vβ profile stimulated depended on the purity of the SEB preparation used.
TiγA+δTCS1+ T cells in human thymus. Analysis of the T cell receptor
Authors: Bosse Roland , Heiken Hans , Kolanus Waldemar , Delany Patricia , Schmidt Reinhold E. , Triebel Frederic 
Published: March 2007

AbstractTcR1+ T cells in peripheral blood have been shown to express in an exclusive fashion either the TiγA or the δTCS1 epitope. Here, we characterize a subset of TcR1+ T cells in fresh thymus co‐expressing the TiγA and δTCS1 epitopes. TcR1dim and TcR1bright clones can be distinguished. Biochemical and molecular studies on both types of clones generated from these thymocytes reveal a unique T cell receptor structure characterized by the use of a Vγ9/Cγ2‐encoded 55‐kDa γ chain nondisulfide linked to a Vδ1‐encoded δ chain.
Complexes of IgG molecules and C3a and C4a complement components in human serum
Authors: Nezlin Roald , Freywald Andrew 
Published: March 2007

AbstractA heterogeneous group of proteins was separated from human serum IgG using 5 M guanidine hydrochloride solution in 0.1 M acetic acid. The protein mixture was fractionated by reverse‐phase high‐performance liquid chromatography and two proteins were isolated and identified as the C3a and C4a complement components (anaphylatoxins) according to their molecular masses and N‐terminal sequences. Using a chemical cross‐linking technique, the capacity of C3a and C4a to reassociate with the heavy and the light chains of IgG was shown. On the basis of the molecular masses of reconstituted complexes one molecule of C3a (or C4a) was bound to one heavy or one light chain of IgG.
Lymphokine profile and activation pattern of two unrelated antigen‐ or idiotype‐specific T suppressor cell clones
Authors: Pauels Hans‐Gerd , Austrup Frank , Becker Christian , Schmitt Edgar , Rüde Erwin , Kölsch Eckehart 
Published: March 2007

AbstractTwo T suppressor (Ts) clones of different specificity have been analyzed for their lymphokine spectrum. BVI/5 is an I‐Ek‐restricted bovine serum albumin (BSA)‐specific Ts cell clone from a CBA/J mouse tolerized by low doses of BSA. It affects directly or indirectly the function of BSA‐specific T helper (Th) cells. The Ts cell clone 178‐4 from a BALB/c mouse is I‐Ed restricted and recognizes the public J558 Id on B cells. It prevents α(1→3)dextran B 1355S (Dex)‐specific IgG antibody production and drives Dex‐specific J558 idiotype‐bearing B cells into an anergic B IgG memory cell state. Both Ts cell clones thus cause specific suppression, yet in different experimental systems using different effector mechanisms. Upon stimulation with concanavalin A or fixed CD3‐specific monoclonal antibody, both clones produce high levels of interferon (IFN)‐γ and tumor necrosis factor (TNF) but in contrast to Th1 cells no interleukin (IL)‐2. Both clones produce low levels of IL‐3 and IL‐6 but no IL‐4, IL‐5 and IL‐9. Furthermore, unlike Th2 cells, both clones do not respond to IL‐1. The mechanism of the idiotype‐specific induction of anergy in Dex‐specific B IgG memory cells by 178‐4 Ts cells is not yet understood. BVI/5 Ts cells suppress in vitro the BSA‐specific proliferation of the BSA‐specific Th cell clone 83/1, as well as the response of BSA‐primed CBA/ LN cells. Whereas the suppressive effect on 83/1 cells is due to IFN‐γ alone the suppression of BSA‐specific lymph node cells can be simulated neither by IFN‐γ nor the combination of IFN‐γ and TNF. Thus these mediators cannot account for the antigen‐specific suppression by BVI/5 Ts cells in polyclonal in vitro responses from lymph node cells and probably not for the induction of in vivo unresponsiveness.
Evidence that mannose recognition by splenic sinusoidal cells plays a role in the splenic entry of lymphocytes
Authors: Weston Susan A. , Parish Christopher R. 
Published: March 2007

AbstractPrevious studies demonstrated that mannan is a potent inhibitor of splenic entry of lymphocytes and mediates its inhibitory effect at an unidentified site in the spleen rather than acting directly on lymphocytes. This report describes the in vivo site of action of mannan. In vivo localization studies with fluoresceinated preparations of mannan (Fl‐mannan) and a mannose‐6‐phosphate‐containing yeast phosphomannan monoester core from P. holstii exopolysaccharide (Fl‐PPME) demonstrated that the polysaccharide specifically localize in the splenic marginal sinuses in cells with a dendritic morphology termed splenic sinusoidal cells (SSC). Uptake of the polysaccharides by SSC was mediated by a mannan‐specific receptor which was saturable and of high avidity. Several lines of evidence suggested that mannan uptake by SSC inhibited splenic entry of lymphocytes. First, the ability of SSC to bind Fl‐mannan and Fl‐PPME closely paralleled the ability of these polysaccharides to inhibit splenic entry of lymphocytes. In fact, doses of mannan and PPME which would saturate SSC mannan receptors completely blocked splenic entry of lymphocytes. Second, SSC are situated at the initial entry point of lymphocytes into spleen and passage of lymphocytes through the SSC region of spleen was profoundly inhibited by mannan. Finally, direct evidence for adhesion between lymphocytes and SSC was obtained with spleen cell suspensions where clustering between Fl‐mannan labeled SSC and lymphocytes was observed. Collectively, these data indicate that mannan (and PPME) inhibit splenic entry of lymphocytes by interacting with SSC, cell which play a critical role in the entry of lymphocytes into the spleen. Whether mannan‐specific receptors on SSC directly mediate lymphocyte‐SSC adhesion or play on indirect role in modifying lymphocyte migration requires further investigation.
A method for rapid screening of recombinant proteins for recognition by T lymphocytes
Authors: Hickling Julian K. , Jones K. Rebecca , Yuan Bin , Rothbard Jonathan B. , Bülow Roland 
Published: March 2007

AbstractA simple, cost‐effective method is described that allows rapid screening of recombinant protein sequences for their ability to stimulate T cells. Individual microcultures of E. coli each expressing a gene product or peptide sequence fused to protein A are grown in 96‐well plates. Following lysis of the bacteria, the fusion peptide is readily captured with immobilized immunoglobulin in tissue culture wells. No further purification is required. T lymphocytes plus appropriate antigen‐presenting cells are added directly to the wells and assayed for proliferation. The DNA in bacteria from wells stimulating T cell proliferation is then sequenced. The technique allows rapid mapping of T cell epitopes by facilitating screening of truncation mutants without extensive purification. Described here is a further application of the technique to study monosubstituted analogues of a known T cell epitope.
Glycosidase inhibitors (castanospermine and swainsonine) and neuraminidase inhibit pokeweed mitogen‐induced B cell maturation
Authors: Karasuno Takahiro , Kanayama Yoshio , Nishiura Tetsuo , Nakao Hirohisa , Yonezawa Takeshi , Tarui Seiichiro 
Published: March 2007

AbstractCastanospermine (CSP), an inhibitor of α‐glucosidase, enhanced immunoglobulin (Ig) release in a Staphylococcus aureus Cowan I (SAC)‐induced lymphocyte culture (Scand. J. Immunol. 1990. 32: 529). In a pokeweed mitogen (PWM)‐human lymphocyte culture, unlike the SAC‐stimulated system. CSP strongly decreased the number of IgG‐, IgA‐ and IgM‐secreting cells as well as that of Ig‐bearing cells. Peripheral blood lymphocytes treated with swainsonine, a mannosidase II inhibitor, or with neuraminidase also showed a reduced response to PWM. In cross‐culture experiments, only a mixture of B cells pretreated with either agent and untreated T cells showed such a suppressive effect. Adhesion was decreased between B cells treated with either agent and untreated T cells, but not between treated T cells and untreated B cells. These results demonstrate that a certain alteration in B cell membrane oligosaccharides inhibited the T cell‐B cell adhesion in the PWM culture, leading to an arrest of B cell maturation. Considering that these inhibitors eventually prevent terminal sialic acid addition, the present study provides evidence that sialic acids on B cell surface oligosaccharides play a biological role in the T cell‐B cell interaction.
Subjugation of dominant immunogenic determinants within a chimeric peptide
Authors: Bhardwaj Vatsala , Kumar Vipin , Geysen H. Mario , Sercarz Eli E. 
Published: March 2007

AbstractThe mechanism of immunodominance was investigated using chimeric peptides from mouse myelin basic protein consisting of the immunodominant I‐Au‐restricted Ac1‐11, attached by a peptide bond to I‐Eu‐restricted 35–47. Our results indicate that this chimeric peptide and certain of its derivatives were excellent immunogens both in vitro and in vivo. Notably, on immunization with Acl‐11:35–47 or Ac1‐11 (Ala4):35–47, the proliferative T cell responses to each of its component peptides were almost completely “subjugated” in favor of neo‐determinants that are I‐Eu restricted. Furthermore, each of 11 hybridomas derived after immunization with Ac1‐11:35–47 had specificity for junctional neo‐determinants and none could be stimulated to produce interleukin‐2 from Ac1‐11 or 35–47. Subjugation of the immunogenicity of the original determinants occurred regardless of their dominance when separate. It did not appear to result from non‐availability of the original determinants because the chimeric peptide was able to induce neonatal tolerance to each of its constituents. These results indicate that in an overlapping multideterminant array, the dominant determinant is unpredictable from historical data about any of the components. Determinant choice, at any stage of processing, may be governed by competitive aspects of determinant capture in an environment where all components ‐antigen, major histocompatibility complex and T cell receptor ‐ are available.
A protective NOD islet‐infiltrating CD8+ T cell clone, I.S. 2.15, has in vitro immunosuppressive properties
Authors: Pankewycz Oleh G. , Guan Jing‐Xin , Benedict John F. 
Published: March 2007

AbstractType 1, insulin‐dependent diabetes mellitus (IDDM) appears to result from a T cell‐dependent destruction of insulin‐producing pancreatic β cells. In non‐obese diabetic (NOD) mice and in other rodent models of human IDDM, final expression of disease may be controlled by protective, as well as, destructive T cell influences. Previously, a CD8+ T cell clone, I.S. 2.15, was isolated directly from islets of disease‐resistant male NOD mice. Upon transfer to young NOD recipients, the non‐cytolytic I.S. 21.5 T cell clone, confers in vivo protection from two forms of accelerated IDDM. The present study demonstrates that I.S. 2.15 T cells induce in vitro immunosuppression. The suppressive effects of I.S. 2.15 T cells are mediated through soluble factor(s) and are independent of T cell activation, cell contact, antigen specificity or the major histocompatibility complex (MHC). By polymerase chain reaction (PCR), I.S. 2.15 T cells contain mRNA species encoding for the potentially immunosuppressive cytokines, interleukin‐10 (IL‐10) and transforming growth factor‐β (TGF‐β). The T cell suppressive effects engendered by I.S. 2.15 T cells closely mimic those observed with TGF‐β. Moreover, I.S. 2.15‐induced immunosuppression correlates with intracellular levels of TGF‐β mRNA. These results establish that immunoregulatory T cells are present within islets in IDDM‐resistant NOD mice and may impact on final disease expression through the production of soluble mediator(s).
Adhesion molecule‐mediated signals regulate major histocompatibility complex‐unrestricted and CD3/T cell receptor‐triggered cytotoxicity
Authors: Galandrini Ricciarda , Albi Nicola , Zarcone Daniela , Grossi Carlo E. , Velardi Andrea 
Published: March 2007

AbstractAppropriate experimental conditions were devised to demonstrate that CD58 (LFA‐3), CD54 (ICAM‐1) and CD11a/CD18 (LFA‐1) adhesion molecules are the source of signals that regulate nonspecific major histocompatibility complexunrestricted and CD3/T cell receptor (TcR)‐triggered cytotoxicity. Using anti‐LFA‐3 monoclonal antibody (mAb)‐treated, interleukin‐2 (IL‐2)‐cultured peripheral blood lymphocytes (PBL) or cloned CD3+/CD8+ cells as lymphocyteactivated killer (LAK) effectors, and ligand (CD2)‐negative tumor cell lines as targets, a down‐regulation of CD3− and CD3+ cell‐mediated LAK activity was consistently observed. Anti‐LFA‐3 mAb also down‐regulated tumor cell lysis when T cell clones were triggered to kill P815 cells through stimulation of the CD3/TcR complex by an anti‐CD3 mAb. The inhibitory effect of anti‐LFA‐3 mAb was not prevented by stimulatory anti‐CD2 mAb. Anti‐ICAM‐1 mAb treatment of IL‐2‐cultured PBL consistently up‐regulated LAK cytotoxicity against tumor target cells. However, this effect was only exerted on CD3− LAK effectors. Anti‐LFA‐1 mAb blocked conjugate formation between effector cells and tumor target cells, thus rendering this model unsuitable to evaluate the regulatory role of LFA‐1. Therefore, a cytotoxicity model system was applied in which a hybrid anti‐CD3/anti‐human red blood cell (HuRBC) mAb triggers cytolytic T cells to lyse HuRBC. In these experiments, anti‐LFA‐1 mAb markedly up‐regulated the lytic ability of IL‐2‐cultured PBL.We conclude that mAb against LFA‐3, ICAM‐1 and LFA‐1 molecules deliver regulatory signals for LAK cells and cytotoxic T lymphocytes. As these stimuli may be delivered by ligands expressed on tumor targets as well as on other immune competent and inflammatory cells, the present observations are relevant in the context of both the host's immune response against tumors and the general functioning of the immune system.
Structural requirements for the peptide‐induced conformational change of free major histocompatibility complex class I heavy chains
Authors: Elliott Tim , Elvin John , Cerundolo Vincenzo , Allen Hamish , Townsend Alain 
Published: March 2007

AbstractIn an attempt to define the structural features of peptides which are important for inducing the folding of free class I heavy chains in the absence of β2‐microglobulin, and to determine whether they are the same as those required to form stable major histocompatibility complex (MHC): peptide adducts, we have used a panel of peptides related to the Db‐binding nonamer ASNENMDAM (influenza nucleoprotein residues 366–374) with altered primary structures, and a number of other peptides which have the Db‐binding “motif”. In this way, we have shown that in addition to the “anchor” residues which define this motif, the α amino and carboxyl groups at the N and C termini also play a major role in both inducing the conformational change in free heavy chain (HC) and formation of a stable Db: peptide complex. We also show that the importance of the key residues is affected by the primary sequence “context” in which they appear. In addition, we have extended our original finding that naturally processed epitopes induce a conformational change in free HC to the H2Kb HC, and show that the effect does not require the presence of the class I α3 domain.
Presence of murine fetal liver cells capable of being induced to differentiate in vitro into T cell receptor‐positive cells
Authors: Shimamura Michio , Oku Manami , Yamagata Tatsuya 
Published: March 2007

AbstractMouse fetal liver cells were analyzed for the surface expression of T cell markers. Fetal liver cells prepared from mouse embryos at 14.5 days of gestation contained a small number of CD4+ cells (1.4%), but virtually no cells positive for any other T cell markers such as CD8, CD3 and T cell receptor (TcR). When a fetal liver cell suspension prepared from BALB/c(♂) × AKR(♀) F1 embryos at 14.5 days of gestation was cultured in medium supplemented with culture supernatants of both WEHI−3 and concanavalin A‐stimulated rat spleen cells, TcR αβ+ and CD4+ cells were generated, whereas CD8+ and TcR γδ+ cells were hardly detectable. Most of TcR αβ+ and CD4+ cells were H‐2d+, thus clearly showing their fetal origin. Treatment with anti‐CD4, anti‐CD3 or anti‐TcR αβ antibodies plus complement or electronic sorting to remove cells expressing these markers failed to inhibit the generation of T cell marker‐positive cells following culture in vitro. On the other hand, depletion of Thy‐1.2+ cells reduced their generation. These findings indicate the presence of some progenitor T cells in fetal liver with the Thy‐1+, CD3−, CD4−, CD8−, TcR− phenotype, which can be induced to differentiate into TcR αβ+ cells in the presence of specific humoral supplements without the influence of the thymus.
Processing and presentation of ovalbumin in mice genetically selected for antibody response
Authors: Vidard Laurent , Rock Kenneth L. , Couderc Jacques , Mouton Denise , Benacerraf Baruj 
Published: March 2007

AbstractLines of mice selected for high or low antibody production to sheep red blood cells (H‐I and L‐I) were studied for their ability to process and present ovalbumin to a panel of 12 T‐T hybridomas in two different H‐2 haplotypes. When H‐I and L‐I spleen cells were used as antigen‐presenting cells, no difference could be observed in the peptide generation by these mice compared to H‐2‐compatible B.10.Q and B.10.S spleen cells, respectively. Neither normal splenic L‐I B‐cells nor L‐I thioglycolate‐induced peritoneal macrophages were defective at presenting native ovalbumin, to six and eight different I‐As‐restricted T‐T hybrids, respectively. Altogether, these results differ from previous findings which had indicated a deficiency in the processing and presentation of antigen by the low line, L‐I.
Differential effect of transforming growth factor β on the synthesis of Th1‐ and Th2‐like lymphokines by human T lymphocytes
Authors: Fargeas Christine , Wu Chang You , Nakajima Toshiharu , Cox David , Nutman Thomas , Delespesse Guy 
Published: March 2007

Abstract(TGF)‐β is a pluripotent cytokine exerting differential effects on distinct components of the immune response. The present report, based on lymphokine determination in culture supernatants and Northern blot analysis of lympokine mRNA, demonstrates that TGF‐β2 markedly inhibits interleukin (IL)‐4 and IL‐5 synthesis by polyclonally activatted human T cells in the absence of any significant effect on (IFN)‐γ, lymphotoxin or IL‐2, suggesting a modulatory effect of TGF‐β2 on the ineterferon Th1/Th2) balance of immune respnses. The inhibitory effect of TGF‐β on IFN‐γ production by unfractionated peripheral blood mononuclear cells is likely to reflect the blunting of natural killer cell activation by TGF‐β.
Active lymphocyte traffic induced in the periphery by cytokines and phytohemagglutinin: Three different mechanisms?
Authors: Binns Richard M. , Licence Stephen T. , Wooding F. B. Peter , Duffus W. Philip H. 
Published: March 2007

AbstractPhytohemagglutinin (PHA) injection induces transient protease‐sensitive traffic of lymphocytes in skin and other tissues in several species. Examination of the possible roles of cytokines in such reactions showed that recombinant bovine and human tumor necrosis factor (TNF)‐α potently induce dose‐dependent lymphocyte traffic in pig skin (and in other tissues including the draining lymph nodes) with early kinetics and a morphology of the inflammatory reaction similar to that of PHA (peaking 9–12 h). Recombinant human interleukin (IL)‐1α also induces dose‐dependent lymphocyte traffic, but it peaks at 4 h. Entry of labeled lymphocytes into inflammatory sites induced by PHA, TNF‐α and IL‐1α, but not into normal skin, is inhibited by approximately 80 % by their pretreatment with trypsin, indicative of the induction of endothelial determinants recognized by protease‐sensitive surface molecules on the lymphocytes. Even the minimal lymphocyte traffic induced by interferon‐γ and lipopolysaccharide was similarly protease sensitive. At the earliest stage (∼2 h) of significant induction of lymphocyte entry by TNF‐α and IL‐1α the inductive signal for each appears easily saturated. Thus lymphocyte entry is little increased by increasing low cytokine doses over 100‐fold: However, these reactions are additive, and this was used to confirm that they are distinct from each other and from PHA. A further distinction was revealed by the homing of lymphocytes pretreated with pertussis toxin: such lymphocytes were >90 % inhibited in their homing to tissues through constitutive high endothelial venules (HEV) and >60 % inhibited in homing to TNF‐α and IL‐1α skin sites, but unaffected in homing to PHA skin sites (like most non‐HEV‐mediated traffic). Moreover, potent chicken anti‐TNF‐α, which prevented TNF‐induced lymphocyte entry, did not affect PHA‐induced traffic. Thus, these three agents which induce peripheral lymphocyte traffic appear to involve different mechanisms as shown by differences in (i) their kinetics; (ii) the effect of anti‐TNF‐α and (iii) the effect of pertussis toxin treatment of the lymphocytes and by the fact that their inductive mechanisms are additive in effect.