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PubMed1995

Interaction of antibody with Forssman antigen in guinea pigs. A mechanism of adaptation to antibody- and complement-mediated injury.

Forssman antigen is a glycosphingolipid with antigenic specificity determined by extra-membrane haptenic sugars similar to blood group antigens and antigens that are the main barrier to xenogeneic organ transplantation. Herein, we describe the localization of Forssman antigen in guinea pig lungs and kidneys and the consequences of its interaction with antibodies in vitro and in vivo (Forssman reaction). Exposure of cultured guinea pig aortic endothelial cells to Forssman antibodies induced rapid redistribution of antigen-antibody complexes at the cell surface, followed by shedding that occurred by blebbing of plasma membrane as vesicles or fragments, and was associated with disappearance of antigen from the cell surface (antigenic modulation). Guinea pigs surviving frequent intravenous infections of increasing amounts of antibodies, for a total of 20 to 40 lethal doses, developed a partial or complete adaptation to generalized Forssman reaction, and adaptation was associated with partial or complete modulation of Forssman antigen at the surface of the pulmonary and, in minor degree, renal endothelial and epithelial cells. These findings support the hypothesis that modulation of endothelial carbohydrate antigens contributes to adaptation of highly vascularized organs exposed to tolerable levels of allo- or xenoantibodies.

Animals↗
PubMed1993

Vascularized osteochondral allografts in an immunosuppressed rat model: graft modulation and host immune tolerance.

The effects of 4 weeks of cyclosporin A (7 mg/kg per day) (CyA) on the survival of vascularized osteochondral grafts between rat strains [DA (donor) and Lewis (recipient)] and the presence and significance of host immune tolerance and graft antigen modulation after cessation of immunosuppression have been examined. Isografts (n = 12) survived without apparent abnormality for 8 weeks but showed signs of wasting after longer periods; unprotected allografts (n = 5) were rejected within 2 weeks. After 4 weeks of CyA, allografts remained healthy for at least 12 weeks but then deteriorated (n = 40). Antigen modulation was examined by graft removal at various intervals after cessation of CyA and reimplantation into a naive recipient (n = 14). All were rejected rapidly. Host tolerance was examined by graft removal at various periods after cessation of CyA and reimplantation of a fresh allograft (n = 15). Some of the second grafts survived at least 4 weeks without immunosuppression. The findings indicate development of incomplete host tolerance but no antigenic modulation of the graft.

Animals↗
PubMed1984

Effects of monoclonal antibody therapy in patients with chronic lymphocytic leukemia.

A phase I clinical trial was initiated to treat patients with stage IV B-derived chronic lymphocytic leukemia (CLL) with the IgG2a murine monoclonal antibody T101. This antibody binds to a 65,000-mol wt (T65) antigen found on normal T lymphocytes, malignant T lymphocytes, and B-derived CLL cells. All of the patients had a histologically confirmed diagnosis of advanced B-derived CLL and were refractory to standard therapy, and more than 50% of their leukemia cells reacted with the T101 antibody in vitro. The patients received T101 antibody two times per week, over two to 50 hours by intravenous administration in 100 mL of normal saline containing 5% human albumin. Twelve patients were treated with a fixed dosage of 1, 10, 50, or 100 mg, and one patient was treated with 140 mg of antibody. It was demonstrated that patients given two-hour infusions of 50 mg developed pulmonary toxicity, with shortness of breath and chest tightness. This toxicity was eliminated when infusions of 50 or 100 mg of T101 were prolonged to 50 hours. All dose levels caused a rapid but transient decrease in circulating leukemia cell counts. In vivo binding to circulating and bone marrow leukemia cells was demonstrated at all dose levels with increased binding at higher dosages. Antimurine antibody responses were not demonstrated in any patients at any time during treatment. Circulating free murine antibody was demonstrated in the serum of only the two patients treated with 100 mg of antibody as a 50-hour infusion and the patient treated with 140 mg of antibody over 30 hours. Antigenic modulation was demonstrated in patients treated at all dose levels but was particularly apparent in patients treated with prolonged infusions of 50 and 100 mg of antibody. We were also able to demonstrate antigenic modulation in lymph node cells, which strongly suggests in vivo labeling of these cells. Overall, T101 antibody alone appears to have a very limited therapeutic value for patients with CLL. The observations of in vivo labeling of tumor cells, antigenic modulation, antibody pharmacokinetics, toxicity, and antimurine antibody formation may be used in the future for more effective therapy when drugs or toxins are conjugated to the antibody.

Antibodies, Monoclonal↗
PubMed1981

Fate of a common acute lymphoblastic leukemia antigen during modulation by monoclonal antibody.

Modulation of a human common acute lymphoblastic leukemia antigen (CALLA) by specific monoclonal antibody (J5) has been studied with the immune precipitation method to identify radiolabeled antigen. Surfaces of leukemic cells have been labeled using 125I both before and after modulation by J5 antibody for different time intervals. Leukemic cells have also been metabolically labeled with 35S-methionine before modulation. These studies indicate that the 100,000-dalton glycoprotein expressing CALLA (gp 100-CALLA) cannot be detected in cells that were modulated with J5 antibody before surface labeling but that it is easily detectable in cells that were surface labeled before modulation for 10 hr. At later time points, gp 100-CALLA is selectively lost from cells that were surface labeled before modulation. Gp 100-CALLA is not detected in the supernatants from cultures of these modulated cells. We conclude that gp 100-CALLA is rapidly internalized during modulation and that CALLA is degraded. Gp 100-CALLA is not shed into the culture media, nor does it remain on the cell surface in an altered form. Incubation of leukemic cells with antisera to beta2-microglobulin or IgM does not affect the expression of gp 100-CALLA.

Antibodies, Neoplasm↗
PubMed1993

Repressor binding to a regulatory site in the DNA coding sequence is sufficient to confer transcriptional regulation of the vir-repressed genes (vrg genes) in Bordetella pertussis.

Five TnphoA fusions to vir-repressed genes (vrg genes) have been identified in the respiratory pathogen Bordetella pertussis. A comparison of vrg DNA sequences suggests a consensus DNA element within the coding regions of four of five vrg genes. To determine the role of this DNA sequence in vrg regulation, a nucleotide substitution mutation in the conserved region of vrg-6 was isolated. This mutant showed constitutively high levels of expression in the absence of antigenic modulators, MgSO4 and nicotinic acid, suggesting that this DNA element may be a control site for vrg repression. Moreover, Northern (RNA) analysis and transcriptional fusion analysis suggest that vrg genes are regulated at the transcriptional level. To determine whether sequences in the coding region were sufficient to respond to antigenic modulation, a vrg-6::TnphoA promoter deletion plasmid that contained a heterologous promoter driving the expression of vrg-6 coding sequences from the vrg-6 translation start site to the TnphoA fusion junction was constructed. This heterologous construct responded to modulators in a vir-dependent fashion, indicating that sequences upstream of the coding sequence are not required for antigenic modulation. Southwestern (DNA-protein) analysis and mutational studies suggest that the vrg consensus DNA sequence is specifically recognized by a 34-kDa vir-activated gene (vag) product, whose binding results in down-regulation of vrg transcript levels. We conclude, at least for the vrg::TnphoA fusion strains, that a site on the DNA that corresponds to a consensus sequence located in the vrg coding region is sufficient to confer the transcriptional regulation (repression) of vrg genes when B. pertussis strains are grown under nonmodulating conditions.

Amino Acid Sequence↗
PubMed2006

The shaving reaction: rituximab/CD20 complexes are removed from mantle cell lymphoma and chronic lymphocytic leukemia cells by THP-1 monocytes.

Clinical investigations have revealed that infusion of immunotherapeutic mAbs directed to normal or tumor cells can lead to loss of targeted epitopes, a phenomenon called antigenic modulation. Recently, we reported that rituximab treatment of chronic lymphocytic leukemia patients induced substantial loss of CD20 on B cells found in the circulation after rituximab infusion, when rituximab plasma concentrations were high. Such antigenic modulation can severely compromise therapeutic efficacy, and we postulated that B cells had been stripped (shaved) of the rituximab/CD20 complex by monocytes or macrophages in a reaction mediated by FcgammaR. We developed an in vitro model to replicate this in vivo shaving process, based on reacting rituximab-opsonized CD20(+) cells with acceptor THP-1 monocytes. After 45 min at 37 degrees C, rituximab and CD20 are removed from opsonized cells, and both are demonstrable on acceptor THP-1 cells. The reaction occurs equally well in the presence and absence of normal human serum, and monocytes isolated from peripheral blood also promote shaving of CD20 from rituximab-opsonized cells. Tests with inhibitors and use of F(ab')(2) of rituximab indicate transfer of rituximab/CD20 complexes to THP-1 cells is mediated by FcgammaR. Antigenic modulation described in previous reports may have been mediated by such shaving, and our findings may have profound implications for the use of mAbs in the immunotherapy of cancer.

Antibodies, Monoclonal↗
PubMed1981

Monoclonal antibodies as probes of acetylcholine receptor structure. 2. Binding to native receptor.

Binding of monoclonal antibodies top Torpedo californica acetylcholine receptor monomers solubilized in Triton X-100 was studied by centrifugation on sucrose gradients. Antibodies to alpha subunits were of two types. One type formed complexes of one antibody and one receptor monomer, independent of antibody/receptor ratio. We conclude that the binding sites for these antibodies are oriented on the two alpha subunits per monomer in such a way that each could be bound by one of the two binding sites of a single immunoglobulin molecule. Most antibodies were of this type. The other type of monoclonal antibody formed complexes of several sizes, including antibody cross-linked receptors, depending on the ratio of antibody to receptor. We conclude that the binding sites for these antibodies are oriented in such a way that the two alpha subunits per monomer could not be cross-linked by a single antibody molecule. A monoclonal antibody of this type raised against Electrophorus electricus receptors was used to show that this receptor also has two alpha subunits per monomer. This antibody cross-reacted with receptor from fetal calf muscle and was able to induce modulation of receptor in muscle cells in culture. This suggests that muscle receptor also has two alpha subunits and that the antibody can cross-link receptor in the plane of the membrane, as it does in solution, and thereby form complexes which enhance endocytosis and increase the rate of receptor destruction. The rate of antigenic modulation decreases at high antibody/receptor ratios, as expected if un-cross-linked complexes of two antibodies and one receptor were not destroyed at a faster rate. Antibodies which cross-link alpha subunits within a receptor monomer are frequent but would not be expected to be able to induce antigenic modulation. This provides one mechanism by which antisera of equivalent antireceptor titer might differ in their ability to induce antigenic modulation. An antibody which binds to denatured delta and gamma subunits forms complexes of only one antibody and one receptor monomer, independent of antibody ratio, as do antibodies thought to cross-link the two alpha subunits in a monomer. It apparently cross-links delta and gamma subunits within the monomer. Some of the monoclonal antibodies to alpha subunits can bind simultaneously to receptor, while the binding of others is mutually exclusive.

Animals↗
PubMed1994

Influence of culture conditions on expression of antigens in Bordetella bronchiseptica.

Bordetella (B.) bronchiseptica isolates from the respiratory tract of rat and pig in their virulent phase-I and their spontaneously developed avirulent phase-III were investigated. The strains were cultured on Bordet-Gengou agar, on nutrition agar with 10% horse blood, and with 5% sheep blood, on yeast agar, on minimal nutrition agar (MM) and Simmon's citrate agar with glycerol, starch, and nicotinic acid. Antigenic modulation was induced by MgSO4 on Bordet-Gengou agar. The B. bronchiseptica strains were cultivated at 37 degrees C for 48 h. The influence of different MgSO4 concentrations after five passages (1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 50, 100 mM/ml and low (20 degrees C) and high (42 degrees C) temperatures on antigenic modulation was investigated on Bordet-Gengou (B-G) agar. B. bronchiseptica colonies were characterized in relation to morphology, haemolysis, slide agglutination with B. bronchiseptica phase-I polyclonal antibodies, haemagglutination with horse and calf erythrocytes and polypeptide and LPS patterns in SDS-PAGE. Cultivation of B. bronchiseptica phase-I on B-G agar and ACMM agar at 37 degrees C for 48 h resulted in strong phase-I antigenic patterns, and, on peptone-rich media, in antigenic modulation. The morphology of B. bronchiseptica phase-I-strain colonies on peptone media was different from that of B-G and ACMM agar. The LPS pattern of both strains resembled that of phase-III strains. MgSO4 concentrations of 1 mM/ml (strain 1636 I) and 3 mM/ml (Ratte I) were able to induce LPS-pattern-like phase III.

Agglutination Tests↗
PubMed2002

Induction of local innate immune responses and modulation of antigen uptake as mechanisms underlying the mucosal adjuvant properties of immune stimulating complexes (ISCOMS).

Lipophilic immune stimulating complexes (ISCOMS) containing the Quil A adjuvant can induce local and systemic immune responses against orally delivered protein antigens. Here, we have examined the possibility that ISCOMS act by modulating local innate immune responses and antigen uptake in the intestine. Feeding ISCOMS to mice induced recruitment of dendritic cells (DCs), activated macrophages (mphi) and lymphocytes into the mesenteric lymph node (MLN), as well as recruitment of macrophages and B cells into the PP. Feeding ISCOMS also enhanced the absorption into circulation of a test feed of ovalbumin (OVA), with accelerated kinetics and increased peak levels. Serum taken 1h after feeding a tolerogenic dose of OVA to mice given ISCOMS orally did not induce the tolerance of systemic delayed type hypersensitivity (DTH) and antibody responses found in mice receiving serum from donors fed OVA alone. Thus, ISCOMS may increase the immunogenicity of intestinal antigen via a combination of effects on antigen uptake and on local accessory cells.

Adjuvants, Immunologic↗
PubMed2005

In vitro preparation and functional assessment of human monocyte-derived dendritic cells-potential antigen-specific modulators of in vivo immune responses.

Dendritic cells (DCs) are highly specialized professional antigen presenting cells that have a potent capacity for stimulating naïve, memory and effector T-cells. They are located in lymphoid organs as well as in almost all nonlymphoid tissues. Immature DCs, residing in the host microenvironment, respond to danger signals with maturation, a differentiation process along which they acquire the ability to direct the extent and the type of primary immune responses according to the type of danger perceived. In this review we present some of our approaches and experiences regarding the isolation of human monocytes from peripheral blood and the in vitro preparation of, first, immature and then mature DCs by applying several maturation factors: bacterial lipopolysaccharide (LPS), a defined mixture of recombinant pro-inflammatory cytokines, monocyte conditioned medium (MCM) and TNF-alpha alone. The assessment of DC phenotypes and their functional capabilities as well as some of the techniques used for tumour associated antigen loading are also presented. The results of such studies represent a basis for optimal in vitro preparation of DCs, which could be clinically used to modulate immune responses in cancer, autoimmune diseases and in the planned onset of tolerance to disparate major histocompatibilty complex (MHC) antigens prior to tissue or organ transplantation.

Antigen Presentation↗
PubMed2000

Capsular polysaccharide and O-specific antigen divergently modulate pulmonary neutrophil influx in an Escherichia coli model of gram-negative pneumonitis in rats.

Enteric gram-negative bacilli cause a severe, often life-threatening pneumonia. An improved understanding of the pathogenesis of this infection may lead to improved treatment. Nearly all of the responsible gram-negative bacilli possess capsular polysaccharides and/or an O-specific antigen as part of their lipopolysaccharide (LPS). We hypothesized that these surface polysaccharides may modulate the pulmonary host response. To investigate this, a rat pneumonitis model was used, and pulmonary neutrophil influx, a critical aspect of host defense, was measured. To assess for the effect of the capsule and O-specific antigen on this host response, three proven, isogenic derivatives that are deficient in capsular polysaccharide alone (CP9.137), the O-specific antigen moiety of the LPS alone (CP921), and both the capsular polysaccharide and O-specific antigen (CP923), as well as their wild-type parent (CP9), were used as challenge strains at various intratracheal challenge inocula (CI). Total lung myeloperoxidase (MPO), a surrogate marker for neutrophils, was measured for 15 h post-bacterial challenge. To determine the effect of capsule and the O-specific antigen on the measured MPO levels, a mathematical model was developed and used to describe the MPO levels as a function of time for each CI of each of the four strains. The results from this analysis demonstrated that in the absence of the K54 capsule, 80.7 times the CI is necessary to achieve the same maximum MPO level relative to K54 positive strains (P < 0.0001). In contrast, a diametric effect was observed in the absence of the O-specific antigen, where 0.13 times the CI was necessary to achieve the same maximum MPO level relative to O4-positive strains (P = 0.0032). No interactive effect was observed between the capsule and the O-specific antigen. These findings demonstrate that these surface polysaccharides modulate pulmonary neutrophil influx and suggest that the K54 capsular polysaccharide is a proinflammatory mediator and that the O4-specific antigen attenuates the proinflammatory response. If these speculations are substantiated, an understanding of how the capsule and the O-specific antigen modulate host response could have significant therapeutic implications. The potential use of biologic modulators directed against the host response, as well as approaches based on inactivating bacterial components (e.g., surface polysaccharides) in attempts to modify sepsis syndromes, could be developed.

Animals↗
PubMedDate not supplied

Modulation for antigen presentation in tuberculosis by using synthetic peptides.

Competition assay technology has been a very useful tool in the study of parasite antigens and has been inferred but never proven that this approach can be applied to select T-cell epitopes by using another microorganisms. In this study, HLA-restricted T-cell clones specific to synthetic peptides derived from the 65 kDa mycobacterial protein were used to investigate whether these peptides are able to compete with each other at the level of MHC-binding sites in tuberculosis. Fixed APCs were pulsed with suboptimal concentration of stimulator peptide in the presence of various concentrations of competitor peptide. The results showed that two peptides from this protein were able to compete with each other inducing a significant inhibition in the proliferation assays while there was no competition by using a control peptide. The amount of cross-reactivity was influenced by the peptide concentrations. More important was the observation that these peptides were able to bind to the same HLA-class II molecules therefore blocking the binding of each other. The fact that these peptides have not an identical amino acid sequence support the idea that the MHC-peptide interaction must have a broad specificity to be able to bind a large number of peptides. These results demonstrate that it is possible to modulate the antigen presentation by blocking the peptide MHC-class II interaction in tuberculosis and support the idea that this approach facilitates the selection of appropriate T-cell epitopes to be incorporated in a vaccine.

Amino Acid Sequence↗
PubMed1998

B cell responses to a peptide epitope. VII. Antigen-dependent modulation of the germinal center reaction.

Germinal center responses to two analogous peptides, PS1CT3 and G32CT3, that differ in sequence only at one position within the B cell epitopic region were examined. In comparison with peptide PS1CT3, peptide G32CT3 elicited a poor germinal center response. By demonstrating equal facility of immune complexes with IgM and IgG Ab isotypes to seed germinal centers, we excluded differences in isotype profiles of early primary anti-PS1CT3 and anti-G32CT3 Ig as the probable cause. Quantitative differences in germinal center responses to the two peptides were also not due to either qualitative/quantitative differences in T cell priming or variation in the frequency of the early Ag-activated B cells induced. Rather, they resulted from qualitative differences in the nature of B cells primed. Analysis of early primary anti-PS1CT3 and anti-G32CT3 IgMs revealed that the latter population was of a distinctly lower affinity, implying the existence of an Ag affinity threshold that restricts germinal center recruitment of G32CT3-specific B cells. The impediment in anti-G32CT3 germinal center initiation could be overcome by making available an excess of Ag-activated Th cells at the time of immunization. This resulted in the appearance of a higher affinity population of G32CT3-specific B cells that, presumably, are now capable of seeding germinal centers. These data suggest that the strength of a germinal center reaction generated is Ag dependent. At least one regulatory parameter represents the quality of B cells that are initially primed.

Amino Acid Sequence↗
PubMed1992

1 alpha,25-dihydroxyvitamin D3 modulates Ia antigen expression induced by interferon-gamma and prostaglandin E2 production in Pam 212 cells.

Recent investigations suggest that 1 alpha,25-dihydroxyvitamin D3 [1 alpha,25(OH)2D3] has an effect on the regulation of immune responses and that keratinocyte (KC) expression of major histocompatibility complex class II antigens may be involved in immune responses. We investigated the modulation by 1 alpha,25(OH)2D3 of Ia antigen expression induced by interferon-gamma (IFN-gamma) and prostaglandin E2 (PGE2) production in Pam 212 cells. 1 alpha,25(OH)2D3 at 10(-6), 10(-8) or 10(-10) M significantly decreased the levels of IFN-gamma-induced Ia antigen expression in Pam 212 cells. Pam 212 cells produced PGE2 and 1 alpha,25-(OH)2D3 enhanced Pam 212 cell PGE2 production. However, indomethacin (1, 5 and 10 micrograms/ml) did not abrogate the inhibitory effect of 1 alpha,25(OH)2D3 on IFN-gamma induction of Ia antigen expression in Pam 212 cells, indicating that the products of the cyclo-oxygenase pathway do not mediate 1 alpha,25(OH)2D3 inhibition of IFN-gamma induction of Pam 212 cell Ia antigen expression. Our studies suggest that in Pam 212 cells the levels of Ia antigen expression induced by IFN-gamma and PGE2 production are negatively and positively regulated by 1 alpha,25(OH)2D3, respectively, and that 1 alpha,25(OH)2D3 may play a role in the regulation of immune responses.

Calcitriol↗
PubMed1980

Antigen induced modulation by shed lymphocyte membrane gangliosides.

A unique regulatory mechanism has been proposed for ganglioside which functions to immune responses to temporarily restrain B lymphocytes of all specificities and at various levels of differentiation. Utilizing antigen competition protocols, experiments was designed to exploit and extend the antigen induction properties of this modulation. Spleen cell cultures were prepared from TNP-BGG primed mice. In vitro stimulation of the cultures with ovalbumin (OVA) followed 24 hours later by addition of TNP-BGG resulted in only one weak TNP hemolytic plaque responses when compared to control cultures which did not receive OVA. OVA induced competitive effects were absorbed by anti-Thy-1 or anti-ganglioside. Glycolipids could be extracted from the culture media supernatants of experimental and control groups as a ganglioside fraction containing Thy-1 determinants. These molecules, when formulated into liposomes, produced the same modulatory effect as that of media from the competitive culture group. These results support and extend the proposal that glycolipids released by antigen stimulated T cells provide unrestricted modulation of B cells to prevent overload during T cell maturation. This regulatory mechanism prevents direct antigen binding and prepares B cell receptivity for further stimuli which orchestrate their terminal differentiation into plasma cells.

Animals↗
PubMed1999

Alpha-galactosyl antibody redistributes alpha-galactosyl at the surface of pig blood and endothelial cells.

The interaction of antibodies with cell surface antigens may induce redistribution of immune complexes, followed by antigen depletion, with increased resistance to injurious effect of antibody and complement (antigenic modulation). Human natural antibodies to Gal alpha 1,3Gal beta 1,4GlcNAc-R (alpha Gal) epitopes expressed at the surface of pig cells are a major obstacle to xenotransplantation. Recent studies have shown that these antibodies do not modulate alpha Gal, but the morphological consequences of the antigen-antibody interaction are unknown. Pig blood and endothelial cells, were exposed to baboon alpha-Gal antibodies, and studied by immunofluorescence and phase contrast microscopy, flow cytometry, and inhibition enzyme-linked immunosorbent assay. In cells studied at 4 degrees C or fixed, alpha Gal was diffusely expressed at the surface. After cross-linking at 37 degrees C, antigenic modulation did not occur, but granular redistribution of alpha Gal immune complexes was seen in all cell types. In other systems a similar redistribution is known to induce perturbation of the plasma membrane/cytoskeletal structure with changes in adhesive properties, gene regulation, and T cell activation, which could be important if pig xenografts will be made to survive for prolonged periods.

Animals↗
PubMed1989

Expression of MHC class II antigens is modulated by ouabain.

Ouabain enhances a modulation effect of lipopolysaccharide (LPS) on the expression of MHC class II antigens. A similar but lesser effect than that of ouabain, which increases intracellular concentration of sodium ions, has been observed when treating cells with ionophores quercetin which increases [Ca2+]i or valinomycin which increases [K+]i. These findings confirm the role of ion flux in cellular activation and differentiation. Optimal concentration of ouabain is 10(-7) M with 10 micrograms of LPS/ml for human and pig peripheral blood cells. The increase in radioactivity of mononuclear human blood cells after the binding of 125I-anti-MHC class II monoclonal antibody is at the fourth hour of cultivation with LPS and ouabain, the number of immunofluorescently positive cells rises at the twelfth hour. A similar modulation has been observed on pig kidney cell line. It can be concluded that the expression of class II antigens on the plasma membrane can be induced by cumulative effect of LPS and agents alterating ion transport.

Animals↗