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Results for “antigen expression and secretion”

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PubMed1999

The effects of dexamethasone, cyclosporine, and vitamin D(3) on the activation of dendritic cells stimulated by haptens.

By their potent antigen-presenting function, dendritic cells (DCs) play a crucial role in the initiation of T cell-mediated immunity, including allergic contact hypersensitivity. To acquire such potent antigen-presenting ability, DCs in tissue must be activated, with increased expression of costimulatory molecules. Recent progress in DC biology has demonstrated that DCs can be activated via a variety of substances, e.g. various cytokines, CD40 ligand, bacterial products, and haptens, to increase their antigen-presenting ability, probably by different mechanisms. Therefore, in this study, to elucidate the mechanisms underlying the efficacy of the immunosuppressive drugs dexamethasone (DEX), cyclosporine A (CY), and vitamin D(3) (Vit D3) in the modulation of allergic contact hypersensitivity reactions, we examined the effects of these drugs on CD86 and HLA-DR antigen expression and TNFalpha secretion by monocyte-derived DCs stimulated with two representative haptens, NiCl(2) and DNCB, in vitro. The augmented expression of CD86 induced by NiCl(2) and DNCB was significantly suppressed by DEX at concentrations in the range 10(-8) to 10(-5) M, which include concentrations less than its therapeutically effective concentration of 10(-7) M. Vit D3 also significantly suppressed NiCl(2)- and DNCB-induced augmented expression of CD86, at concentrations in the ranges 10(-9) to 10(-7) M and 10(-10) to 10(-7) M, respectively. In contrast, significant suppressive effects of CY on the NiCl(2)- or DNCB-induced augmented expression of CD86 were seen only at concentrations in the range 10(-6) to 10(-5) M, which are more than ten times higher than its effective concentration for T cell suppression. The augmented expression of HLA-DR antigen, which was only induced by stimulation with NiCl(2), was resistant to treatment with these three drugs. Only DEX suppressed HLA-DR antigen expression at 10(-5) M. TNFalpha secretion by stimulated DCs was suppressed by DEX and Vit D3, although their effects were not statistically significant. Thus DEX and Vit D3 could modulate allergic contact dermatitis by their clearly demonstrated suppressive effects on the activation of DCs by haptens.

Antigens, CD↗

PubMed1992

Identification of a prenylation site in delta virus large antigen.

During replication, hepatitis delta virus (HDV) switches from production of small to large delta antigen. Both antigen isoforms have an HDV genome binding domain and are packaged into hepatitis B virus (HBV)-derived envelopes but differ at their carboxy termini. The large antigen was shown to contain a terminal CXXX box and undergo prenylation. The large, but not the small, antigen formed secreted particles when expressed singly with HBV surface antigen. Mutation of Cys211 in the CXXX box of the large antigen abolished both prenylation and particle formation, suggesting that this site is important for virion morphogenesis.

3T3 Cells↗

PubMed1996

Biology of colorectal and gastric cancer cell lines.

Cell lines established from the human colorectal and gastric cancers may provide very useful tools to the study of the disease and to develop and test new therapeutic approaches, and a large bank of well-characterized cell lines should reflect the diversity of tumor phenotypes and provide adequate models for the study of tumor heterogeneity. Colorectal lines are relatively easy to establish, while gastric cancer cell lines remain extremely difficult to propagate in long-term culture, and the number of cell lines is very limited. In this paper, we describe the up-to-date results of the characteristics of our nine colorectal cancer cell lines and four gastric cancer cell lines. Based on culture, xenograft, and ultrastructural morphologies, these cell lines could be subtyped into well-differentiated, moderately differentiated, poorly differentiated, and mucinous carcinomas. Basic properties concerning expression and secretion of antigens, neuroendocrine features, receptor binding of various gastrointestinal hormones and neurotransmitters, cytogenetic studies, gene amplification and expression, and chemosensitivity profiles are described. In particular, a greater number of receptors for hormones and neurotransmitters are expressed on human colorectal cancer cell lines compared to gastric cancer cell lines, raising the possibility that gastrointestinal hormones may have a greater autocrine effect on colon cancer cell growth. Despite major differences in the biology of colorectal cancer and gastric cancer as indicated by clinical studies, the multiple properties that we examined reveals marked similarities between the colorectal and gastric cancer cell lines. However, in vitro chemosensitivity patterns to cytotoxic drugs are very different in colorectal and gastric cell lines. Some of these observations may be due to the relatively low expression of the multidrug-resistance-associated (MDR1) gene in gastric cancer cell lines. In addition, colorectal cancer cell lines express receptors for peptide hormones more frequently.

Adenocarcinoma↗

PubMed1995

Recombinant Listeria monocytogenes as a live vaccine vehicle for the induction of protective anti-viral cell-mediated immunity.

Listeria monocytogenes (LM) is a Gram-positive bacterium that is able to enter host cells, escape from the endocytic vesicle, multiply within the cytoplasm, and spread directly from cell to cell without encountering the extracellular milieu. The ability of LM to gain access to the host cell cytosol allows proteins secreted by the bacterium to efficiently enter the pathway for major histocompatibility complex class I antigen processing and presentation. We have established a genetic system for expression and secretion of foreign antigens by recombinant strains, based on stable site-specific integration of expression cassettes into the LM genome. The ability of LM recombinants to induce protective immunity against a heterologous pathogen was demonstrated with lymphocytic choriomeningitis virus (LCMV). LM strains expressing the entire LCMV nucleoprotein or an H-2Ld-restricted nucleoprotein epitope (aa 118-126) were constructed. Immunization of mice with LM vaccine strains conferred protection against challenge with virulent strains of LCMV that otherwise establish chronic infection in naive adult mice. In vivo depletion of CD8+ T cells from vaccinated mice abrogated their ability to clear viral infection, showing that protective anti-viral immunity was due to CD8+ T cells.

Amino Acid Sequence↗

PubMed2002

High-level heterologous expression and secretion in Streptomyces lividans of two major antigenic proteins from Mycobacterium tuberculosis.

Two major antigens from Mycobacterium tuberculosis were produced by Streptomyces lividans as secreted extracellular proteins. An expression-secretion vector had been constructed that contained the promoter of xylanase A and the signal sequence of cellulase A. The latter contained two initiation codons preceded by a Shine-Dalgarno sequence plus eight nucleotides complementary to the 16S rRNA. The genes encoding the 38-kDa (Rv0934) and 19-kDa (Rv3763) proteins, respectively, were amplified by polymerase chain reaction and cloned into that vector. The recombinant proteins were then purified from the culture supernatants of the clones. The yields after purification were 80 mg/L for the 38-kDa protein and 200 mg/L for the 19-kDa protein. Sequence analysis of the N-terminal sequences showed a deletion of seven or eight amino acids for the 38-kDa protein, while in the 19-kDa protein 22 or 23 amino acids were lost, as compared with the respective wild-type proteins. However, the 19 kDa recombinant protein had the same N-terminal sequence as the one recovered from the M. tuberculosis culture supernatant. The high yields obtained for these two proteins demonstrated the potential of S. lividans as an alternative host for the production of recombinant proteins from M. tuberculosis. The culture conditions have yet to be worked out to minimize proteolytic degradation and to recover intact products.

Antigens, Bacterial↗

PubMed1988

Nickel antigen induces IL-2 secretion and IL-2 receptor expression mainly on CD4+ T cells, but no measurable gamma interferon secretion in peripheral blood mononuclear cell cultures in delayed type hypersensitivity to nickel.

Nickel sulphate antigen-induced peripheral blood lymphocyte activation in vitro was characterized by lymphokine measurement (IL-2, IFN-gamma) and phenotyping of the IL-2 responsive cells. Mononuclear cells from nickel-sensitive patients synthesized more DNA, produced more IL-2 and had more IL-2 receptor positive cells in response to nickel than did those of the control subjects. On the other hand no IFN-gamma was detectable in the nickel supernatants, while PPD, used as the control antigen, induced pronounced quantities of IFN-gamma with an equal amount of DNA synthesis. The increase in IL-2 receptor positive cells was due to activation of CD4+ (helper/inducer) T cells. T cells with HLA-DR antigen surface markers were more numerous on each day of culture than cells with IL-2 receptors. These two activation markers were co-expressed on the same cells only to a certain extent, thus perhaps reflecting different types or phases of activation. In conclusion, nickel-induced peripheral blood mononuclear cell activation in vitro differs from microbial antigen-induced activation with respect to its modest or non-existent IFN-gamma response.

Adult↗

PubMed1996

Immune infiltrates and cytokines in gliomas.

Frozen sections of 21 gliomas were analysed to characterize inflammatory infiltrating cells, HLA-DR antigen expression and cytokine secretion. Mononuclear cells infiltrating the tumours were mostly macrophages, which were detected in 100% of cases, and expressed HLA-DR antigens. Lymphocytes were less frequently seen and expressed the CD8 phenotype. Interleukin-1 beta (IL-1 beta) and Interleukin-6 (IL-6), two cytokines mainly produced by activated cells of the macrophage lineage, were demonstrated especially in neoplastic astrocytes. IL-1 beta immunoreactivity was detected in all tumours, and was prevalent in more anaplastic gliomas; IL-6 was found in anaplastic gliomas and in glioblastomas. IL-1 receptors were expressed by both infiltrating macrophages and neoplastic astrocytes in the gliomas analysed. These findings suggest that cytokine production in gliomas seems not related to immune reactions against the tumour and their synthesis by anaplastic astrocytes could follow an unregulated activation of many metabolic processes after neoplastic transformation.

Astrocytes↗

PubMed1989

Complete characterization of the gene coding for the Epstein-Barr virus major membrane antigen gp 220/340 and selective expression of a secreted form of gp 220.

The gene which encodes the Epstein-Barr gp 220/340 was inserted into a eukaryotic expression vector. A cDNA clone corresponding to the mature mRNA coding for gp 220 was isolated from an Epstein-Barr virus cDNA library and inserted in the same expression vector, enabling us to identify the precise location of the intron within the gp 220/340 coding sequence. The recombinant plasmids direct the expression of membrane proteins detected by immunofluorescence experiments using an anti-gp 220/340 monoclonal antibody in transfected human cells. The region of the gp 220/340 gene encoding the domain for membrane anchorage was removed from the two recombinant plasmids and the sequence containing the intron produced secreted forms of both truncated gp 220 and gp 340 whereas only the former was obtained with the intronless sequence.

Antigens, Viral↗

PubMed1982

Antigenicities of mucins - their relevance to tumour associated and stage specific embryonic antigens.

It can now be envisaged that there exists a distinct set of differentiation antigens formed by linear (i type) or branched (I-type) oligosaccharides and their fucosylated (and perhaps sialylated) derivatives. Several of these antigens are expressed in secreted glycoproteins (mucins) which are relatively abundantly available. Thus mucins can serve as valuable sources of oligosaccharide haptens of differentiation antigens just as they have done in the past with the major blood group antigens.

Animals↗

PubMed1997

Normal B cells fail to secrete interleukin-12.

Interleukin-12 is a key regulatory cytokine produced by antigen-presenting cells (APC) which drives the development of interferon-gamma (IFN-gamma)-producing cells and promotes cell-mediated immunity. Following subcutaneous immunization with protein antigen in adjuvant, dendritic cells (DC) but not small nor large B cells in immune lymph nodes express antigenic complexes and secrete substantial amounts of bioactive IL-12 p75 upon antigen-specific interaction with T cells. We have analyzed secretion of IL-12 p40 and p75 by cell populations enriched in DC, macrophages or B cells in response to nonspecific stimulation or to interaction with antigen-specific CD4+ cells. These APC populations do not produce IL-12 constitutively but, upon stimulation with heat-fixed Staphylococcus aureus and IFN-gamma, IL-12 p40 and p75 are secreted by DC and macrophages, whereas B cells fail to produce IL-12. B cells also fail to secrete IL-12 in response to stimulation with LPS and IFN-gamma. Co-culture with CD4+ T hybridoma cells and antigen induces IL-12 secretion by DC. Up-regulation of IL-12 secretion by interaction with antigen-specific CD4+ T cells is abrogated by anti-class II monoclonal antibodies (mAb), by soluble CD40 molecules and by anti-CD40 ligand mAb, demonstrating a positive feedback between T cells and DC mediated by TCR-peptide/class II and by CD40-CD40 ligand interactions. Expression of class II and CD40 molecules is comparable in B cells and DC, and both APC types activate CD4+ T cells. Yet, even upon interaction with antigen-specific T cells, B cells fail to secrete IL-12. The capacity of B cells to present antigen but not to secrete IL-12 may explain their propensity to selectively drive T helper type 2 cell development.

Amino Acid Sequence↗

PubMedDate not supplied

Cytotoxic CD4+ T cells associated with the expression of major histocompatibility complex class II antigen of mouse myeloma cells secreting interferon-gamma are cytolytic in vitro and tumoricidal in vivo.

Vaccination of mouse myeloma V(K)C(K)-gamma (I) cells secreting interferon (IFN)-gamma and expressing enhanced major histocompatibility complex (MHC) class I antigen (Ag) resulted in protective immunity that was mainly mediated by CD8+ T cells. V(K)C(K)-gamma (I/II) cells expressing both enhanced MHC class I and class II Ags were isolated from V(K)C(K)-gamma (I) cells. These V(K)C(K)-gamma (I/II) cells were used to study the relationship between IFN-gamma secretion of tumor cells, its tumorigenicity, and its induced immunity, as well as to evaluate the cellular immunocomponents mediating this immunity. Our animal studies showed that IFN-gamma secretion by V(K)C(K)-gamma (I/II) cells curtailed its tumorigenicity in syngeneic BALB/c mice and further induced protective immunity against a subsequent graft of parental V(K)C(K) tumor. This immunity is mediated by both CD4+ and CD8+ T cells. The activation of CD4+ T cells is associated with enhanced expression of MHC class II Ag of V(K)C(K)-gamma (I/II) cells. These CD4+ T cells are tumor specific and cytolytic in an MHC-restricted fashion in vitro, and are tumoricidal in a T-cell adoptive transfer experiment in vivo. Our data thus demonstrate that vaccination of genetically modified tumor cells secreting IFN-gamma may provide beneficial antitumor effects by inducing both cytolytic CD4+ and CD8+ cytotoxic T lymphocytes, provided that these tumor cells express both enhanced MHC class I and class II Ags.

Animals↗

PubMed1985

Acquisition of cytotoxic T lymphocyte-specific carbohydrate differentiation antigens.

Cytotoxic T cell (CTL)-specific activation antigens, termed CT determinants, have been detected by monoclonal antibodies (mAb) that inhibit CTL function. At the cell surface, the CT antigens are associated with the T200 glycoproteins and two other proteins of Mr 140,000 and 85,000 and are present on a secreted protein, gp155. Periodate treatment followed by binding analysis and immunoprecipitation experiments using tunicamycin-treated cells indicated that carbohydrate is necessary for CT antigen expression. Furthermore, gp155 is secreted in the presence of tunicamycin while retaining the CT antigens, and the CT determinants are added late in T200 biosynthesis, suggesting that the CT glycans are O-linked. Finally, interleukin 2 was shown to dramatically influence the expression of the CT mAb-reactive oligosaccharides present at the CTL cell surface.

Animals↗

PubMed2003

Genetic manipulation of immunoglobulin binding proteins of Haemophilus somnus.

The relationship of the 76kDa immunoglobulin binding, surface antigen (p76) of Haemophilus somnus to the high molecular weight immunoglobulin binding proteins (HMW IgBPs) was investigated. The kanamycin resistance gene from pLS88 was used via homologous recombination with allelic exchange to replace a portion of the gene encoding IgBPs of H. somnus strain 8025. Recombinants were shown by Western immunoblotting to express and secrete truncated antigens of approximately 200kDa and not to produce p76. The truncated HMW IgBP variants retained the ability to bind bovine IgG2 by the Fc portion as demonstrated by Western immunoblotting against IgG2 anti-DNP. This data indicated that the deleted 1.8kb BglII fragment was not required for secretion or immunoglobulin Fc binding by the HMW IgBPs but was required for expression of the downstream p76 gene. Functional studies showed that, in addition to Fc binding of IgG2 to truncated HMW IgBPs, the mutant strain 8025 Kan1 was equally resistant to killing by mouse complement but less virulent than the wild type parent (8025) in a mouse septicemia model of H. somnus infection. However, mutant strain 8025 Kan1 did adhere less well than the wild type to bovine pulmonary artery endothelial cells. It is probable that p76 and the missing peptides of the HMW IgBPs play a role in this aspect of virulence and perhaps other aspects.

Animals↗

PubMed2000

Protective effect of DNA immunization against mycobacterial infection is associated with the early emergence of interferon-gamma (IFN-gamma)-secreting lymphocytes.

The development of more effective anti-tuberculosis (TB) vaccines would contribute to the global control of TB. Understanding the activated/memory T cell response to mycobacterial infection and identifying immunological correlates of protective immunity will facilitate the design and assessment of new candidate vaccines. Therefore, we investigated the kinetics of the CD4+ T cell response and IFN-gamma production in an intravenous challenge model of Mycobacterium bovis bacille Calmette-Guérin (BCG) before and after DNA immunization. Activated/memory CD4+ T cells, defined as CD44hiCD45RBlo, expanded following infection, peaking at 3-4 weeks, and decreased as the bacterial load fell. Activated/memory CD4+ T cells were the major source of IFN-gamma and the level of antigen-specific IFN-gamma-secreting lymphocytes, detected by ELISPOT, paralleled the changes in bacterial load. To examine the effects of a DNA vaccine, we immunized mice with a plasmid expressing the mycobacterial secreted antigen 85B (Ag85B). This led to a significant reduction in mycobacteria in the liver, spleen and lung. This protective effect was associated with the rapid emergence of antigen-specific IFN-gamma-secreting lymphocytes which were detected earlier, at day 4, and at higher levels than in infected animals immunized with a control vector. This early and increased response of IFN-gamma-secreting T cells may serve as a correlate of protective immunity for anti-TB vaccines.

Adjuvants, Immunologic↗

PubMed2002

IKKalpha, IKKbeta, and NEMO/IKKgamma are each required for the NF-kappa B-mediated inflammatory response program.

The IKKbeta and NEMO/IKKgamma subunits of the NF-kappaB-activating signalsome complex are known to be essential for activating NF-kappaB by inflammatory and other stress-like stimuli. However, the IKKalpha subunit is believed to be dispensable for the latter responses and instead functions as an in vivo mediator of other novel NF-kappaB-dependent and -independent functions. In contrast to this generally accepted view of IKKalpha's physiological functions, we demonstrate in mouse embryonic fibroblasts (MEFs) that, akin to IKKbeta and NEMO/IKKgamma, IKKalpha is also a global regulator of tumor necrosis factor alpha- and IL-1-responsive IKK signalsome-dependent target genes including many known NF-kappaB targets such as serum amyloid A3, C3, interleukin (IL)-6, IL-11, IL-1 receptor antagonist, vascular endothelial growth factor, Ptx3, beta(2)-microglobulin, IL-1alpha, Mcp-1 and -3, RANTES (regulated on activation normal T cell expressed and secreted), Fas antigen, Jun-B, c-Fos, macrophage colony-stimulating factor, and granulocyte-macrophage colony-stimulating factor. Only a small number of NF-kappaB-dependent target genes were preferentially dependent on IKKalpha or IKKbeta. Constitutive expression of a trans-dominant IkappaBalpha superrepressor (IkappaBalphaSR) in wild type MEFs confirmed that these signalsome-dependent target genes were also dependent on NF-kappaB. A subset of NF-kappaB target genes were IKK-dependent in the absence of exogenous stimuli, suggesting that the signalsome was also required to regulate basal levels of activated NF-kappaB in established MEFs. Overall, a sizable number of novel NF-kappaB/IKK-dependent genes were identified including Secreted Frizzled, cadherin 13, protocadherin 7, CCAAT/enhancer-binding protein-beta and -delta, osteoprotegerin, FOXC2 and FOXF2, BMP-2, p75 neurotrophin receptor, caspase-11, guanylate-binding proteins 1 and 2, ApoJ/clusterin, interferon (alpha and beta) receptor 2, decorin, osteoglycin, epiregulin, proliferins 2 and 3, stromal cell-derived factor, and cathepsins B, F, and Z. SOCS-3, a negative effector of STAT3 signaling, was found to be an NF-kappaB/IKK-induced gene, suggesting that IKK-mediated NF-kappaB activation can coordinately illicit negative effects on STAT signaling.

Animals↗

PubMed2004

Immune responses to a class II helper peptide epitope in patients with stage III/IV resected melanoma.

The importance of CD8(+) cytolytic T cells for protection from viral infection and in the generation of immune responses against tumors has been well established. In contrast, the role of CD4(+) T-helper cells in human infection and in cancer immunity has yet to be clearly defined. In this pilot study, we show that immunization of three resected, high-risk metastatic melanoma patients with a T-helper epitope derived from the melanoma differentiation antigen, melanoma antigen recognized by T cells-1, results in CD4(+) T-cell immune responses. Immune reactivity to that epitope was detected by DR4-peptide tetramer staining, and enzyme-linked immunospot assay of fresh and restimulated CD4(+) T cells from patients over the course of the 12-month vaccine regimen. The postvaccine CD4(+) T cells exhibited a mixed T-helper 1/T-helper 2 phenotype, proliferated in response to the antigen and promiscuously recognized the peptide epitope bound to different human leukocyte antigen-DRbeta alleles. For 1 DRbeta1*0401(+) patient, antigen-specific CD4(+) T cells recognized human leukocyte antigen-matched antigen-expressing tumor cells, secreted granzyme B, and also exhibited cytolysis that was MHC class II-restricted. These data establish the immunogenicity of a class II epitope derived from a melanoma-associated antigen and support the inclusion of class II peptides in future melanoma vaccine therapies.

Age Factors↗

PubMed2002

CTLA-4 expression on antigen-specific cells but not IL-10 secretion is required for oral tolerance.

CD4(+) T cells play a vital role in mediating the tolerance induced at mucosal sites following exposure to non-pathogenic stimuli, and further understanding of the precise mechanisms by which these cells prevent aberrant responses is required. We have developed a model using transfer of DO11.10 TCR-transgenic bone marrow into irradiated recipients in which it has been possible to track antigen-specific CD4(+) cells in mesenteric lymph nodes (mLN), Peyer's patches (PP) and lamina propria following primary exposure to antigen. Using this model we have demonstrated initial activation in all three gut-associated lymphoid tissue compartments characterized by increases in the frequency of transgenic cells expressing CD69 and CD25. These cells subsequently enter a state of hyporesponsiveness both locally in the mLN and PP and in the periphery following feeding and challenge. Investigating the role of CTLA-4 either using anti-CTLA-4 mAb or by generating chimeras using DO11.10xCTLA-4(-/-) mice as donors we have clearly shown that antigen-specific cells require the expression of this regulatory molecule for oral tolerance. In contrast, oral tolerance was intact in chimeras generated using DO11.10xIL-10(-/-) cells, indicating that secretion of this cytokine by antigen-specific cells is not required.

Abatacept↗

PubMed2002

Effects of triamcinolone acetonide on adult human lung fibroblasts: decrease in proliferation, surface molecule expression and mediator release.

BACKGROUND: Lung fibroblasts may have a pivotal role in airway inflammation as they are involved in continuous cycles of mediator secretion, proliferation, activation and cross-talk with recruited inflammatory cells. The role of fibroblasts as intermediate participants in the inflammatory network suggests that they could represent an important target for drugs commonly used in asthma; thus, we investigated the effects of triamcinolone acetonide (TAA) on primary human lung fibroblasts. METHODS: The in vitro activity of increasing concentrations (10(-9) to 10(-7) M) of TAA in fibroblast cultures was evaluated as regards the following parameters: proliferation, extracellular matrix (ECM) release, cytokine/chemokine secretion and surface antigen expression. RESULTS: All concentrations of TAA decreased fetal calf serum (FCS)-induced fibroblast proliferation, whereas in the presence of FCS plus basic fibroblast growth factor TAA was only effective at 10(-8) and 10(-7) M. TAA failed to decrease ECM, whereas at 10(-8) and 10(-7) M it decreased IL-6 and IL-8 secretion to different extents. In the presence of IFN-gamma the drug was able to reduce VCAM-1 expression at all of the tested concentrations; on the other hand, in TGF-beta 1-driven cultures a decrease in CD54 expression was detected with TAA at 10(-8) and 10(-7) M. CONCLUSIONS: TAA acts on some functional properties of human lung fibroblasts that make these cells active participants in the inflammatory network. The ability of TAA to inhibit lung fibroblast proliferation may prevent or even reverse some of the histological changes that characterize airway remodeling in chronic inflammatory diseases; moreover, IL-6, IL-8 and surface molecule decreases by TAA may suggest a direct anti-inflammatory effect of the drug by suppression of resident lung cell function.

Cell Division↗