bluuebunny/crossref_metadata_2025_split huggingface dataset:
induction of human in vitro ige synthesis via stimulation by anti‐cd3 antibody
Authors: Yang Xiao‐Dong , Weck Alain L. De , Stadler Beda M. 
Published: March 2007

AbstractMitogens such as pokeweed mitogen, Staphylococcus aureus Cowan I, con‐canavalin A and phytohemagglutinin and monoclonal anti‐CD antibodies were examined for their‐ capacity to induce IgE synthesis by peripheral blood leukocytes obtained from both atopic and nonatopic individuals. While lectins failed to induce IgE synthesis, monoclonal anti‐CD3 antibodies were very potent stimuli for the induction of human in vitro IgE synthesis, possibly due to the activation of T cells. Activation via CD4 or CD8 molecules by OKT4 or OKT8 antibodies did not lead to a T cell‐dependent modulation of IgE synthesis. PWM acted in synergy with the enhancing effect of anti‐CD3 antibodies for IgE synthesis. In vitro IgG production was less affected. These results indicate that activation of T cell via CD3 molecules may be important in the regulation of IgE immune responses in man. Furthermore, the successful induction of IgE synthesis by anti‐CD3 antibody in unfractionated peripheral blood leukocytes culture provides a simple model for investigation of human IgE regulatory mechanism in vitro.
Anti‐suppressor effect of cyclophosphamide on the development of spontaneous diabetes in nod mice
Authors: Yasunami Reiko , Bach Jean‐FrançOis 
Published: March 2007

AbstractIn the NOD mouse, an autoimmune process beginning by 5 weeks of age with lymphocyte infiltration and destruction of insulin‐secreting beta cells leads to overt diabetes which begins to appear by 11 weeks of age. Although there is a high incidence of insulitis by 10 weeks of age (> 80%) in both males and females, by 30 weeks of age diabetic symptoms have occurred in 53‐80% of females and in 1240% of males. Intraperitoneal injection of a high dose (200 mg/kg) of cyclophosphamide (CY) consistently induces the onset of diabetes in male and female NOD mice at an age when spontaneous diabetes rarely occurs. Spleen T cells from CY‐induced diabetic mice are capable of transferring the disease into irradiated nondiabetic syngeneic recipients. This indicates that the diabetogenic effect of CY is not mediated by direct toxicity on pancreatic beta cells but is mediated by abrogation of a suppressor mechanism which may prevent activation of T cells responsible for the development of diabetes in the NOD mouse. Additionally, CY is only effective in NOD mice and not in F1 hybrids between NOD and other strains of mice. Thus, the potential beta cell aggressor mechanism is not present in these hybrids as it is in homozygous mice, which indicates that it is not under the control of dominant genes.
In vivo function of natural killer cells as regulators of myeloid precursor cells in the spleen
Authors: Hansson Mona , Petersson Max , Koo Gloria C. , Wigzell Hans , Kiessling Rolf 
Published: March 2007

AbstractIn order to study the in vivo effect that natural killer (NK) cells may have on hematopoietic precursor cells in the autologous host, NK‐depleted mice were constructed by injection of an anti‐NK‐1.1 monoclonal antibody. Only the spleen, and not the bone marrow, of such NK‐depleted mice shows an increase in the number of myeloid precursur cells able to form colonies in soft agar as compared to control mice with normal levels of NK activity. The increase in number of hematopoietic immature cells due to lack of a regulatory cell (i.e. NK cell) is selective for the committed myeloid precursur cells, and not evident for erythroid or pluripotent progenitor cells. This is direct evidence in support of the hypothesis that NK cells in the autologous host serve as a regulator of extramedullary myelopoiesis.
The role of protein kinase C in early activation vs. growth of T lymphocytes
Authors: Friedrich Bengt , Gullberg Martin 
Published: March 2007

AbstractProtein kinase C (PKC) has been implicated in the signaling of a number of cellular responses including activation of T cells. In an approach to study the role of PKC in both early activation and interleukin 2 (IL2)‐dependent growth, we have used in vivo phosphorylation of endogenous substrates as a marker for PKC activation. In the present report the requirements for CD3‐specific activation of PKC are defined, and it is shown that the conditions required for optimal activation coincide with the induction of a proliferative response. Moreover, it is also shown that IL2 receptor interactions induce only low levels of PKC substrate phosphorylation and that IL2 does not cooperate with CD3‐specific signals on the level of PKC activation.
Long‐term depletion of cd8+ t cells in vivo in the rat: no observed role for cd8+ (cytotoxic/suppressor) cells in the immunoregulation of experimental allergic encephalomyelitis
Authors: Sedgwick Jonathon D. 
Published: March 2007

AbstractA method is described for the long‐term depletion of CD8+ T cells in the rat. Employing Lewis rats depleted of this cell type it is shown that such animals acquire, and subsequently recover from both passively and actively induced experimental allergic encephalomyelitis (EAE) in a comparable fashion to normal animals. Furthermore, after spontaneous recovery from the initial bout of disease, CD8+ T cell‐depleted rats do not show any signs of relapse and, like normal rats following recovery from active EAE, are still resistant to further attempts at disease induction. Overall, these data do not support a role for the classic cytotoxic/suppressor (CD8+) T cell in the immunoregulation of EAE in the Lewis rat.
Interferon‐γ is not an antiviral, but a growth‐promoting factor for t lymphocytes
Authors: Landolfo Santo , Gariglio Marisa , Gribaudo Giorgio , Jemma Cristina , Giovarelli Mirella , Cavallo Giorgio 
Published: March 2007

AbstractThe effects of interferon (1FN)‐γ or IFN‐α/β on virus yield, (2′‐5′)oligo(A) synthetase activation, H‐2 antigen expression and proliferation of T lymphocytes have been investigated. Under the culture conditions used, vesicular stomatitis virus or Semliki Forest virus replication in T cells was not impaired by the addition of IFN‐γ, whereas it was completely inhibited by the addition of IFN‐α/β. In contrast, B cell lines, macrophage‐transformed cell lines and fibroblasts were fully protected by both IFN‐γ as well as IFN‐α/β following virus infection. The lack of sensitivity of T lymphocytes to the antiviral effects of IFN‐γ was not due to absence of specific membrane receptors, since in saturation binding experiments with 125I‐labeled murine IFN‐γ most T cell lines displayed a number of binding sites and a degree of affinity comparable to those found on B cells, which are fully sensitive to IFN‐γ antiviral activity. Analysis of IFN‐induced dsRNA‐dependent (2′‐5′)oligo(A) synthetase activity, one of the biochemical markers for cellular responses to IFN, showed that it was not induced in T lymphocytes after IFN‐γ treatment, whereas IFN‐α/β induced high levels. Both IFN‐γ and IFN‐α/β enhanced H‐2 antigen expression on T cells as well as on cells of different histological type. Moreover, when IFN‐γ was tested for its antiproliferative activity on T cells, it was found to consistently potentiate the response of these cells to mitogens or growth factors, rather than inhibit their proliferation. Taken as a whole these results suggest that on T lymphocytes IFN‐γ should not be regarded as an antiviral agent, but rather as a modulator of T cell growth and functional differentiation, transducing intracellular signals dissimilar to those observed with target cells of different origin.
An acquired immune suppression in mice caused by infection with lymphocytic choriomeningitis virus
Authors: Roost Hanspeter , Charan Shiv , Gobet Rita , Rüedi Edith , Hengartner Hans , And Alana Althage , Zinkernagel Rolf M. 
Published: March 2007

AbstractA murine model of virally induced acquired immunodeficiency was analyzed in mice. The effect of systemic infection with various isolates of lymphocytic choriomeningitis virus (LCMV) on the capacity of mice to mount a T cell‐independent IgM and a T cell‐dependent IgG neutralizing antibody response against a subsequent infection with vesicular stomatitis virus (VSV) was analyzed. DBA/2 mice infected with the LCMV‐WE isolate were impaired in their IgM and IgG responses to VSV. Immune suppression was not caused by interferons inhibiting proper VSV antigen expression, since responses to inactivated VSV were also suppressed. The higher the dose of the LCMV and the lower the dose of the challenging VSV infection the more drastic was the apparent lack of immune responsiveness and the longer it lasted. Kinetics of induction of suppression of the T cell‐independent IgM responses closely followed that of a normal cytotoxic T cell response to LCMV‐WE, starting on day 6 and reaching maximal levels by day 8 to 10. The T cell‐dependent IgG response to VSV was suppressed with a kinetics that was shifted by about 6 days when compared with suppression of IgM responses, i.e. LCMV infection on the same day or before (but not after) VSV infection led to suppression of IgG responses that are usually first detected by day 6‐7 after initiation of the VSV infection. Severity and duration of immunosuppressiveness depended upon the LCMV isolate and the mouse strain used: LCMV‐WE and LCMV‐Docile were most, whereas LCMV‐Armstrong was in general least immunosuppressive. Antibody responses to VSV‐NJ seemed to be more subject to LCMV‐induced immune suppression than VSV‐IND‐specific responses. Mouse strains differed considerably with respect to extent of suppression, dependent upon both major histocompatibility genes (MHC) and non‐MHC genes. DBA and Swiss type mice were generally more susceptible than C57BL and CBA mice, and H‐2q and H‐2k seemed to be more susceptible than H‐2b or H‐2d mice.Mice infected with LCMV‐WE showed signs of acquired immunodeficiency diseases since they were more susceptible to superinfection with VSV and developed paralytic disease and tended to die from VSV infection. Since LCMV is basically a noneytopathic virus, this murine model of virally induced immune suppression may serve to analyze immune pathogenesis of virus‐induced acquired immunodeficiency.
Signal transduction through cd4 receptors: stimulatory vs. inhibitory activity is regulated by cd4 proximity to the cd31t cell receptor
Authors: Ledbetter Jeffrey A. , June Carl H. , Rabinovitch Peter S. , Grossmann Angelika , Tsu Theta T. , Imboden John B. 
Published: March 2007

AbstractThe binding of antibody to the CD4 molecule inhibits mobilization of cytoplasmic free calcium ([Ca2+]i) in response to CD3 cross‐linking on resting T cells. Similarly, when CD3 and CD4 are independently and simultaneously cross‐linked, calcium mobilization is inhibited when compared to that induced by cross‐linking CD3 alone. In contrast, when anti‐CD4 and anti‐CD3 are cross‐linked together, calcium mobilization is substantially higher than from CD3 cross‐linking alone. A heteroconjugate consisting of covalently bound CD3 and CD4 monoclonal antibodies (mAb) retains the ability to mobilize [Ca2+]i in CD4 cells at protein concentrations approximately two orders of magnitude lower than the free CD3 mAb, and the activity of the heteroconjugate is inhibitable by free CD4 mAb. The CD3/CD4 heteroconjugate also shows significantly greater activity in stimulation of inositol phosphate IP1, IP2 and IP3 synthesis in T cells than the CD3 mAb alone, and again the activity is inhibited by free CD4 mAb. The activity of the CD3/CD4 heteroconjugate is not simply due to oligomerization, since CD3/CD3 or CD4/CD4 homoconjugates or homoconjugate mixtures did not show increased activity. Other heteroconjugates (CD3/CD5 and CD3/CD28) were not different than the CD3/CD3 homoconjugate in their ability to increase [Ca2+]i. Purified CD4 T cells that do not respond to CD3 mAb in solution do respond to the CD3/CD4 heteroconjugate in solution by proliferating in the presence of a CD28 mAb, with a significant fraction of CD4 cells entering the second cycle within the first three days of stimulation. The CD3/CD4 heteroconjugate co‐modulates the CD3 and CD4 receptors, indicating that the heteroconjugate is not simply anchoring the T cell receptor to the T cell surface like anti‐CD3 on a solid surface. These results suggest that CD4 plays an active role in signal transduction when brought into close physical proximity to the CD3/T cell receptor complex during major histocompatibility complex class II‐restricted antigen presentation.
Characterization and functional properties of a novel monoclonal antibody which identifies a T cell receptor in chickens
Authors: Cihak Josef , Ziegler‐Heitbrock H. W. LöMs , Trainer Hans , Merkenschlager Michael , Lösch Uli 
Published: March 2007

AbstractA monoclonal antibody, mAb6, was produced that specifically bound to chicken T lymphocytes. Immunofluorescence analysis using a fluorescence‐activated cell sorter revealed that the antibody reacted with approximately 50% of blood lymphocytes and with approximately 40% of splenocytes and thymocytes. It did not react with bursa1 cells and erythrocytes. Among different types of hemopoietic cell lines, only a T cell line was reactive with mAb6. When coupled to Sepharose 4B beads, mAb6 was found to be highly mitogenic for chicken T cells. In soluble form, mAb6 inhibited concanavalin A‐induced T cell proliferation and the cytotoxic activity of allosensitized T cells, the inhibition occurring in a dose‐dependent manner for both assays. Thus, the tissue distribution and the effects of this antibody on T cell responses suggest that mAb6 recognizes a T cell receptor present on a large proportion of chicken T cells.
Differential expression of two t cell receptors, tcr1 and tcr2, on chicken lymphocytes
Authors: Chen Chen‐Io H. , Cihak Josef , Lösch Uli , Cooper Max D. 
Published: March 2007

AbstractA monoclonal antibody, TcR2, has been shown to recognize an avian homologue of the mammalian α/β T cell receptor (TcR). The TcR2‐reactive molecule was found to be a T3‐associated heterodimer with relative molecular mass of 90‐kDa consisting of disulfide‐linked 50‐kDa and 40‐kDa polypeptides. The sizes of the deglycosylated TcR2 polypeptides differed from those of TcR1, an avian homologue of the mammalian γ/δ T cell receptor. Immunofluorescence analysis revealed that TcR1 and TcR2 are expressed on separate populations of T cells during their development first in the thymus and then in the periphery. Ontogenetic studies revealed that the TcR1+ thymocytes are generated first and the generation of TcR2+ cells begins approximately 3 days later. While most TcR2+ cells in the thymus expressed both CT4 and CT8, TcR2+ cells in blood and the spleen were either CT4+ or CT8+. The TcR1+ cells in blood and thymus were CT4−CT8−, but the majority of TcR1+ cells in the spleen surprisingly expressed the CT8 marker. The data suggest that TcR1 and TcR2 cells are generated in the thymus as separate T cell sublineages.
Class‐specific suppression of human b cell maturation by iga‐binding factors
Authors: Millet Isabelle , Samarut Christiane , Revillard Jean‐Pierre 
Published: March 2007

AbstractIgA‐binding factors (IgA‐BFs) were prepared by chromatography on Sepharose 4B beads covalently linked to dimeric and polymeric monoclonal IgA1 from supernatants of peripheral blood mononuclear lymphocytes (PBMC) and human B cell lines incubated in serum‐free medium. Receptors for IgA, as revealed by the binding of biotinylated monoclonal IgA1, were expressed on monocytes, T‐enriched and T‐depleted lymphocytes. IgA‐BFs or control eluates were added to pokeweed mitogen (PWM)‐stimulated PBMC cultures, and their effects on the terminal differentiation of polyclonally activated human B cells were assessed by enumeration of intracytoplasmic IgM‐, IgG‐ or IgA‐containing cells. A selective decrease of IgA‐containing cells was observed in the presence of IgA‐BFs whereas IgM‐ and IgG‐containing cells remained unchanged. Differential counts of B blasts and plasma cells revealed that only the former were decreased following addition of IgA‐BFs. Kinetic studies indicated that maximum inhibition of IgA‐containing cell generation was achieved when IgA‐BFs were added during the first 5 days of PWM‐stimulated PBMC cultures, whereas no inhibition could be demonstrated when IgA‐BFs were added 24 h before harvesting. IgA‐BFs did not decrease [3H]thymidine incorporation in PWM‐stimulated PBMC cultures. They diminished the proliferation of the surface IgA+ monoclonal human B cell line DAKIKI, but not that of the surface IgA− IM‐9 cell line. Several control eluates obtained from the same cell supernatants absorbed on Sepharose 4B, Sepharose 4B‐IgG or Sepharose 4B‐β2‐microglobulin had no effect. Finally, IgA‐BFs prepared from supernatants of two human B cell lines bearing receptors for IgA selectively depressed the generation of intracytoplasmic IgA+ cells in PBMC cultures stimulated by PWM. Altogether the data indicate that IgA‐BFs obtained by spontaneous release from heterogeneous mononuclear cell suspensions or from IgA receptor‐positive human monoclonal B cell lines selectively depress the maturation of B cells into IgA plasma cells and the proliferation of a surface IgA+ B cell line.
The effect of immunization with a 14‐kda streptococcal antigen on primate t cell and b cell responses
Authors: Fellowes Raymond , Fortune Farida , Bergmeier Lesley A. , Lehner Thomas 
Published: March 2007

AbstractA streptococcal antigen (SA) of 185 kDa was isolated from Streptococcus mutuns and this antigen induced in vitro helper, suppressor and contrasuppressor activities with primate peripheral blood lymphocytes. The 185‐kDa SA was then treated by sodium dodecyl sulfate and yielded a 4‐kDa SA which was capable of eliciting only helper activity. We have now cleaved the 185‐kDa SA with cyanogen bromide, in an attempt to identify suppressor and contrasuppressor determinants. A 14‐kDa SA was separated from the cyanogen bromide digest and its ability to elicit T cell and B cell functional activities was tested in rhesus monkeys. Whereas the 185‐kDa SA (and 4‐kDa SA) elicited high serum anti‐SA antibodies and the CD4 cells showed an increase in DNA synthesis, this was not demonstrable with the 14‐kDa SA. However, the 14‐kDa SA, unlike the 185‐kDa SA, activated a significant proportion of CD4 and CD8 cells to bind the Viciu villosu lectin (VV) and this is a characteristic feature of contrasuppressor cells. We then studied the effect of sequential immunization of monkeys with the 14‐kDa SA, followed by the 185‐kDa SA. The results of this showed suppression of the CD4 proliferative response, in the presence of a normal antibody production. We suggest that the split tolerance between the T cell proliferative and B cell differentiating functions might be interpreted on the basis of suppressor CD8 cells inhibiting the CD4 proliferative phase and the W‐adherent CD8 cells contrasuppres‐sing B cell antibody formation.
Ontogeny of human complement receptors cr1 and cr3: expression of these molecules on monocytes and neutrophils from maternal, newborn and fetal samples
Authors: Adinolfi Matteo , Cheetham Mark , Lee Tak , Rodin Adam 
Published: March 2007

AbstractHigher levels of the expression of CR1 and CR3 molecules were detected on the surface of monocytes and neutrophils from maternal and newborn (cord) blood samples than in adult controls. Chemotactic factors such as formyl‐methionyl‐leucylphenylalanine or leukotriene B4 induced an increase of the expression of CR1 and CR3 which was more pronounced on cells from maternal and cord samples than from nonpregnant adult controls. CR1 and CR3 molecules were detected in monocytes and neutrophils from peripheral blood obtained from fetuses more than 14 weeks old and on subpopulations of cells in bone marrow, spleen and thymus.
Expression of receptors for iga on mitogen‐stimulated human t lymphocytes
Authors: Millet Isabelle , Panaye Genevikve , Revillard Jean‐Pierre 
Published: March 2007

AbstractThis study demonstrates that activation of human peripheral blood mononuclear cells (PBMC) by the T cell mitogens phytohemagglutinin (PHA) and concanavalin A (Con A) induces the expression of receptors for IgA without addition of IgA to the culture medium. Cells bearing receptors for IgA were determined by indirect immuno‐fluorescence using human secretory IgA and fluoresceinated goat anti‐human IgA or goat anti‐secretory component antibodies. Among freshly isolated PBMC, 4.7 ± 1.7% of T cells, 12.7 ± 12.5% of B cells and 14.4 ± 7.6% of monocytes were found to be IgA receptor positive. In unstimulated PBMC cultures the percentage of IgA receptor‐positive cells slightly increased at 48 h and was more elevated after 7 days. In Con A‐stimulated cultures 24.3 ± 18.5% of the cells expressed receptors for IgA after 48 h. Then, the number decreased and rose again thereafter. PHA stimulation induced an increase of smaller magnitude with similar kinetics. Induction of receptor for IgA on activated T cells was demonstrated by double‐labelling experiments showing more CD8+ than CD4+ cells with receptors for IgA among Con A‐activated PBMC. Furthermore, PHA or Con A stimulation of B cell‐depleted PBMC suspensions resulted in a marked increase of cells bearing receptors for IgA. Expression of these receptors was down‐regulated by recombinant interferon‐γ (250 units/ ml) and by prostaglandin PGE2 (100 nM) both on unstimulated and mitogen‐activated PBMC. The receptor for IgA was distinct from the asialoglycoprotein receptor and did not cross‐react with the poly‐Ig receptor of epithelial cells. It was concluded that, in the absence of inducing exogenous IgA, T cell mitogens trigger the expression of receptors for IgA. Therefore, T cell activation is associated with the down‐regulation of receptors for IgM and the increased expression of receptors for IgG, IgA and IgE.
The human t cell receptor α‐δ locus: a physical map of the variable, joining and constant region genes
Authors: Griesser Henrik , Champagne Erik , Tkachuk Douglas , Takihara Yoshihiro , Lalande Marc , Baillie Eric , Minden Mark , Mak Tak W. 
Published: March 2007

AbstractIn this study a physical macro‐restriction map of the entire human a locus that spans about 1000 kilobase pairs and includes the Vα Jα and Cα genes is presented. Evidence is provided that gene duplications were involved in the increase of genomic diversity of Vα genes. In addition, we show a detailed map of a 40‐kb region located approximately 100 kg upstream of the human Cα gene. Direct evidence is provided to support that the human a chain locus, like the murine, also contains another T cell constant region gene in the a chain locus, the human σ chain gene. In addition, two J segments and one D segment have been identified. Using these genomic probes, we show that several T cell lines, including those known to express the surface γ/σ heterodimer, have rearranged this region. The design of two separate centers of rearrangement within one locus that are involved in rearrangement events at different times, and the presence of high number of J segments in this region, may render the locus highly vulnerable to chromosomal translocation during T cell developement.