bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prolonged growth of activated B lymphocytes requires interaction with helper T cells
Authors: Rajasekar Ramanujam , Andersson Jan , Leanderson Tomas 
Published: March 2007

AbstractResting B lymphocytes acquire upon activation responsiveness to soluble factors that support their growth and differentiation. We have studied the growth requirements of anti‐μ pre‐activated B lymphocytes in vitro. We found that activated B lymphocytes did respond to soluble factors from helper T cells by entering the cell cycle but cell‐cell contact with specific helper T cells was required for prolonged growth of activated B lymphocytes. Thus, activated B lymphocytes must receive activation signals from helper T cells in order to stay in the proliferative phase of the cell cycle.
Activation of specific T cell lines by the antigens avidin and myelin basic protein in the absence of antigen‐presenting cells
Authors: Altmann Daniel M. , Lider Ofer , Douek Daniel C. , Cohen Irun R. 
Published: March 2007

AbstractWe have investigated the specific activation by soluble antigen of rat or mouse longterm T helper cell lines using antigen‐presenting cell (APC)‐free culture conditions. Some T cell lines specific for avidin or myelin basic protein responded to native antigen in the absence of added APC. Responses in the absence of APC were substantial and specific although, as would be expected, lower than in the presence of APC. Proliferation could not be inhibited by culture with anti‐Ia antibodies and the ability of lines to respond to antigen in the absence of APC did not correlate with the endogeneous surface Ia expression of the lines. Furthermore, irradiated T cells were unable to act as presenting cells for line cells of the same or a different specificity. This suggests that the T cells did not present antigen to each other, and demonstrates, along with other data shown, that activation cannot be attributed to undetected APC remaining in the cultures. Anti‐avidin T cell lines differed markedly in their ability to respond to avidin in the absence of added APC.S2, an anti‐avidin line of H‐2s genotype consistently responded well to avidin seen in the absence of added APC; K2, an H‐2k anti‐avidin line, responded moderately and B3, and H‐2b anti‐avidin line, although the most prolific responder in the presence of APC, never responded to antigen in their absence. Z1a, a Lewis rat‐derived T cell line specific for myelin basic protein, proliferated well in response to the antigen in the absence of added APC. The present findings demonstrate that some T cells can recognize and respond to native antigens without the mediation of specialized APC.
Four epitopes on the rat 55‐kDa subunit of the interleukin 2 receptor as defined by newly developed mouse anti‐rat interleukin 2 receptor monoclonal antibodies
Authors: Mouzaki Athanasia , Diamantstein Tibor 
Published: March 2007

AbstractFour new mouse monoclonal antibodies (mAb), ART‐38, ART‐35, ART‐75 and ART‐94, directed against the rat interleukin 2 receptor (IL 2R) have been developed. As shown by immunoprecipitation studies they all recognize specifically the 55‐kDa subunit of the rat IL 2R. These mAb were compared to three previously characterized mouse mAb directed against the 55‐kDa molecule of the rat IL 2R, namely the ART‐18, ART‐65 and OX‐39 mAb. Out of all seven mAb, only ART‐18 and OX‐39 were found to inhibit the IL 2 binding to activated T cells, while IL 2R inhibited the binding of ART‐18 alone. ART‐18 was the only mAb found to inhibit the IL 2‐dependent proliferation of cells carrying the IL 2R. Scatchard plot analyses showed gross differences in the numbers of mAb‐binding sites ranging between 30000 (ART‐65) and 165000 (ART‐75) as well as in their affinities which ranged between 2.5 × 10−9 M (ART‐38) and 8.3 × 10−10 M (OX‐39). Cross inhibition studies revealed that the mAb recognize four different epitopes on the 55‐kDa rat IL 2R subunit.
Immunomodulation of murine visceral leishmaniasis by administration of monoclonal anti‐Ia antibodies: differential effects of anti‐I‐A vs. anti‐I‐E antibodies
Authors: Blackwell Jenefer M. , Roberts Morven B. 
Published: March 2007

AbstractOn a B10 genetic background noncure and cure phenotypes for murine visceral leishmaniasis are controlled by H‐2. In this report results are presented which show the effects of administering specific anti‐I‐A and anti‐I‐E monoclonal antibodies to B10.D2/n (H‐2d) noncure mice prior to and during 85 days of infection with Leishmania donovani LV9. The effects of the two anti‐Ia antibodies were precisely equivalent in diminishing circulating anti‐leishmanial IgG levels throughout infection, possibly as a direct effect of the anti‐Ia antibodies in reducing the splenic B cell population. In terms of resolution of liver and spleen parasite loads, which is known to be dependent upon induction of a cell‐mediated immune response, dramatically different results were obtained with the two anti‐Ia antibodies. Anti‐I‐A treatment resulted in prolonged exacerbation of disease in liver and spleen. Anti‐I‐E treatment was associated with enhanced clearance of liver and spleen parasite loads beyond 30 days of infection. The results are consistent with the hypothesis that blocking major histocompatibility complex‐restricted antigen presentation by one class II molecule allows T cell responses controlled by the other to predominate. Hence, in H‐2d mice, I‐E controls suppressor activity while I‐A is associated with helper activity for cell‐mediated control of infection. The results offer some prospect for the development of haplotype‐ and class II molecule‐specific immunotherapeutic regimens in the host which might prevent the undesirable expansion of T cell populations which exacerbate disease without compromizing development of a curative cell‐mediated immune response.
Anti‐Thy‐1‐induced proliferation of immature thymocytes expressing the CD3‐associated γ/δ heterodimer
Authors: MacDonald H. Robson , Miescher Guido C. , Howe Rawleigh C. 
Published: March 2007

AbstractA series of rat monoclonal antibodies (mAb) directed against the Thy‐1 molecule have been evaluated for their ability to stimulate immature (CD4−8−) murine thymocytes. CD4−8− thymocytes could be induced to proliferate by several anti‐Thy‐1 mAb provided that exogenous inteleukin 1 or interleukin 2 was provided. Apparently nonstimulatory anti‐Thy‐1 mAb could be rendered stimulatory if cross‐linked by a rabbit anti‐rat immunoglobulin reagent. Anti‐Thy‐1‐stimulated CD4−8− thymoctes were found to uniformly express CD3 but did not stain positively with F23.1, a mAb reactive with α/β T cell receptors utilizing the Vβ8 gene family. Immunoprecipitation analysis of such stimulated CD4−8− thymocytes indicated that they expressed a CD3‐associated heterodimer of 45 kDa/35 kDa most likely corresponding to the product of the γ and (putative) δ T cell receptor genes. Taken together, these data demonstrate that anti‐Thy‐1 mAb selectively activate a subset of CD4−8− thymocytes committed to the γ/δ T cell receptor lineage.
Activation of murine CD8+ lymphocytes: Two distinct signals regulate c‐myc and interleukin 2 receptor RNA expression
Authors: Hardt Conny 
Published: March 2007

AbstractResting cytotoxic T lymphocyte precursors (CTL‐P; CD8+) constitutively express T cell receptors (TcR) on their cell surfaces. CTL‐P are preactivated if binding of the corresponding antigen (mitogens, allogeneic major histocompatibility complex (MHC) determinants, viral proteins or haptens in conjunction with self MHC structures) to the TcR takes place. Using a myc specific probe I show that within 12 h antigen binding leads to optimal c‐myc RNA expression which seems to be the first sign that resting CTL‐P are preactivated. Thereafter, c‐myc RNA expression was remarkably reduced only at day 5. Antigen alone, however, is not sufficient for interleukin 2 receptor (IL 2R) RNA expression. A monocyte‐derived, soluble mediator termed IL 2R‐inducing factor (RIF) acts in conjunction with antigen to induce the expression of IL 2R RNA and functional IL 2R on the cell surface. RIF is a 44‐kDa heat‐labile protein produced by accessory cells and its function is restricted to CD8+ lymphocytes. IL 2R RNA is first expressed 12 h after onset of culture, maximally expressed on day 3 and it decreases thereafter. Cells kept in long‐term culture without mitogen but in the presence of IL 2 do not express high amounts of IL 2R RNA. Expression of IL 2R RNA can be very efficiently reinduced, however, by mitogenic stimulation. In contrast to primary cultures, IL 2R RNA expression peaks earlier and is independent of RIF. The results obtained here show that (a) for CD8+ lymphocytes of primary cultures two distinct activation signals (mitogen and RIF) are necessary for c‐myc and IL 2R RNA expression and (b) for CD8+ lymphocytes of secondary cultures the mitogenic signal alone is sufficient for re‐expression of IL 2R RNA.
Unusual forms of T cell γ mRNA in a human T cell leukemia cell line: Implications for γ gene expression
Authors: Tighe Lynette , Forster Alan , Clark David M. , Boylston Arthur W. , Lavenir Isabella , Rabbitts Terence H. 
Published: March 2007

AbstractThe expression and rearrangement of T cell rearranging (TRG) γ genes in human leukemic cell lines has been examined. The cell line MOLT‐17 produces abundant γ mRNA which is translated into a protein found on the cell surface which is associated with the CD3 molecule. The analysis of the γ mRNA sequences in MOLT‐17, by cDNA cloning, shows transcripts of aberrantly rearranged genes as well as the productively rearranged allele. The productive allele consists of a rearranged V 8 gene joined to Jγ2. Two forms of aberrant transcript originate from the other rearranged γ allele. One of these initiates just upstream of the unrearranged Jγ2 segment, and the other initiates from a Vγ8 gene segment joined to another Jγ segment, upstream of Jγ2. An unusual feature of the latter transcript is that polyadenlyation has occurred at the end of the first exon of Cγ2, where two conserved poly(A) addition signals occur. The MOLT‐4 cell line, on the other hand, has productively and nonproductively rearranged γ alleles, from which relatively little transcription occurs. These results define new Jγ segments in the human TRG γ locus and suggest that positive activation of the γ locus is necessary for high level transcription after rearrangement.
Abrogation of the lethal graft‐vs. ‐host reaction developed to non‐H‐2 antigens: involvement of T suppressor cells distinct from veto cells
Authors: Halle‐Pannenko Olga , Pritchard Linda L. , Bruley‐Rosset Martine 
Published: March 2007

AbstractThe mortality induced by graft‐vs.‐host reaction (GVHR) in (DBA/2 × B10.D2)F1 recipients transplanted with cells from H‐2d‐identical B10.D2 donors can be abrogated by preimmunizing the donors with parent‐strain spleen cells from normal DBA/2 mice. The experiments described here were designed to explore the possibility that the observed protection might be mediated by veto cells contained in the immunizing cell inoculum; the reasoning was based on an analogy with the cytotoxic T lymphocyte response to non‐H‐2 antigens where suppression can be mediated by veto cells, present in the spleens of normal mice, which are radiosensitive and largely Lyt‐2+. We show that the intensity of the protection against GVHR mortality is a function of the immunizing cell dose, and that protection remains effective when optimal doses of immunizing cells are (a) irradiated or (b) pretreated with anti‐Thy‐1 serum. GVHR suppression is abrogated when, before transfer to F1 recipients, suppressor cells from spleens of immunized donors are pretreated with antiserum directed against Lyt‐1.2 (expressed by B10.D2 but not by DBA/2, which expresses Lyt‐1.1); in contrast, it is not significantly affected when these same cells are pretreated with anti‐Lyt‐2.2 alloantiserum. We conclude that when the antigen load is great enough the immunizing cells play a largely passive role in the observed suppression. The protection against GVHR mortality seen in this H‐2‐compatible combination is transferable by Lyt‐1+2− suppressor T cells originating in mice given high doses of alloantigen. These suppressor cells are therefore distinct from the splenic veto T cells effective against cytotoxic T lymphocyte responses to non‐H‐2 antigens. The mechanism of the observed suppression and its relationship to Mlsa product(s) are discussed.
Differentiation of B cell progenitors in vitro: Generation of surface IgM+ B cells, including Ly‐1 B cells, from Thy‐l− asialoGM1+ cells in newborn liver
Authors: Hardy Richard R. , Kishimoto Tadamitsu , Hayakawa Kyoko 
Published: March 2007

AbstractWe have established a stromal adherent cell line (ST2) from fetal liver that promotes growth and differentiation of early B lineage cells. Many cells in the “null population” (3–5%) from newborn liver that lack antigens found on mature erythroid, myeloid or lymphoid cells proliferate extensively on this ST2 layer. Further division of this cell fraction on the basis of Thy‐1 and asialoGMl (aGMI) expression discriminates cells that predominantly proliferate from those that differentiate on the ST2 layer. Among four populations, Thy‐1+ aGM1− cells proliferate most but yield few B220+ cells. In contrast, Thy‐1− aGM1+ cells proliferate to a very limited extent, but most (> 90%) start to express B220 and a large fraction (up to 50%) become surface IgM+ after 2 weeks of culture. These B cells include cells expressing the pan‐T cell molecule Ly‐1, that is, Ly‐1 B cells. Curiously, this Thy‐1− aGM1+ cell population is largely absent from bone marrow in adult mice.
Selective effects of cholera toxin on the activation of mouse B cells by different polyclonal activators
Authors: Klaus Gerry G. B. , Vondy Karen , Holman Mary 
Published: March 2007

AbstractMurine B cells were stimulated in vitro with anti‐immunoglobulin (Ig) antibodies, lipopolysaccharide, or with various combinations of phorbol dibutyrate and ionomycin. Very low concentrations (ca. 10−14 M) of cholera toxin inhibited anti‐Ig‐stimulated DNA synthesis, while the response to LPS was only abrogated by 2 × 104‐105‐fold greater concentrations of the toxin. Earlier responses in anti‐Ig‐stimulated B cells, such as increases in Ia antigen levels, were not affected by the toxin. Protein kinase C‐activating phorbol esters, together with Ca2+ ionophores, are believed to stimulate DNA synthesis in lymphocytes by mimicking the two second messengers resulting from ligation of the antigen receptors. However, concentrations of cholera toxin which totally abolish anti‐Ig‐induced B cell proliferation significantly enhanced DNA and RNA synthesis induced by phorbol dibutyrate plus ionomycin. The results are discussed in terms of possible effects of cholera toxin on guanine nucleotide‐binding (G) proteins controlling receptor coupling to second messenger‐generating systems in B cells.
HIV env glycoprotein shares a cross‐reacting epitope with a surface protein present on activated human monocytes and involved in antigen presentation
Authors: Beretta Alberto , Grassi Fabio , Pelagi Micaela , Clivio Alberto , Parravicini Carlo , Giovinazzo Giovanna , Andronico Franca , Lopalco Lucia , Verani Paola , Butto Stefano , Titti Fausto , Rossi Giovanni Battista , Viale Giovanna , Ginelli Enrico , Siccardi Antonio G. 
Published: March 2007

AbstractA serological cross‐reactivity between env gp120 glycoprotein of the human immunodeficiency virus (HIV) and a human cellular surface protein has been defined by a monoclonal antibody (M38) raised against HIV. The cellular antigen is a protein of ca. 80 kDa expressed on a small fraction of mononuclear cells in peripheral blood and in lymph nodes. The protein behaves as an activation antigen of the monocytic lineage since it is expressed by monocytes in plastic‐adherent culture conditions and by interferon‐γ‐treated monocytes and pro‐monocytic U937 cells. The protein is involved in antigen presentation since the antibody efficiently inhibits the proliferation of responsive lymphocytes in autologous tetanus toxoid presentation assays. In the T lymphoblastoid line H9, the protein is present in very small amounts, is not induced by interferon‐γ and increases after HIV infection. Sera from lymphoadenopathy syndrome and acquired immunodeficiency syndrome (AIDS) patients fail to detect the cellular protein, although containing antibodies reacting with gp120. We propose that both viral and cellular structures recognized by the monoclonal antibody (mAb) are involved in interactions with CD4 molecules of T helper lymphocytes and that such molecular mimicry might be relevant in the pathology of HIV infection. This view is supported by the finding that BL/10T4, a CD4‐specific mAb, binds to M38 neutralizing its interactions with HIV and with monocytes. mAb M38 thus behaves as the internal image of CD4. This single property would explain all its diverse binding characteristics.
Activation of macaque T cells and B cells with agonistic monoclonal antibodies
Authors: Clark Edward A. , Draves Kevin E. 
Published: March 2007

AbstractA series of mouse monoclonal antibodies (mAb) to human differentiation antigens known to have agonistic activity for human T or B cells was found to bind specifically to macaque T or B cell subsets. Most of these mAb also stimulated macaque lymphocyte proliferation, implying that they recognize functional homologues in monkeys. Anti‐CD3, anti‐CD28 (9.3), and anti‐Lp220 (CD45R) mAb stimulated proliferation of both human and macaque T cells; similarly, anti‐IgM and anti‐CDw40 mAb stimulated both human and macaque B cells. In contrast, anti‐CD20 and anti‐CD39 mAb, which are known to stimulate human B cells, did not stimulate macaque B cells. A human low‐molecular weight B cell growth factor (BCGF) and anti‐IgM were co‐stimulatory for macaque splenic B cells but not for blood B cells, suggesting that B cell subpopulations may differ in their responsiveness to BCGF. The results show that functional epitopes on some lymphocyte surface molecules such as CD28 or CDw40 are conserved in primate evolution. Functional epitopes on other cell surface molecules such as CD3 and CD20 may have more complex evolutionary constraints.
Impairment of immunogenicity by antigen presentation in liposomes made from dimyristoylphosphatidyl‐ethanolamine linked to the secretion of prostaglandins by macrophages
Authors: Bakouche Quahid , David François , Gerlier Denis 
Published: March 2007

AbstractThe induction of antibody response in syngeneic rats by the Gross virus cell surface antigen (GCSAa) was dependent on the presentation of GCSAa into liposomes made from distearoylphosphatidylcholine (DSPC). GCSAa liposomes made from dimyristoylphosphatidylethanolamine (DMPE) were nonimmunogenic, even when used as anamnestic immunogens. Spleen cells, from rats twice immunized with GCSAa‐DSPC‐liposomes and used to transfer the anti‐GCSAa immune response into naive recipients after a tertiary immunostimulation in vitro in the presence of naive peritoneal exudate cells (PEC), responded to soluble GCSAa only after irradiation at 500 rds and to GCSAa‐DMPE‐liposomes only when indomethacin was added during the in vitro stimulation. The preincubation of these cells with empty DMPE liposomes or the addition of supernatant from PEC fed with DMPE liposomes abrogated the response to GCSAa‐DSPC liposomes. Using a specific radioimmunoassay, prostaglandin E2 was demonstrated to be produced by PEC when fed with DMPE liposomes, and not when fed with DSPC liposomes. This prostaglandin E2 secretion by PEC induced by DMPE liposomes was inhibited by indomethacin.
Purified lymphocyte function‐associated antigen‐3 and T11 target structure are active in CD2‐mediated T cell stimulation
Authors: Tiefenthaler Georg , Hünig Thomas , Dustin Michael L. , Springer Timothy A. , Meuer Stefan C. 
Published: March 2007

AbstractIn this study we have used cells expressing LFA‐3 or T11TS, the human and sheep forms of the ligand of CD2, as well as the purified LFA‐3 and T11TS molecules themselves to study their effects on T cell activation via the CD2‐mediated “alternative pathway”. Sheep red blood cells, which bind to CD2 via T11TS in E‐rosette formation, and human autologous monocytes, which express the LFA‐3 molecule, both induce proliferation of resting T cells in the presence of per se submitogenic concentrations of anti‐T112 plus anti‐T113 monoclonal antibodies (mAb). This effect is blocked by mAb to LFA‐3, T11TS and CD2 known to inhibit CD2‐ligand interaction. In addition, purified LFA‐3 and T11TS, when added at ng amounts to cultures containing submitogenic concentrations of anti‐T112 + 3 mAb, are also strongly mitogenic for resting human T cells. Thus, both LFA‐3 and T11TS are potent co‐stimulators of the alternative pathway of T cell activation but by themselves do not provide a mitogenic signal. This finding is discussed with regard to a physiological role of CD2‐LFA‐3 interaction in T cell activation.
Anti‐interferon‐γ antibody protects mice against the generalized Shwartzman reaction
Authors: Billiau Alfons , Heremans Hubertine , Vandekerckhove Filip , Dillen Chris 
Published: March 2007

AbstractA generalized Shwartzman reaction was found to occur in non‐SPF‐NMRI mice given a local injection of S. marcescens lipopolysaccharide (LPS) in the footpad, followed, with an interval of 24 h, by an i.v. injection. The reaction occurred several hours after the second injection. It was characterized by disseminated subcutaneous bleedings at the mouth, anus, conjuctiva, nose tip and tail end. Most mice died within 24–48 h. The size of the LPS dose given in the footpad (5 μg) was found to be critical in that the reaction failed to occur with higher as well as lower doses. The reaction was found to be completely absent in mice that had received one or more systemic injections of monoclonal antibodies with neutralizing potential for murine interferon‐γ (IFN‐γ). Mice treated with control preparations, including a monoclonal antibody with binding but no neutralizing activity for murine IFN‐γ, remained sensitive to induction of the reaction. These observations assign a crucial role to endogeneous IFN‐γ in the elicitation of the generalized Shwartzman reaction and open perspectives for the prevention or therapy of clinical conditions related to the Shwartzman reaction by the use of antibodies to IFN‐γ.
Alloreactive T cell clones transformed by Theileria parva retain cytolytic activity and antigen specificity
Authors: Baldwin Cynthia L. , Teale Alan J. 
Published: March 2007

AbstractTheileria parva is a protozoan parasite which infects and transforms bovine lymphocytes. This study examined the effects of Theileria‐induced transformation on phenotype and function, in terms of cytolytic potency and specificity, of class I and class II‐specific alloreactive T cell clones. Alloreactive T cell clones infected with T. parva (Muguga) retained expression of the T cell differentiation antigens BoT2, BoT4, BoT8 and the mature T cell antigen recognized by monoclonal antibody ILA27, as well as cytolytic function and antigen specificity, over a period of 3–4 months in continuous culture. These features were identical to those expressed by the uninfected parent clones. During this period, neither antigenic stimulation nor exogenous growth factors were required for the maintenance of proliferation, function or antigen specificity. Thereafter, cytolytic activity declined and was eventually lost, which may reflect degenerative changes normally associated with T cell senescence rather than result from parasitization per se.