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At least 847 records · Page 47Linked to original sources
PubMed1986

Rapid phosphorylation and modulation of the T4 antigen on cloned helper T cells induced by phorbol myristate acetate or antigen.

A cell surface protein known as T4 (CD4, Leu3), Mr = 55,000, is expressed on the subset of human T lymphocytes which provides helper function for B cell and cytotoxic T cell activities. We show that T4 is constitutively phosphorylated and that phorbol myristate acetate (PMA) induces a rapid serine phosphorylation which is followed by a fast dephosphorylation. Within 5 min after PMA treatment, there is a 24% reduction of T4 on the cell surface, by 4 h the loss is nearly complete, and by 20 h T4 is re-expressed. Addition of antigen to a T4+ antigen-reactive T cell clone induces both phosphorylation and dephosphorylation with kinetics similar to that described for PMA. Antigen also causes reduction of cell surface T4, although to a lesser degree than stimulation with PMA. The rapid phosphorylation/dephosphorylation of T4 as well as its movement from the cell surface suggest that T4 functions as a receptor for an unknown ligand.

Amino Acid Sequence↗
PubMed1986

Presentation by peritoneal macrophages: modulation by antibody-antigen complexes.

The effects of immune complex formation on presentation was studied. Immune complexes between an IgG2a monoclonal anti-DNP antibody and TNP-KLH were produced, and the presentation of the carrier molecule by peritoneal macrophages to KLH-primed T cells was monitored. Complex formation was found to enhance the proliferative response of the T cells. This enhancement was specific, was not mediated by lymphokine release, and required antibody with an intact Fc portion. The significance of these results in terms of immune regulation and antigen presentation is discussed.

Animals↗
PubMed1986

Modulation of B16 melanoma antigen expression by lymphokines and dimethyl sulfoxide.

We have developed two monoclonal antibodies, designated 152 E12 D7 and 153 C7 A6, which have reactivity with cell surface antigens expressed on the B16 mouse melanoma. These monoclonal antibodies are produced by hybridomas resulting from the fusion of splenocytes taken from C57BL/6 mice bearing the B16-F10 tumor. The monoclonal antibodies are of the immunoglobulin M class and have been shown to react with three variants of the B16 and another mouse melanoma but no normal murine tissues. Exposure of B16 melanoma cells to a concanavalin A stimulated spleen cell mixed lymphokine preparation (LK) and to dimethyl sulfoxide (DMSO) enhanced the expression of the cell surface antigens recognized by these monoclonal antibodies. The cultures stimulated with LK or DMSO contained a greater proportion of cells expressing the antigens recognized by monoclonal antibodies 152 E12 D7 and 153 C7 A6 than did unstimulated controls. In addition to increasing the proportion of antigen-positive cells, the antigen expression per cell, as measured by fluorescence intensity, was substantially increased following exposure to LK and DMSO. The effects of treatment with LK or DMSO were apparent after 24 h exposure but did not persist after the agent was removed from the cultures, suggesting that the enhancement of antigen expression was a transient event rather than a permanent differentiation of the melanoma cells.

Animals↗
PubMed1985

Interferon-gamma modulates HLA class II antigen expression on cultured human thymic epithelial cells.

Cultures of human thymic epithelial cells (TEC) were tested for the expression of HLA class I (A, B, C) and class II (DR and DC) antigens by indirect immunofluorescence. The epithelial nature of the cells was proven by using an antikeratin antiserum. A high level of expression (close to 100% positive cells) of HLA class I antigens was observed on TEC at the beginning of the culture and remained unchanged for up to 12 days. In contrast, HLA class II antigen expression (85% DR+ and 75% DC+ cells on day 2) decreased gradually and reached very low levels (less than 5% DR+ or DC+) by day 7 of culture. This loss of class II antigen expression was not seen when cultures were performed in the presence of supernatants from activated T cells containing interferon-gamma (IFN-gamma). Furthermore, the presence of recombinant IFN-gamma (rIFN-gamma) in the medium from the onset of culture maintained HLA-DR and DC antigen expression on a high number of cells (comparable to that observed on day 2 of culture). A large percentage of rIFN-gamma-treated cells also showed intracytoplasmic HLA-DR antigen expression. Addition of rIFN-gamma at various times after the onset of the culture led to a reinduction of DR and DC antigen expression. This effect of rIFN-gamma was observed in 48 hr with concentrations as low as 10 IU/ml and was apparently specific for this IFN species, in that rIFN-alpha was unable to modify HLA class II antigen expression at concentrations up to 1000 IU/ml. The increased expression of HLA class II antigen was truly due to induction in individual TEC, rather than selection of class II-positive cells, because induction under the influence of IFN-gamma was reversible and occurred in the absence of proliferation in mitomycin-treated or gamma-irradiated cultures. Our results indicate that synthesis and membrane expression of class II HLA antigens are enhanced by IFN-gamma in TEC cultures. This finding raises the possibility that IFN-gamma participates in the mechanisms that assure the permanent expression of DR and DC antigens observed in TEC in vivo, with potentially important functional consequences in terms of education for self recognition.

Cell Survival↗
PubMed1993

Modulation of protectin (CD59 antigen) cell surface expression on human neoplastic cell lines.

The ability of cytokines (IFN alpha, IFN gamma, TNF alpha, IL-1 alpha, IL-6), all-trans retinoic acid, 1,25(OH)2-vitamin D3 and the tumor promoting phorbol ester TPA to regulate cell surface expression of protectin (CD59 antigen) on human hematopoietic and non-hematopoietic neoplastic cell lines was examined with the aid of immunocytofluorometric measurements. The tumor promoting phorbol ester TPA induced a marked up-regulation of protectin in all examined cell lines with the exception of promyelocytic leukemia HL-60, where TPA significantly decreased protectin cell surface expression. All-trans retinoic acid weakly down-regulated cell surface protectin on K-562, while 1,25(OH)2-vitamin D3 produced such effect on HL-60 cells. None of the examined cytokines induced a significant protectin down-regulation in the examined cell lines.

Antigens, CD↗
PubMed1995

Modulation of immunogenicity and antigenicity of proteins by maleylation to target scavenger receptors on macrophages.

We have maleylated proteins to target macrophage-specific scavenger receptors and have used this system to study changes in the epitopes and immunogenicity of such proteins. We show that maleylation of diphtheria toxoid (DT) induces targeting to macrophage scavenger receptors and enhances its immunogenicity. DT does not evoke detectable serum Ab responses upon injection as soluble protein. However, maleylated DT (mDT) does generate a significant Ab response. Furthermore, immunization with soluble mDT leads to a better T cell proliferative response in vitro than immunization with DT can generate, thereby demonstrating that maleylation leads to enhanced T cell immunogenicity in vivo. We also find that maleylation disrupts the native B cell epitopes of DT and creates new epitopes, because antisera to DT and mDT do not cross-react. At least some of the new epitopes generated are maleylation specific, because antisera against various maleylated proteins do cross-react. In contrast, maleylation does not significantly modify the repertoire of T cell epitopes generated from DT, because T cells generated by either DT or mDT immunization are cross-reactive, and both DT and mDT can stimulate T cells that are specific for single synthetic DT peptide. Maleylated proteins are better presented in vitro than are their native counterparts, and this enhancement of presentation is blocked by unrelated maleylated proteins. These results suggest that Ags targeted to scavenger receptors on macrophages by maleylation are better presented to T cells and are immunogenic in vivo without adjuvant.

Animals↗
PubMed1993

Phorbol ester-induced modulation of cell surface antigens on U-937 cells in protein-free medium: effect of protein kinase and calmodulin inhibitors.

Phorbol ester (PMA) induced decrease in cell surface expression of CD4 antigen was potentiated on human monoblastoid cell line U-937 cultured and induced in protein-free culture medium. Down-regulation of the CD4 antigen was partially inhibited by the isoquinoline protein kinase inhibitor H7 and unaffected by the calmodulin inhibitor R24571 (calmidazolium). PMA-induced increase of the monocyte-associated CD14 antigen was dependent the presence of fetal bovine serum (FBS) in culture medium and partially abolished by calmodulin inhibitor R24571. H7 inhibitor partially abrogated this up-regulation in 4 out of 8 induction experiments. PMA-induced down-regulation of MHC class I antigen was found in both FBS-supplemented and protein-free culture media. This effect was partially inhibited by both H7 and R24571 inhibitors.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Bis azo dyes--studies on the mechanism of complex formation with IgG modulated by heating or antigen binding.

The mechanism of binding of azo dyes (bis azo) to immunoglobulin G of altered conformation, induced by heating or interaction with antigen was analysed in this work. Azo dyes: Congo Red, Evans Blue and Trypan Blue were selected for these studies. The molecules of Congo Red and Evans Blue associate readily in water and exist as polymolecular micellar species of liquid crystalline organization. Such organization of molecules appeared necessary for these dyes to interact with antibodies and to affect the formation of immune complex. It was proved by studying the properties of isomeric dyes Evans Blue and Trypan Blue, whose ability to form polymolecular conglomerates in water differs, being high for Evans Blue and low for Trypan Blue. The dyes seem to influence the formation of the immune complex generally by interacting with individual immunoglobulin molecules. The rate of exchange of dye molecules in conglomerate bound to protein varies and is the lowest for the portion of molecules which are engaged directly in the complex with protein. Electron microscopic studies also confirmed the polymolecular form of the dye in the dye-protein complex. The computational simulation of dye-dye and dye-protein interaction was performed in a model system. The micelle in the system was represented by three molecules of Congo Red. The peptide loop composed of amino acids 68-88 originating from VL IgG domain, was selected to represent protein. Amino acid side chains of this fragment were reduced to C beta. The best fitness was found for peptide chains of twisted beta conformation and independently optimized conformation of the dye in a form of "twisted ribbon" micelle. It was concluded that the IgG domains become accessible for penetration of the dye after being relaxed in the result of heating or interaction with the antigen.

Agglutination Tests↗
PubMed1989

Modulation by cytokines of HLA antigens, intercellular adhesion molecule 1 and high molecular weight melanoma associated antigen expression and of immune lysis of clones derived from the melanoma cell line MeM 50-10.

Clones were isolated from the cultured human melanoma cell line MeM 50-10, which metastasizes in nude mice with a pattern similar to that in patients with melanoma. Analysis with monoclonal antibodies detected heterogeneity among the clones in the expression of HLA class I antigens, HLA class II antigens, intercellular adhesion molecule 1 and high molecular weight melanoma associated antigen. The clones MeM A16 and MeM A18 were also shown to display differential susceptibility to modulation by immune interferon (IFN-gamma) and/or tumor necrosis factor (TNF-alpha) of the expression of the four types of antigens analyzed. In spite of differences in the antigenic profile, the two clones did not differ in their susceptibility to lysis by lymphokine-activated killer (LAK) cells and by anti-HLA-A2 cytotoxic T cells. The increase in the expression of HLA class I antigens induced by IFN-gamma and/or TNF-alpha on the two clones was associated with an increased susceptibility to lysis by anti-HLA-A2 cytotoxic T cells. Because of the metastasizing properties of cultured melanoma cells MeM 50-10, the clones we have isolated, with their distinct antigenic profile and differential susceptibility to modulation by cytokines, may represent useful models to investigate the role of distinct antigenic structures in the metastatic process.

Antigens, Neoplasm↗
PubMed2003

Memory and effector T cells modulate subsequently primed immune responses to unrelated antigens.

Memory and effector T cells modulate subsequently primed T cell responses to the same antigen. However, little is known about the impact of pre-existing memory and effector T cell immunity on subsequently primed immune responses to unrelated antigens. Here, we show that an antigen-primed first wave of Th1 and Th2 immunity enhanced or inhibited the subsequently primed T cell immunity to an unrelated antigen, depending on whether the second antigen was administered in the same or opposite type of adjuvant. The regulatory effects of the first wave of T cell immunity on the subsequent T cell responses to an unrelated antigen attenuated over time. Notably, following challenge with the second antigen, there was a mutual cross-regulation between the first and second wave of humoral responses to unrelated antigens. Thus, immunization with one antigen not only primes immune responses to that antigen, but also influences subsequently primed immune responses to unrelated antigens.

Animals↗
PubMed1998

The RcsB-RcsC regulatory system of Salmonella typhi differentially modulates the expression of invasion proteins, flagellin and Vi antigen in response to osmolarity.

Entry into intestinal epithelial cells is an essential feature in the pathogenicity of Salmonella typhi, which causes typhoid fever in humans. This process requires intact motility and secretion of the invasion-promoting Sip proteins, which are targets of the type III secretion machinery encoded by the inv, spa and prg loci. During our investigations into the entry of S. typhi into cultured epithelial cells, we observed that the secretion of Sip proteins and flagellin was impaired in Vi-expressing strains. We report here that the production of Sip proteins, flagellin and Vi antigen is differentially modulated by the RcsB-RcsC regulatory system and osmolarity. This regulation occurs at both transcriptional and post-translational levels. Under low-osmolarity conditions, the transcription of iagA, invF and sipB genes is negatively controlled by the RcsB regulator, which probably acts in association with the viaB locus-encoded TviA protein. The cell surface-associated Vi polysaccharide, which was maximally produced under these growth conditions, prevented the secretion of Sip proteins and flagellin. As the NaCl concentration in the growth medium was increased, transcription of iagA, invF and sipB was found to be markedly increased, whereas transcription of genes involved in Vi antigen biosynthesis was greatly reduced. The expression of iagA, whose product is involved in invF and sipB transcription, occurred selectively during the exponential growth phase and was maximal in the presence of 300mM NaCl. At this osmolarity, large amounts of Sips and flagellin were secreted in culture supernatants. As expected from these results, and given the essential role of Sip proteins and motility in entry, RcsB and osmolarity modulated the invasive capacity of S. typhi. Together, these findings might reflect the adaptive response of S. typhi to the environments encountered during the different stages of pathogenesis.

Antigens, Bacterial↗
PubMedDate not supplied

Modulation of class II histocompatibility antigen expression by maternal serum.

Human maternal serum has been shown to down-regulate the expression of MHC class II antigen in three distinct circumstances. Cord blood mononuclear cells, incubated in the mother's own serum, showed significant modulation of class II antigen expression. This was also the case for unrelated donor lymphocytes, incubated in pooled maternal serum. One neoplastic line (Daudi) was further shown to down-regulate class II antigen expression. In this last case, the down-regulating effect persisted over a 10-day period during which maternal serum was renewed regularly. Retroplacental serum was more MHC class II-inhibiting than peripheral serum. This down-regulating effect does not apply to maternal lymphocytes. The inhibitory effect is thought to be due to a factor, yet to be defined, included in the maternal IgG fraction. Regular assays made throughout pregnancy showed that the class II inhibiting component appears early (5th week), reaches its peak value at the 12th week, and disappears 2 or 3 weeks after delivery.

Antigen-Antibody Complex↗
PubMed1986

N-myc amplification causes down-modulation of MHC class I antigen expression in neuroblastoma.

Amplification of the N-myc gene is correlated with increased metastatic ability of human neuroblastomas. We show here that overexpression of the N-myc gene in a rat neuroblastoma cell line following gene transfer causes down-modulation of class I histocompatibility antigen expression and increases in the in vivo growth rate and metastatic ability of these cells. N-myc-mediated down-modulation of MHC class I antigen expression could be reversed by treatment with interferon without affecting the steady state level of N-myc mRNA. No effect on MHC class I antigen expression was found when the N-myc gene was expressed in rat fibroblasts, indicating that some of the effects caused by N-myc gene amplification are cell-type-specific.

Animals↗
PubMed1994

Diabetes enhancement and increased islet antigen expression following neonatal injections of glucose and arginine in non-obese diabetic mice.

Modulation of beta-cell antigens at birth may affect the course of type I diabetes. Since the functional state of beta cells modulates antigen expression, we investigated whether neonatal injections of glucose and arginine (G-A) influence diabetes in non-obese diabetic (NOD) mice. Two groups of 90 mice (45 female, 45 male) were injected for the first 6 days of life with G-A or saline. To determine whether these injections influenced beta cell functional maturation, isolated islets were characterized according to insulin response to glucose or arginine. Modulation of antigens for islet-cell autoantibodies (ICA antigens) was analyzed by indirect immunofluorescence using ICA-positive human sera. Variations of pancreatic glutamic acid decarboxylase 67-kD (GAD 67) mRNA were evaluated by polymerase chain reaction (PCR), hybridization with a 32P-labeled probe, and densitometry of the autoradiographic bands. Female NOD mice treated with G-A displayed diabetes earlier and with a higher incidence (P < .01) than control mice, whereas the diabetes incidence was not statistically modified in G-A-treated male NOD mice. Insulitis was more severe (P < .03) in 2-month-old G-A-treated female NOD mice than in control mice, but was not statistically modified in male NOD mice. In both sexes, ICA antigens and GAD 67 mRNA were higher in G-A-treated mice than in control mice (P < .01). Islets isolated after neonatal G-A injections exhibited improved insulin sensitivity to both stimuli (P < .01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗