Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P30536 (PBS)
 9,886 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A monoclonal antibody-based sandwich enzyme immunoassay (EIA) for bovine interferon-gamma (IFN-gamma) has been developed and can be used in conjunction with a whole blood culture system to diagnose tuberculosis in cattle. During its development, normal bovine plasma samples were tested to establish background levels of circulatory IFN-gamma. Of 191 samples tested, 81 (42.4%) were positive (OD > 0.1) when tested undiluted in intact monoclonal antibody (IgG1)-coated wells compared to only 8 (4.2%) in F(ab')2-coated wells, which suggested non-specific interference in the EIA rather than circulatory IFN-gamma. Reactivity of all remaining samples was removed by diluting plasmas 1/2 with 1% casein-PBS-0.05% Tween 20 supplemented with an optimum amount (5%) of normal mouse serum (NMS). Serum pools derived from BALB/c, DBA/2, C3H/HeJ, CBA/CaH and Swiss, but not C57BL/6J, mice were found to inhibit equally the reactions of five strong false-positive bovine plasma samples but had no effect on the titre of IFN-gamma in the sample. Sera from other species tested were less effective. This suggests that the interfering factors possess a high degree of specificity, since the immunoglobulin heavy chain of IgG1 produced by all these five strains of mice are allotypically identical and different to IgG1 produced by C57BL/6J mice. The use of F(ab')2 antibody fragments to coat plate wells and sample diluent containing 5% NMS has resulted in an EIA for bovine IFN-gamma that is virtually free from false-positive reactions, has a high degree of reproducibility and a sample detection limit equivalent to approximately 80 pg/ml recombinant bovine IFN-gamma.
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PMID:Removal of false-positive reactions from plasma in an enzyme immunoassay for bovine interferon-gamma. 143 Nov 51

The effect of recombinant rat interferon-gamma (rRIFN-gamma) on allograft rejection was studied in two rat heart transplantation models. Recipients were treated with rRIFN-gamma by intraperitoneal or intravenous injection, either by bolus or continuous infusion. Treatment was started after transplantation and continued during a period ranging from 4 to 10 days; dosages varied from 2.5 x 10(2) U/kg/day to 3 x 10(6) U/kg/day. Controls were infused with PBS. Treatment with rRIFN-gamma had no effect on allograft survival, irrespective of the route of administration, the dosage used or the duration of treatment. Higher dosages of rRIFN-gamma induced serious morbidity and mortality. In conclusion, systemic treatment of cardiac allograft recipients with rRIFN-gamma has no effect on graft rejection and is associated with serious toxicity and mortality when high dosages are used.
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PMID:Treatment with rIFN-gamma has no effect on cardiac allograft rejection. 190 27

The present study was initiated to study the efficacy of donor pretreatment with interferon-gamma to induce class II antigen expression in heart tissue, and to investigate whether this pretreatment would influence heart allograft survival. BN rats were used as donors, and LEW rats as recipients. During a period of 3 consecutive days prior to transplantation, IFN-gamma was administered to BN rats via continuous intravenous infusion at dosages of 10(3), 10(4), and 5.10(4) U/hr. Control animals were infused with PBS; each group consisted of 9 animals. Analysis of IFN-gamma induced class II expression by immunoperoxidase staining revealed a significant, fourfold increase in the number of dendriticlike cells, irrespective of the IFN-gamma dose given (controls: 15 +/- 4 vs. highest dose group: 57 +/- 9 cells/mm2; P less than 0.005). Endothelial cells of arteries and venules remained class II antigen negative. Grafting of hearts from IFN-gamma perfused donors to untreated recipients (6 animals per group), did not result in a shortened or prolonged survival time in any of the experimental groups, as compared to controls. These results indicate that upgrading of class II antigen expression on dendriticlike cells is not likely to be of importance for the process of rejection.
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PMID:Increase of major histocompatibility complex class II--positive cells in cardiac allografts by interferon-gamma has no impact on graft survival. 251 99

Mouse monoclonal antibodies (mAbs) against human interferon-gamma (IFN-gamma) were produced after immunization with recombinant IFN-gamma. Two mAbs (1-D1K and 7-B6-1) recognizing distinct epitopes on natural IFN-gamma were selected for the development of a two-site ELISA. The sensitivity was similar for IFN-gamma diluted in PBS with 1% bovine albumin, spent culture medium or fetal calf serum but reduced to approximately 50% when diluted in normal human serum. Individual normal human sera were tested and three of 14 gave false reactivities in the ELISA. One serum factor with major impact on the individual variation and the decreased sensitivity could be adsorbed to and eluted from protein A-Sepharose. Based on these observations we established a new ELISA protocol which made it possible to test for low levels of IFN-gamma in human serum and plasma samples. The modifications in this protocol are easy to apply with basic laboratory equipment.
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PMID:Monoclonal antibody two-site ELISA for human IFN-gamma. Adaptation for determinations in human serum or plasma. 251 32

Thymopentin (TP-5) is a synthetic pentapeptide that corresponds to the active 32-36 amino acid sequence of the thymic hormone thymopoietin, of which it retains all the immunomodulatory properties. In this study, we have evaluated the effects of long term prophylactic treatment with TP-5 on the clinical, immunological and histological parameters of the SLE-like syndrome that spontaneously occurs in MRL/lpr-lpr (MRL-lpr) mice. TP-5, administered (s.c.) to these mice at the doses of 1, 10 and 100 mg/kg, was given daily, five times a week, from the 9th to the 26th weeks of life. The prophylactic treatment with TP-5 prolonged in a clear dose-dependent fashion the lifespan of MRL-lpr mice as compared with PBS-treated control mice, and the effect reached statistical significance at the doses of 10 and 100 mg/kg. In parallel ex vivo studies, this clinical effect was associated with multiple profound modifications of the immune system including: (i) the reduction of the spontaneous and Con A-induced release of interleukin-4 (IL-4); (ii) the increased secretion of interferon-gamma (IFN-gamma) and IL-6 upon polyclonal mitogenic stimulation, and (iii) the amelioration of the defective Con A-induced lymphoproliferative response. In contrast, although the drug diminished the severity of proteinuria in MRL-lpr mice, it neither reduced histological signs of lupus nephritis nor diminished the serum titres of anti-native DNA and anti-histone autoantibodies. These results indicate that TP-5 displayed powerful immunodulatory activities in a well known model of human SLE.
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PMID:The effects of thymopentin on the development of SLE-like syndrome in the MRL/lpr-lpr mouse. 797 60

We have evaluated the effects of a treatment with soluble interleukin-1 receptor (sIL-1R) in the accelerated model of autoimmune diabetes induced by cyclophosphamide (CY) in the non-obese diabetic (NOD) mouse. Prior to the CY challenge (350 mgkg body weight), female euglycemic NOD mice were randomly divided into three groups (A-C). Groups B and C were treated daily from 1 day before to 13 days after the CY challenge with sIL-1R at doses of 0.2 and 2 mg/kg body weight. Group A was treated with PBS. By 2 weeks after CY administration, an acute form of autoimmune diabetes with glycosuria, hyperglycemia and severe insulitis occurred in the majority (13/20, 65%) of the control mice (group A). In contrast, repeated injections with sIL-1R protected NOD mice from insulin-dependent diabetes mellitus (IDDM) development in a dose-dependent fashion; the incidence of IDDM was 53.3% (8/15) in the mice treated with 0.2 mg/kg and only 6.7% (1/15) in those treated with 2 mg/kg. However, none of the doses of the sIL-1R reduced the extent of insulitis in NOD mice. Importantly, the anti-diabetogenic property of sIL-1R may not involve major T cell function impairment; accordingly, in parallel experiments, splenic lymphoid cells from NOD mice not challenged with CY, but treated with 2 mg/kg sIL-1R for 5 consecutive days showed a normal distribution of mononuclear cell subsets and maintained their capacity to secrete interferon-gamma and IL-2 and to proliferate in response to polyclonal mitogenic stimulation with concanavalin A.
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PMID:Protection from experimental autoimmune diabetes in the non-obese diabetic mouse with soluble interleukin-1 receptor. 805 41

The histologic and cytologic responses of heifer mammary glands infected with Staphylococcus aureus were studied after infusion of interleukin-2 or interferon-gamma. Two groups of 4 heifers each, which were infected experimentally with S. aureus in all 4 mammary quarters, were infused in diagonal quarters with 7.5 x 10(5) units of interleukin-2 or 10(5) units of interferon-gamma; remaining quarters received PBS. Heifers in both trials were slaughtered 14 d after cytokine infusion, and mammary tissues were collected for histological examination. Uninfected quarters from 2 additional heifers were left untreated to compare infected with uninfected tissues for both trials. Morphologic evaluation and leukocyte infiltration scores were performed on tissue sections stained with hematoxylin and eosin, and plasma cells were quantified on sections stained with immunoperoxidase. Infected quarters had lower percentages of alveolar epithelial and luminal areas and higher percentages of stromal area than did uninfected quarters in the interleukin-2 trial, but no differences were observed between infected quarters that had been treated with PBS or interleukin-2. Likewise, interferon-gamma treatment had no effect on mammary parenchymal components in the infected quarters. Interleukin-2 treatment significantly elevated leukocytosis into the mammary gland parenchyma compared with infected quarters treated with PBS and uninfected quarters. Among the leukocyte types evaluated, eosinophilic infiltration was elevated in interleukin-2 quarters over that of PBS controls. In both trials, concentrations of plasma cells bearing Ig were elevated in infected versus uninfected quarters. Plasma cell concentrations also were higher in cytokine than PBS controls, especially in interleukin-2 quarters. Results suggested that neither cytokine influenced the histology of infected mammary tissues, but both interleukin-2 and interferon-gamma increased, although insignificantly, the prevalence of all isotypes of plasma cells bearing Ig, suggesting enhancement of the local immune response to IMI.
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PMID:Histologic response of the heifer mammary gland to intramammary infusion of interleukin-2 or interferon-gamma. 822 19

Experimental autoimmune myasthenia gravis (EAMG) in the Lewis rat, induced by a single injection of acetylcholine receptor (AChR) protein, is a model used to study human myasthenia gravis (MG). The production of anti-AChR antibodies in the animal model and human MG is T cell-dependent, and AChR-specific T cells have been considered as a potential target for specific immunotherapy. Intrathymic injection of antigens induces antigen-specific tolerance in several T cell-mediated autoimmune models. We examined the effect of intrathymic injection of AChR on T cell responses and the production of antibodies to AChR in EAMG rats. Primed lymph node cells from rats receiving intrathymic injection of AChR exhibited reduced proliferation to AChR with marked suppression of interferon-gamma (IFN-gamma) secretion in the antigen-stimulated culture, compared with those of rats injected with PBS. However, neither anti-Narke AChR nor anti-rat AChR antibody production was suppressed or enhanced in intrathymically AChR-injected animals compared with that of animals injected intrathymically with PBS or perithymically with AChR. This 'split tolerance' may be attributable to the suppression of type-1 T helper cells (Th1). Our results suggest that the suppression of Th1 function alone may not be sufficient for the prevention of antibody-mediated autoimmune diseases.
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PMID:'Split tolerance' induction by intrathymic injection of acetylcholine receptor in a rat model of autoimmune myasthenia gravis; implications for the design of specific immunotherapies. 853 58

Oral and nasal administration of nicotinic acetylcholine receptor (AChR) to Lewis rats prior to myasthenogenic immunization with AChR and complete Freund's adjuvant (CFA) resulted in prevention or marked decrease of the severity of experimental autoimmune myasthenia gravis (EAMG) and suppression of AChR-specific B-cell responses and of AChR-reactive T-cell function. To examine the involvement of immunoregulatory cytokines and the underlying mechanisms involved in tolerance induction, in situ hybridization with radiolabeled cDNA oligonucleotide proves was adopted to enumerate mononuclear cells (MNC) expressing mRNA for the proinflammatory cytokine interferon-gamma (IFN-gamma), the B cell-stimulating interleukin-4 (IL-4), and the immunosuppressive transforming growth factor-beta (TGF-beta). Popliteal and inguinal lymph nodes from EAMG rats contained elevated numbers of AChR-reactive IFN-gamma, IL-4, and TGF-beta mRNA-expressing cells, compared to control rats receiving PBS orally or nasally and injected with CFA only. Oral and nasal tolerance was accompanied by decreased numbers of AChR-reactive IFN-gamma and IL-4 mRNA-expressing cells and strong up-regulation of TGF-beta mRNA-positive cells in lymphoid organs when compared to nontolerized EAMG control rats. The results suggest that IFN-gamma and IL-4 are central effector molecules in the development of EAMG and that TGF-beta plays an important role in tolerance induction to EAMG.
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PMID:Mucosal tolerance to experimental autoimmune myasthenia gravis is associated with down-regulation of AChR-specific IFN-gamma-expressing Th1-like cells and up-regulation of TGF-beta mRNA in mononuclear cells. 861 Sep 80

(BALB/c x SJL)F1 mice, perinatally injected with peptide-N-glyconase F-treated, deglycosylated IgE heavy chain or recombinant IgE heavy chain (CH epsilon 2-CH epsilon 4), were profoundly inhibited in antigen-specific IgE production. There exist minimally two tolerogenic IgE peptides, residing in the CH epsilon 2 and CH epsilon 4 domains. Peptide I, generated by V8 protease, comprises 39 amino acids within CH epsilon 2, beginning at amino acid 103. Peptide E begins at amino acid 312 of the CH epsilon 4 domain and extends through the CH epsilon 4 domain. The total lack of antigen-specific IgE responses in IgE peptide-treated mice was not due to overproduction of interferon-gamma, nor lack of interleukin (IL)-4, as predicted by the Th2/IL-4 paradigm for IgE production. IgE-tolerant mice exhibited comparable levels of circulating anti-IgE antibodies to those of PBS-treated control mice. IgG obtained from sera of both sources failed to inhibit IgE responses in vitro. Moreover, IgE responses of spleen cells from IgE peptides-treated mice were restored by CD4+ T cells from PBS-treated control mice. We hypothesize that regulation of antigen-specific IgE responses is mediated by CD4+ T cells which normally recognize IgE peptides on IgE precursor B cells, and can be rendered tolerant by perinatal IgE peptide treatment.
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PMID:Peptides derived from IgE heavy chain constant region induce profound IgE isotype-specific tolerance. 864 65


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