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Results for “Antigenic Modulation”

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PubMed1988

Modulation of HLA antigens in response to the binding of epidermal growth factor by A431 cells.

In a previous study [(1984) J. Cell Biol. 98, 725-731] we showed that the level of human MHC, HLA antigens on A431 carcinoma cells is reduced after these cells bind epidermal growth factor (EGF). Here we use flow cytometry to determine the effects of various doses and times of EGF treatment on HLA expression. We then show that the reduction in HLA expression is associated with a reduction in the level of phosphorylation of immunoprecipitable surface HLA antigens, although longer exposure of cells with EGF increased both surface HLA expression and their phosphorylation levels. Lateral diffusion of HLA antigens is lower in EGF-treated than in control cells. The lower diffusion coefficients measured may be causally related to the decreased phosphorylation of HLA antigens.

Aged↗
PubMed1993

Down-modulation of CD4 antigen during programmed cell death in U937 cells.

It has been hypothesized that programmed cell death (PCD), an active cell suicide process occurring in place of necrosis, can be associated with the pathogenesis of acquired immunodeficiency syndrome (AIDS). The entry of human immunodeficiency virus (HIV) into competent cells is mediated by the CD4 molecule present on the surface of certain lymphocyte subpopulations as well as on some cultured cell lines, e.g. U937 myelomonocytic cells. The present paper focuses on some specific aspects of PCD induced by the cytokine tumor necrosis factor (TNF). The results obtained indicate that the exposure of U937 cells to cycloheximide facilitates TNF-mediated PCD via a short term cell death program and modifies the expression of CD4 surface molecules. This change in surface antigen expression, manifested by internalization of the CD4 molecule, occurs in cells in which apoptosis has been triggered, but not in cells undergoing necrosis. These results indicate that the progression of cell death could be associated with specific alterations of certain surface molecules and could have a role in the entry of HIV into cells.

Apoptosis↗
PubMed1991

Differential hormonal modulation of brain antigens recognized by the AB-2 monoclonal antibody.

The expression of monoclonal antibody AB-2 immunoreactivity is age- and sex-dependent in radial glia of developing rat hypothalamus and is regulated by prenatal exposure to gonadal steroids. In the present study, several proteins were recognized by AB-2 and were distributed selectively in subcellular fractions from neonatal hypothalamus (HYP), remaining forebrain (FB), and brainstem regions. Immunoblots revealed polypeptide bands in 3 major molecular weight classes: one at approximately 195 kDa in the cytosolic compartment; and two doublets at 220 kDa and 340 kDa in both microsomal and crude mitochondrial membrane fractions. The 220 kDa and 340 kDa doublets were also Triton-insoluble, suggesting a cytoskeletal association. The 195 kDa-AB-2-immunoreactive band was present in both Triton-soluble and insoluble fractions. AB-2 also recognized several acidic glycolipids extracted from postnatal rat brain regions on immunoblots following high performance thin layer chromatography. One of the bands from postnatal rat brain extracts migrated similarly to purified bovine brain sulfatide, which was also immunoreactive with AB-2. AB-2 immunoreactivity with proteins, polar lipids, and sulfatide suggests that the epitope is a carbohydrate present in multiple cellular compartments. AB-2 recognized the same molecular bands in males and females. Testosterone treatment selectively decreased the level of the 195 kDa AB-2-immunoreactive polypeptide. The 195 kDa AB-2-immunoreactive polypeptide possibly acts in radial glia in the determination of sexually dimorphic neurons in the preoptic area/hypothalamus.

Animals↗
PubMed1991

Modulation of MHC antigen expression by viruses and oncogenes.

It is becoming increasingly clear that regulation of MHC antigen expression by viruses and oncogenes, leading to either immune evasion or autoimmunity, is widespread and important in disease. At a recent meeting*, which brought together workers interested in tumour immunology, viral infection and the MHC, a number of mechanisms for the regulation of MHC antigen expression were revealed and the importance of balanced expression of MHC gene products to effective immunity was underlined.

Animals↗
PubMed2004

Electrochemical modulation of antigen-antibody binding.

The label-free amperometric detection of a rabbit IgG antigen by an anti-rabbit IgG antibody is achieved by observing the electrochemistry at a glassy carbon electrode modified with antibody entrapped in an electrodeposited polypyrrole membrane. In a flow injection apparatus the electrode is pulsed between -0.2 and +0.4 V versus Ag/AgCl. The pulsing of the electrode switches the polypyrrole membrane between the oxidised and reduced states. When antigen is injected into the flow stream a change in current is observed at the electrode despite the antigen or antibody being redox inactive at the potentials employed. It is proposed that this current is due to a change in the flux of ions into and out of the polypyrrole matrix during a pulse when the poly-anionic antigen is present. The immunoreaction was reversible because the 200 ms pulse at each potential was too short to allow secondary bonding forces (hydrogen bonding and hydrophobic forces) which are responsible for the strength of the antibody-antigen complex to be established. The consequence of the reversibility of the antigen-antibody binding is a low apparent affinity constant but an easily regenerated recognition interface.

Animals↗
PubMed2005

Modulation of the antigen transport machinery TAP by friends and enemies.

The transporter associated with antigen processing (TAP) is a key factor of the major histocompatibility complex (MHC) class I antigen presentation pathway. This ABC transporter translocates peptides derived mainly from proteasomal degradation from the cytosol into the ER lumen for loading onto MHC class I molecules. Manifold mechanisms have evolved to regulate TAP activity. During infection, TAP expression is upregulated by interferon-gamma. Furthermore, the assembly and stability of the transport complex is promoted by various auxiliary factors. However, tumors and viruses have developed sophisticated strategies to escape the immune surveillance by suppressing TAP function. The activity of TAP can be impaired on the transcriptional or translational level, by enhanced degradation or by inhibition of peptide translocation. In this review, we briefly summarize existing data concerning the regulation of the TAP complex.

ATP-Binding Cassette Transporters↗
PubMed2003

Ribotoxic stress activates p38 and JNK kinases and modulates the antigen-presenting activity of dendritic cells.

Initiation of adaptive immunity requires activation of dendritic cells (DC) by "danger" signals. This study examines the functional consequences of activating a cellular stress response in human DC. Anisomycin, a potent inducer of this "stress" response, selectively activates p38 kinase in DC at low concentrations, and both p38 kinases and JNKs at higher concentrations. Activation of p38, was accompanied by an increase in the potency of dendritic cells to activate T cells. In contrast to LPS, anisomycin had no effect on the expression of several DC activation markers. Anisomycin synergised with LPS in driving release of IL-12 and TNF-alpha. Anisomycin also enhanced the formation of clusters between DC and T cells. Enhanced cytokine release and clustering were both inhibited by the selective p38 alpha and p38 beta inhibitor SB203580. This study demonstrates that the cellular stress response, mediated via p38 kinases, plays an important role in the regulation of several aspects of DC function.

Anisomycin↗
PubMed2000

Genetic modulation of tumor antigen presentation.

An effective cancer-cell vaccine is created by expressing major-histocompatibility-complex (MHC) class II molecules without the invariant chain protein (Ii) that normally blocks the antigenic-peptide-binding site of MHC class II molecules at their synthesis in the endoplasmic reticulum. Such tumor-cell constructs are created either by the transfer of genes for MHC class IIalpha and beta chains, or by the induction of MHC class II molecules and Ii protein with a transacting factor, followed by Ii suppression using antisense methods. Preclinical validation of this approach is reviewed with the goal of using this immunotherapy for metastatic human cancers.

Animals↗
PubMed1996

Modulation of antigen-specific T and B cell responses influence bacterial clearance of non-typeable Haemophilus influenzae from the lung in a rat model.

This study investigates antigen-specific B and T cell responses following mucosal immunization with the major outer membrane protein, P2, from non-typeable Haemophilus influenzae (NTHi) and the role of these responses in bacterial clearance following pulmonary challenge. Modification of the immunization preparation by the inclusion of sodium dodecyl sulphate (SDS) with the adjuvant, incomplete Freund's, differentially affects the T and B cell responses to the P2 antigen. Rats received an intra-Peyer's patch-immunization with P2 with or without the inclusion of 1% (w/v) SDS, were boosted via an intratracheal administration of P2 alone on day 14, and challenged with live NTHi in the lungs on day 21. There were significant differences in the rate of bacterial clearance between the different P2-immunized groups and the non-immune group. The inclusion of SDS with P2 resulted in enhanced bacterial clearance. This clearance corresponded to an enhancement of P2-specific lymphocyte proliferation by CD4+ T helper cells but a decrease (reduced approximately 75%) in anti-P2 IgG and IgA in both serum and bronchoalveolar lavage washings. P2-specific IgM levels were not altered. IgG subclass analysis indicated that the inclusion of SDS had caused a significant reduction in IgG2a and an increase in IgG1. The data indicates that the magnitude of antibody levels to P2 may not be as important as T cell responses in enhancing clearance of NTHi in the lung, in vivo, and that immunization targeting enhancement of antigen-specific T cells may be important to inducing effective immunity to NTHi.

Animals↗
PubMed1998

Modulation of the antigen presentation activity in foot and mouth disease virus (FMDV) vaccines by two adjuvants: avridine and a water soluble fraction of Mycobacterium sp.

We have previously demonstrated that the presence of the antigen presenting cells (APC) is critical in the induction and maintenance of the immune response in animals infected or immunized with inactivated FMDV. The use of immunological adjuvants has been repeatedly shown to be essential for the improvement of the immunogenicity in FMDV vaccines. Specifically, we have previously shown that the addition of the synthetic lipoamide Avridine (AVR) or a water soluble fraction of Mycobacterium sp. (WSF) significantly increased the immune response and protection against FMDV challenge. Here, we study the effect of these adjuvants on the induction of APC activity in mice immunized with inactivated FMDV. Both adjuvants were able to induce a long lasting antibody response which correlates with an efficient APC activity. Experiments using sequential cell transfers showed that the presence of the APC activity is not related with the efficiency of keeping free antigen in the vaccinated host. Interestingly, APC from animals immunized with AVR as adjuvant elicited virus neutralizing antibodies, while those APC obtained from donors vaccinated using WSF as adjuvant (or just an oil emulsion) induced anti-FMDV detectable only by ELISA. The analysis of the antibody response to a well studied synthetic peptide raised evidences that indicate that this difference could be explained by a differential presentation of viral B epitopes when different adjuvants were used. These results suggest that the induction of APC should be considered as one of the critical factors in the process of improving the immunogenicity of experimental FMDV vaccines.

Adjuvants, Immunologic↗
PubMed1976

Spontaneous shedding and antibody induced modulation of histocompatibility antigens on murine lymphomata: Correlation with metastic capacity.

The lability of cell surface histocompatibility antigens of 2 murine lymphomata was examined. These 2 tumours differ greatly in their capacity to metastasize in syngeneic hosts. Cells of the metastatic lymphoma released histocompatibility antigens in vivo and in vitro at a greater rate than cells of the non-metastasizing lymphoma. Antigen/antibody complexes formed by the addition of allo-antiserum to intact cells disappeared more rapidly from the surface of cells of the metastatic line. We propose that the instability of surface antigens may be an integral feature of malignant cells and that there may be a quantitative relationship between the lability of membrane components and the capacity of the tumour to metastasize.

Animals↗
PubMed1987

In vitro modulation of antigen-primed T cells by a glycosylation-inhibiting factor that regulates the formation of antigen-specific suppressive factors.

BDF1 [(C57BL/6 X DBA/2)F1] mice were primed with alum-absorbed ovalbumin, and their spleen cells were cultured with ovalbumin to activate antigen-primed T cells. The activated T cells were then propagated in interleukin 2-containing medium in the presence or absence of affinity-purified glycosylation-inhibiting factor (GIF). Upon incubation with ovalbumin-pulsed macrophages, T cells propagated in the absence of GIF produced IgE-potentiating factor and glycosylation-enhancing factor. In contrast, T cells propagated in the presence of GIF produced IgE-suppressive factor and GIF. The ovalbumin-primed T cells propagated in the presence of GIF constitutively produced the 13-kDa GIF that lacked affinity for ovalbumin. However, stimulation of the same T cells with ovalbumin-pulsed macrophages resulted in the production of 80- and 35-kDa GIF that had affinity for ovalbumin. Both the antigen-specific GIF and nonspecific GIF from the activated BDF1 T cells had I-Jb determinants. Since the ovalbumin-specific GIF is derived from Lyt-2+, I-J+ ovalbumin-specific suppressor T cells and suppresses the anti-hapten antibody response to dinitrophenyl-coupled ovalbumin, the results strongly suggest that the presence of GIF during the propagation of antigen-primed T cells facilitates the generation of antigen-specific suppressor T cells.

Animals↗
PubMed1998

An inhibitor of HIV-1 protease modulates proteasome activity, antigen presentation, and T cell responses.

Inhibitors of the protease of HIV-1 have been used successfully for the treatment of HIV-1-infected patients and AIDS disease. We tested whether these protease inhibitory drugs exerted effects in addition to their antiviral activity. Here, we show in mice infected with lymphocytic choriomeningitis virus and treated with the HIV-1 protease inhibitor ritonavir a marked inhibition of antiviral cytotoxic T lymphocyte (CTL) activity and impaired major histocompatibility complex class I-restricted epitope presentation in the absence of direct effects on lymphocytic choriomeningitis virus replication. A potential molecular target was found: ritonavir selectively inhibited the chymotrypsin-like activity of the 20S proteasome. In view of the possible role of T cell-mediated immunopathology in AIDS pathogenesis, the two mechanisms of action (i.e., reduction of HIV replication and impairment of CTL responses) may complement each other beneficially. Thus, the surprising ability of ritonavir to block the presentation of antigen to CTLs may possibly contribute to therapy of HIV infections but potentially also to the therapy of virally induced immunopathology, autoimmune diseases, and transplantation reactions.

Animals↗
PubMed2001

SHP-1 requires inhibitory co-receptors to down-modulate B cell antigen receptor-mediated phosphorylation of cellular substrates.

Signaling through the B cell antigen receptor (BCR) is negatively regulated by the SH2 domain-containing protein-tyrosine phosphatase SHP-1, which requires association with tyrosine-phosphorylated proteins for activation. Upon BCR ligation, SHP-1 has been shown to associate with the BCR, the cytoplasmic protein-tyrosine kinases Lyn and Syk, and the inhibitory co-receptors CD22 and CD72. How SHP-1 is activated by BCR ligation and regulates BCR signaling is, however, not fully understood. Here we demonstrate that, in the BCR-expressing myeloma line J558L mu 3, CD72 expression reduces the BCR ligation-induced phosphorylation of the BCR component Ig alpha/Ig beta and its cytoplasmic effectors Syk and SLP-65. Substrate phosphorylation was restored by expression of dominant negative mutants of SHP-1, whereas the SHP-1 mutants failed to enhance phosphorylation of the cellular substrates in the absence of CD72. This indicates that SHP-1 is efficiently activated by CD72 but not by other pathways in J558L mu m3 cells and that inhibition of SHP-1 specifically activated by CD72 reverses CD72-induced dephosphorylation of cellular substrates in these cells. Taken together, BCR-induced SHP-1 activation is likely to require inhibitory co-receptors such as CD72, and SHP-1 appears to mediate the negative regulatory effect of CD72 on BCR signaling by dephosphorylating Ig alpha/Ig beta and its downstream signaling molecules Syk and SLP-65.

B-Lymphocytes↗
PubMed1994

Drug modulation of antigen-induced paw oedema in guinea-pigs: effects of lipopolysaccharide, tumour necrosis factor and leucocyte depletion.

1. In guinea-pigs previously sensitized with ovalbumin, the intra-plantar administration of the antigen induced dose-dependent and sustained oedema. An intense infiltrate of neutrophils and eosinophils was observed at the peak of the oedema (4 h). 2. Oedema induced by ovalbumin at the doses of 50 or 200 micrograms/paw was not inhibited by antihistamines (meclizine and cetirizine), a PAF antagonist (BN 50730), a cyclo-oxygenase inhibitor (indomethacin), a lipoxygenase inhibitor (MK-886), a dual type lipo- and cyclo-oxygenase inhibitor (NDGA), a bradykinin antagonist (Hoe 140) or the combination of cetirizine, MK-886, indomethacin and BN 50730. These drugs did inhibit paw oedema induced by their specific agonists or by carrageenin. These results suggest that histamine, PAF, prostaglandins, leukotrienes or bradykinin are not important in the development of immune paw oedema in guinea-pigs. 3. Dexamethasone (10 mg kg-1) inhibited oedema induced by ovalbumin (50 or 200 micrograms/paw, P < 0.05). This effect apparently does not result from inhibition of arachidonate metabolism, since indomethacin, MK-886 and NDGA were without effect. 4. Oedema induced by ovalbumin (50 or 200 micrograms/paw) was also inhibited by azelastine. This effect was not due to the anti-histaminic property of azelastine since two other potent-antihistamines, meclizine and cetirizine, were ineffective. 5. Intravenous injection of lipopolysaccharide (LPS) dose-dependently inhibited the oedema induced by ovalbumin (200 micrograms/paw). This effect could not be attributed to hypotension or leucopenia since the maximal dose applied (81 micrograms kg-1) did not induce significant changes in the blood pressure or in the white blood cell levels of the animals. It is suggested that the effect of LPS is mediated by the endogenous release of cytokines, including tumour necrosis factor (TNF alpha). Murine TNF alpha dose dependently(9-81 microg kg-1) inhibited the paw oedema induced by ovalbumin.7. The anti-oedematogenic effects of LPS and/or TNF alpha are possibly associated with their capacity to inhibit leucocyte emigration. Accordingly, guinea-pigs rendered leucopenic with vinblastine exhibited less intense oedema after ovalbumin. Vinblastine did not affect oedema induced by PAF or bradykinin,indicating that vascular responsiveness was not involved.

Animals↗
PubMed1998

In vitro modulation of activation antigens on human lymphocytes by beta-estradiol.

PROBLEM: The possible in vitro immunomodulating effect of beta-estradiol on phytohemagglutinin-stimulated human lymphocyte cultures was studied. METHOD OF STUDY: Lymphocyte cultures from 12 healthy men and women aged 25-35 years were set up for 12 hr in the presence and in the absence of beta-estradiol, and the expression of the activation markers CD25, CD69, and CD71 was examined by flow cytometric analysis with specific fluorescent conjugated antibodies. RESULTS: Although the number of cases is small, in 10 of 12 cases in the presence of beta-estradiol in two different concentrations, a significantly decreased expression of CD69 could be observed. A slight decrease could also be observed for the Interleukin-2 receptor expression; however, the difference, in the presence or absence of beta-estradiol, was not significant. CONCLUSIONS: The results suggest that in vitro addition of beta-estradiol can inhibit, to a certain degree, specific activation markers on phytohemagglutinin-stimulated lymphocytes from young men and women. The present study could not define the role of sex differences because of the small number of samples. A comparison between men and women at various ages in a greater number of cases, as well as studies on activation markers after treatments with estrogens, would be useful.

Adult↗
PubMed1978

Unusual antibody-induced modulation of surface antigens in the cell coat of a bloodstream trypanosome.

Unlike other eukaryotic cells, Trypanosoma lewisi forms caps at 0 degrees C when incubated with rabbit immunoglobulin G(IgG) directed against surface IgG from the rat host. The host IgG, which is specific for parasite antigens, probably does not cause capping of these antigens in vivo, since trypanosomes treated with Fab fragments directed against rat IgG are uniformly labeled and do not cap at 0 degrees C or 37 degrees C.

Animals↗