Inhibition of modulation of thymus-leukemia antigens by concanavalin A.
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Animals↗
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Results for “Antigenic Modulation”
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Murine delayed hypersensitivity (DHS): modulation of in vitro antigen-induced responsiveness of lymph node cells from mice expressing DHS to human gamma-globulin by lymphocyte populations from normal syngeneic animals.
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Animals↗
Modulation of MHC class I antigen decreases pancreatic islet immunogenicity.
Pretreatment regimens directed at reducing the immunogenicity of pancreatic islets have emphasized the elimination or alteration of the major histocompatibility complex (MHC) class II-positive dendritic cells within the islet. Unfortunately, the efficacy of such pretreatment regimens has been extremely variable and the relative contribution of the dendritic cells to the overall immunogenicity of pancreatic islets has remained ambiguous. Recent evidence has suggested that the MHC class I antigen present on the endocrine cells within the islets may play an important role in the alloimmune response. This study utilized the in vitro mixed lymphocyte-islet co-culture system to determine if pretreatment of whole islets with an anti-MHC class I monoclonal antibody specific to the donor strain would block the generation of cytotoxic T lymphocytes (CTL) in the in vitro mixed lymphocyte-islet coculture. Pretreatment of B10.BR (H-2k) and DBA/2J (H-2d) islets with an allospecific anti-MHC class I monoclonal antibody blocked the generation of allospecific CTL when the pretreated islets were placed into coculture with C57Bl/6 (H-2b) splenocytes. If such a pretreatment regimen is similarly effective in vivo, it could potentially be used as an antirejection strategy in pancreatic islet allotransplantation.
Animals↗
Detection of antigen in the coelomocytes of the earthworm, Eisenia foetida (Annelida).
Earthworms, Eisenia foetida, are able to respond to antigenic stimulation by the formation of the antigen-binding molecules by coelomocytes--the effector cells of annelids' defence reactions. The ability to react with gold-labelled antigen was detected in agranular coelomocytes by electron microscopy. Furthermore, flow cytometry analysis used for quantitative evaluation of antigen binding showed significant increase of both antigen-binding cells and the amount of antigen bound per cell after stimulation. The antigen binding was inhibited by preincubation of cells with several similar proteins, although the most potent inhibitor was the immunizing antigen.
Animals↗
Selection of a Borrelia burgdorferi antigenic variant by cultivation in the presence of increasing amounts of homologous immune serum.
This investigation was undertaken to select antigenic variants of a Borrelia burgdorferi strain in vitro. The original strain BITS was cultivated in BSK medium supplemented with increasing concentrations of homologous hyperimmune serum raised in rabbits. After a few serial passages starting from a subinhibitory serum dilution of 1:800 in BSK up to 1:200, a variant named BITSv was obtained; it grew abundantly like the control culture in the presence of hyperimmune serum. Analysis of the antigenic pattern of the original and derived variants by Western blotting revealed that BITSv, compared to the original strain BITS, had lost the reactivity with the immune serum at the level of the oligosaccharide moiety. These experiments, designed to mimic the possible action of antibodies that arise during a Borrelia infection, suggest that lipopolysaccharides are surface located and that they play a role in the integrity of the outer membrane during the multiplication of Borrelia burgdorferi.
Antibodies, Bacterial↗
The CD19-CR2-TAPA-1 complex, CD45 and signaling by the antigen receptor of B lymphocytes.
A paradigm describing the response of T lymphocytes to antigen holds that signals from antigen receptors must be modulated by non-antigen-specific, accessory membrane proteins for an appropriate cellular response to occur, such as differentiation, activation and tolerance. Recent studies suggest that this paradigm applies also to B lymphocytes. Signaling through membrane IgM in these cells requires CD45, a phosphotyrosine phosphatase, and is amplified by a complex containing CD19, complement receptor 2 (CD21), and TAPA-1, which recruits the intracellular enzyme, phosphatidylinositol 3-kinase.
Animals↗
Modulation of human leukocyte antigen-DR on monocytes and CD16 on granulocytes in patients with septic shock using hemoperfusion with polymyxin B-immobilized fiber.
BACKGROUND: Hemoperfusion with PMX-F (polymyxin B covalently immobilized on fibers) has been reported to be safe and effective for patients with septic shock. However, the molecular mechanism of this usefulness is not yet clear. The purpose of this study was to evaluate whether the expression of CD14, human leukocyte antigen (HLA)-DR on monocytes, and the expression of CD16, CD11b/CD18 on neutrophils, are altered in septic patients according to the severity, and whether PMX-F treatment affects the clinical parameters and the expression of leukocyte surface antigen expression. PATIENTS AND METHODS: Thirty-four patients who were taken to the National Defense Medical College hospital at emergency, and who had an identified focus of infections, were enrolled in this study. The patients were divided into three groups: non-systemic inflammatory response syndrome [SIRS]) group, sepsis group, and septic shock group. Peripheral blood samples were collected at the time of admission to our hospital. The CD14, HLA-DR expression on monocytes and the CD11b/CD18, CD16 expression on granulocytes were evaluated using flowcytometry, and the serum interleukin (IL)-6 and IL-10 levels were measured using enzyme-linked immunosorbent assay. Treatment with a PMX-F column was performed in 10 patients with septic shock. RESULTS: The HLA-DR expression on monocytes and the CD16 intensity on granulocytes in patients with septic shock were significantly lower than those in patients with sepsis. The serum IL-6 and 10 levels in patients with septic shock were significantly higher than those in patients with sepsis. The mean systolic blood pressure in patients with septic shock was significantly increased after the PMX-F treatment; furthermore, the HLA-DR expression on monocytes and the CD16 intensity on granulocytes were significantly increased after the PMX-F treatment. The serum IL-10 levels were significantly decreased after the PMX-F treatment. CONCLUSIONS: We showed that the surface antigens, HLA-DR on monocytes and CD16 on granulocytes, are extremely decreased in patients with septic shock, and that PMX-F treatment is effective for beneficially increasing the surface antigen expression on leukocytes. This therapy might be a new strategy for helping patients recover from immunoparalysis in septic conditions.
Aged↗
The role of the humoral immune system in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE).
The pathogenic events in multiple sclerosis (MS) that result in immune cell infiltration, multifocal demyelination and axonal loss have been focused by the strong impact of the classical MS model experimental autoimmune encephalomyelitis (EAE) towards the hypothesis that MS is an entirely T cell-mediated disease. Although conspicuous humoral immune responses have been known since Kabal's seminal finding of elevated immunoglobulins (Igs) in the cerebrospinal fluid (CSF), only in the past few years evidence derived from recent studies of the MS lesion of anti-myelin antibodies (Abs) in patients with early MS and of MS animal models has led to a renewed interest in the role for B cells, plasma cells and their products in the pathogenesis of MS. This review surveys the actual data concerning the role of the humoral immune system in MS and EAE and explains potential modes of action and long-time persistence in the inflamed brain tissue as a B cell-supportive microenvironment in MS. These mechanisms include the modulation of antigen presentation and costimulation to T cells, increased myelin opsonisation und recruitment of inflammatory cells to the CNS, but also immunoregulatory influences on the remyelination by anti-myelin B cells and Abs. So, affecting the humoral immune system in MS would be a reasonable therapeutic option.
Animals↗
Anatomy of a murder--signal transduction pathways leading to activation of natural killer cells.
Natural killer (NK) cells control the early phases of viral infections, modulate antigen-specific immune responses, and participate in the rejection of tumours and bone marrow grafts. A fine balance between inhibitory and activating receptors tightly regulates NK cell activation. Biochemical studies in human cell lines and primary cells have revealed some of the activating NK cell signalling pathways, however animal models are instrumental to understand the physiological implications of these findings for immune responses in vivo. Gene targeting in mice and biochemical studies in cells are helping to dissect out the various signal transduction pathways that control NK cell activation. A clearer view of these pathways may eventually help designing more effective immune therapies based on the use of NK cells.
Animals↗
Antigenic profile of human recombinant PrP: generation and characterization of a versatile polyclonal antiserum.
We describe the quality of a rabbit polyclonal antiserum (Sal1) that was raised against mature human recombinant prion protein (rhuPrP). Epitope mapping demonstrated that the Sal1 antiserum recognized six to eight linear antigenic sites, depending on the animal species. The versatility of the antiserum was evident from the range of animal species and immunochemical techniques where it could be applied successfully. Antigen absorption studies revealed differences in the location and number of epitopes remaining after incubation with soluble or aggregated antigen.Our knowledge concerning immunoprophylaxis against prion diseases and the important role played by conformational changes of PrP is increasing rapidly. The findings reported here should add to this body of knowledge.
Amino Acid Sequence↗
Immunotherapeutic approaches in multiple sclerosis.
The progress in understanding the mechanisms of T cell activation, inactivation and modulation has been translated into different immunotherapeutic strategies aiming at treating multiple sclerosis (MS). Key attack points for selective immunointervention in MS include modulation of antigen recognition, costimulation blockade, induction of regulatory cells, deviation to non-pathogenic or protective responses, neutralization of proinflammatory cytokines and administration of anti-inflammatory cytokines. In addition, several attempts have been made using less specific forms of immunointervention. The two resounding successes in the immunotherapy of MS, IFN-failed and glatiramer acetate, contrast with the many attempts, equally based on sound reasoning and promising animal data. Nevertheless, antigen-based immunointervention will continue to be tested clinically, and we will certainly witness the application of more articulate strategies able to selectively target cytokine production by Th1 or Th2 cells or to modify the Th1/Th2 balance. Perhaps, an effective manipulation of pathogenic and protective cells in MS may eventually rely on a combination of antigen- and cytokine-based approaches to selectively target autoreactive T cells and divert them from autoaggression. Most importantly, new avenues are opening, such as the use of chemokine receptor antagonists, and others look very promising, as targeting dendritic cells to favour their capacity to induce regulatory T cells.
Animals↗
Mapping the anatomy of a Plasmodium falciparum MSP-1 epitope using pseudopeptide-induced mono- and polyclonal antibodies and CD and NMR conformation analysis.
Antigen structure modulation represents an approach towards designing subunit malaria vaccines. A specific epitope's alpha carbon stereochemistry, as well as its backbone topochemistry, was assessed for obtaining novel malarial immunogens. A variety of MSP-1(38-61) Plasmodium falciparum epitope pseudopeptides derived were synthesised, based on solid-phase pseudopeptide chemistry strategies; these included all-L, all-D, partially-D substituted, all-Psi-[NH-CO]-Retro, all-Psi-[NH-CO]-Retro-inverso, and Psi-[CH2NH] reduced amide surrogates. We demonstrate that specific recombinant MSP-1(34-469) fragment binding to red blood cells (RBCs) is specifically inhibited by non-modified MSP-1(42-61), as well as by its V52-L53, M51-V52 reduced amide surrogates and partial-D substitutions in K48 and E49. In vivo tests revealed that reduced amide pseudopeptide-immunised Aotus monkeys induced neutralising antibodies specifically recognising the MSP-1 N-terminus region. These findings support the role of molecular conformation in malaria vaccine development.
Amino Acid Sequence↗
Granuloma formation in vitro requires B-1 cells and is modulated by Paracoccidioides brasiliensis gp43 antigen.
The mechanisms that determine granuloma formation and the significance of this type of inflammatory response in the pathogenesis of fungal diseases such as paracoccidioidomycosis are far from fully understood. We developed a granuloma model in vitro using beads to evaluate the role of isolated mouse peritoneal macrophages and B-1 cells. We also investigated granuloma formation in the presence of gp43, the main antigenic component of Paracoccidioides brasiliensis, which is secreted exocellularly. To determine whether B-1 cells, macrophages, or both, participate in granuloma formation, peritoneal cells from Xid mice, which lack B-1 cells, were used. Granuloma-like structures were not formed with Xid peritoneal cells or with cells from wild type mice that had their peritoneal and pleural cavities irradiated before the cultures were established. Granulomas were observed either when total adherent peritoneal cells or when isolated B-1 cells were added to macrophage cultures. The data strongly suggest that an interaction of B-1 cells and macrophages plays an important role in granuloma-like formation in this experimental model and that the presence of gp43 strongly stimulates this response.
Animals↗
Inhibition of infection with human immunodeficiency virus type 1 by sulfated gangliosides.
Four kinds of gangliosides, namely GM1a, GD1a, GD1b and GT1b and their sulfated derivatives were examined for antiviral activities against human immunodeficiency virus type 1 and abilities to modulate CD4 antigen on the cell surface. The infection of human T cells with the virus was markedly inhibited by treatment with the sulfated gangliosides at a concentration of 10 micrograms/ml, while the non-sulfated gangliosides had only weak antiviral activities. The sulfated gangliosides completely inhibited syncytium formation induced by HIV-1 at 30 micrograms/ml. The CD4 antigen on the surface of T cells became hardly detectable after treatment with them. They did not damage cells, nor prolong the activated partial thromboplastin time at concentrations of up to 100 micrograms/ml, suggesting that they may have little side effect in vivo.
Animals↗
Nitric oxide modulates eosinophil infiltration in antigen-induced airway inflammation in rats.
The influence of nitric oxide (NO) on eosinophil infiltration into the airways was investigated in rats actively sensitized with ovalbumin. The animals were treated chronically with the NO synthase inhibitor, N omega-Nitro-L-arginine methyl ester (L-NAME; 75 mumol rat-1 day-1), for 4 weeks. Bronchoalveolar lavage was performed at 6, 24, 48 and 72 h after intratracheal injection of ovalbumin. Intratracheal challenge of the sensitized rats with ovalbumin caused a significant increase in total leucocyte infiltration in bronchoalveolar lavage fluid both 24 and 48 h post-ovalbumin injection. Neutrophils and eosinophils peaked, respectively, at 24 h (29%) and 48 h (30%) in bronchoalveolar lavage fluid whereas the mononuclear cell did not differ significantly from the counts in non-sensitized rats at any time. At both 6 and 24 h post-ovalbumin injection, the chronic treatment of the animals with L-NAME affected neither the total nor the differential leucocyte content. However, at 48 h post-ovalbumin challenge, the total cell count was reduced by approximately 48% in the L-NAME-treated animals and this was associated with a marked inhibition (81%) of the eosinophil influx. Histological examination of the lungs from these animals (48 h post-ovalbumin challenge) also showed a prominent reduction (69.5%; P < 0.05) of the eosinophil infiltration in the respiratory segments. Our results demonstrate that NO plays a pivotal role in the eosinophil infiltration in airways of actively sensitized rats.
Animals↗
Advances in molecular biology. Potential impact on diagnosis and treatment of disorders of the thyroid.
Advances in molecular biology research continue to have a major impact on clinical medicine. These advances have provided a means to produce proteins previously available in limited supply and allow for the production of novel proteins that are improved agonists or else antagonists with greater specificity for therapeutic targets. Newer drug delivery systems should facilitate delivery of these proteins. By combining the capabilities to produce drug targets in acceptable quantities with improved methods for determining the three-dimensional structures of these targets, novel organic therapeutic molecules that act on these targets will be designed. Gene transfer therapy using genes that express important proteins or that encode "antisense" RNAs that inhibit the translation of specific mRNAs will soon become a reality. The use of RFLPs and PCR methodologies promises increased means to diagnose specific genetic diseases and infections. Most importantly, molecular biology is helping to understand the mechanisms of disease such that novel diagnostic and therapeutic approaches can be described. These advances are providing an understanding of the mechanisms involved in cancers of the thyroid gland. They have already led to an enhanced understanding of (1) the growth factors that control proliferation of the thyroid gland, (2) the potential steps in thyroid nodule and neoplasia development, (3) particular mutations that may occur as thyroid cancers develop, (4) oncogenes that are expressed in thyroid cancers, and (5) the genetic defects that are responsible for thyroid gland malignancies in the multiple endocrine neoplasia (MEN) syndromes. With the latter, the RFLP technology has already provided an enhanced means to diagnose the disorder. With further progress, enhanced means for diagnosis and treatment should emerge. Molecular biology techniques are contributing to an increased understanding of the mechanisms of development of autoimmune thyroid disease as with Graves' disease and Hashimoto's thyroiditis. The potential role of infections, histocompatibility antigens, thyroid gland and extraglandular antigens, immune modulators, subpopulations of T-cells such as suppressor and helper cells, other cells involved in immune responses, and a combination of influences of several different functions on the thyroid gland are being defined. This knowledge should soon suggest improved means for diagnosis and treatment. Understanding of the function of the thyroid hormone receptors should have clinical importance. This knowledge suggests a means to develop thyroid hormone antagonists that may be used to more rapidly ameliorate the effects of hyperthyroidism and could be useful in nonthyroidal disorders such as cardiac arrhythmias.(ABSTRACT TRUNCATED AT 400 WORDS)
DNA, Recombinant↗
Expansion or elimination of B cells in vivo: dual roles for CD40- and Fas (CD95)-ligands modulated by the B cell antigen receptor.
Signals from CD4+ T cells induce two opposite fates in B cells: clonal proliferation of B cells that bind specifically to foreign antigens and clonal deletion of equivalent B cells that bind self-antigens. This B cell fate decision is determined by the concerted action of two surface proteins on activated T cells, CD40-and Fas-ligands (CD40L and FasL), whose effects are switched by signals from the B cell antigen receptor (BCR). Foreign antigens that stimulate the BCR acutely cause CD40L and FasL to promote clonal proliferation. CD40L and FasL trigger deletion, however, when the BCRs become desensitized by chronic stimulation with self-antigens or when BCRs have not bound an antigen. The need for both Fas and CD40L to correctly regulate self-reactive B cell fate may explain the severe autoantibody disorders in Fas- or CD40L-deficient children.
Animals↗
Modulation of HLA-DR antigens expression in human myeloid leukaemia cells by cytarabine and 5-aza-2'-deoxycytidine.
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Azacitidine↗