Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.2.1.17 (lysozyme)
21,489 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The induction of tolerance, particularly by intervention before established immunity, is widely accepted. We studied the effects of intravenous (i.v.) administration of hen egg lysozyme (HEL), before as well as after immunization, on a HEL-induced arthritis. Arthritis and also cartilage destruction were almost completely suppressed when 100 micrograms HEL was injected before immunization. Antigen-specific proliferative T cell responses and IL-2 production in vitro were inhibited. Antigen-specific immunoglobulin and IgG1 titres were equal in control and tolerized mice, in contrast to lowered IgG2a titres in tolerized animals. Detailed histological studies showed that the immune complex-dependent polymorphonuclear cell phase (< 24 h after arthritis induction) was equal for control and HEL-injected mice. Only in the T cell-dependent phase of the arthritis (> 24 h), did suppression become pronounced in tolerized mice. I.v. administration of 100 micrograms HEL after immunization could only marginally reduce infiltrate and exudate, and no reduction of cartilage destruction was seen. An elegant way to interfere in an established immunity can be offered by creation of bystander suppression. We show that i.v. administration of HEL followed by triggering with HEL, at the moment either of immunization or of arthritis induction, does not reduce a methylated bovine serum albumin (BSA)-arthritis. We conclude that arthritis can be suppressed almost totally when HEL is injected intravenously before immunization. Treatment after immunization is less effective. The i.v. induced suppression is T cell-mediated and and antigen-specific: no bystander suppression circuit can be generated.
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PMID:Suppression of hen egg lysozyme-induced arthritis by intravenous antigen administration: no role in this for antigen-driven bystander suppression. 814 64

Recombinant interleukin-2 (rIL-2) therapy has been shown to be of value in the treatment of some cases of melanoma and renal cell carcinoma. However its use can be limited by severe systemic toxicity. Targeting rIL-2 to the tumour should improve the anti-tumour immune response and decrease the systemic toxicity. With this aim we have employed recombinant DNA techniques to construct a single chain antibody interleukin-2 fusion protein (SCA-IL-2). The protein used in this model system comprises the variable domains of the anti-lysozyme antibody D1.3 fused to human IL-2. It has been expressed by secretion from Escherichia coli and the purified product possesses antigen binding specificity and retains the immunostimulatory activities of rIL-2. This approach can be taken to generate SCA-IL-2 proteins that bind to appropriate cellular antigens. In vivo administration of a tumour binding SCA-IL-2 should result in a localised high concentration of IL-2 in tumour tissues, maximising the anti-tumour immune response, whilst keeping systemic side effects to a minimum.
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PMID:A recombinant single chain antibody interleukin-2 fusion protein. 843 59

The ability of non-professional antigen-presenting cells (APC) to process and present antigen to the immune system has been the subject of debate in autoimmunity and tumour immunology. The role of muscle cells in the processing and presentation of antigen to T cells via class I and class II MHC pathways is of increasing interest. Muscle cells are the targets of autoimmune attack in the inflammatory muscle diseases, and direct intramuscular injection of antigen-expressing DNA constructs is under scrutiny as a means of vaccination. Furthermore, the immunological properties of muscle cells are of relevance in attempts to transfer myoblasts as replacement cells in dystrophic diseases or as depot cells for the secretion of certain molecules in deficiency states. Using class I and class II MHC transfectant clones of the C2C12 myoblast cell line, myoblasts have been shown to be capable of presenting antigen to, and stimulating secretion of IL-2 by, T cell hybridomas via both of these pathways. The epitopes which are dominantly presented by professional APC after processing of native antigens were also presented by the myoblast cell line after processing of either ovalbumin (class I) or hen egg lysozyme (class II). Further, antigen processing and presentation via the class II pathway were enhanced by pretreatment of the myoblasts with interferon-gamma (IFN-gamma). Up-regulation of invariant chain expression by this treatment may have contributed to this enhanced presentation, but an effect of IFN-gamma on the expression of other molecules such as H-2 DM may have also played a role. The demonstration of the antigen-presenting properties of these myoblasts is of relevance to all three areas mentioned above. In each situation myoblasts comprise a significant population within muscle. In the case of inflammatory muscle diseases the process of muscle degeneration and regeneration is on-going, while in the vaccination procedure some muscle damage occurs, and vaccination is more effective when muscle damage has preceded inoculation.
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PMID:Antigen processing and presentation by a murine myoblast cell line. 853 81

The oral administration of 100 mg/Kg/day of hen egg-white lysozyme (Lysozyme) for 8 consecutive days to mice bearing advanced MCa mammary carcinomas and treated with 5-fluorouracil (5-FU) increases the efficacy of 5-FU on primary tumor growth and on lung metastasis formation and particularly on the postsurgical survival time. These effects are accompanied by the correction of the reduced in vitro response to ConA of lymphocytes obtained from the spleen of the treated mice. In vitro, lysozyme is capable of inducing proliferative activity in a population of blast cells, obtained by a mixed population of mononuclear cells harvested from the spleen of healthy mice, and of evoking a marked proliferative effect to IL-2 in a condition in which, in lysozyme untreated lymphocytes, IL-2 is completely uneffective. These data stress the effects of lysozyme on host immunity following oral administration and moreover indicate the beneficial role of this peptide in conditions in which the increase of host responses can significantly contribute to the success of the treatment.
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PMID:Lysozyme stimulates lymphocyte response to ConA and IL-2 and potentiates 5-fluorouracil action on advanced carcinomas. 857 73

Our previous study suggested that peripheral sympathetic nerve played an important role in the electroacupuncture (EA)-induced immunomodulation. The aim of this study is to explore the role of peripheral parasympathetic nerve in it. All mice are preimmunized with SRBC (sheep red blood cell) 4 days before experiment. The animals in different groups were injected i.p. with Hemicholine-3 (HC-3, an ACh synthesis blocker) or physiological saline 3 hr before EA. The main results are as follows: 1. In saline group, the LTT (lymphocyte transformation test), IL-2 (interleukin-2) of spleen and lymphocyte number of thymus are markedly increased, and the other immune parameters have no change after EA. 2. In HC-3 control group, the LTT, IL-2 are decreased significantly and the other immune parameters have not shown influence. 3. In the HC-3 with EA group, the magnitude of LTT, IL-2 did not significantly change as compared with HC-3 alone, it is especially noteworthy that the other unchanged parameters by HC-3 such as spleen weight, spleen index, thymus weight, thymus index, number of spleen cells, spleen LZM(lysozyme) and thymus LZM are clearly decreased after EA. The above results suggest that peripheral parasympathetic nerve may play some promoting effect in the EA-induced immunomodulation. Its effect may be mediated by ACh released from parasympathetic nerve endings.
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PMID:[Effect of HC-3 on electroacupuncture-induced immunoregulation]. 870 74

To investigate the role of B cells as APCs in acquired tolerance induced by low dose soluble protein Ags, normal and B cell-deficient adult mice were injected i.v. with repeated low doses (10 microgram) of deaggregated OVA, then challenged with OVA in CFA. In animals treated with deaggregated OVA, the in vitro proliferative responses of lymph node T cells to OVA were significantly reduced, and production of the Th1 cytokine, IFN-gamma, in response to OVA was reduced to undetectable levels. This occurred in both normal and B cell-deficient treated animals. B cells were also unnecessary for self tolerance of T cells to the transgenic self Ag, hen egg lysozyme, in a strain with a very low serum lysozyme concentration. Partial low zone tolerance induced by deaggregated, low dose OVA was selective for T cell responses as measured by in vitro proliferation and IL-2 and IFN-gamma production, because Ab responses of B cell-sufficient mice to this T cell-dependent Ag were largely unaffected. Both treated and untreated animals produced equivalent titers of anti-OVA Abs, predominantly of the IgG1 and IgG2b isotypes, following challenge with OVA in CFA.
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PMID:Analysis of low zone tolerance induction in normal and B cell-deficient mice. 875 99

Chemical modification of proteins with monomethoxypolyethylene glycol (mPEG) will reduce the immunogenicity of proteins. In the present study, we evaluated the effect of mPEG modification on the capacity of hen egg-white lysozyme (HEL) to stimulate T cells. Lymph node cells (LNCs) from mice immunized with HEL or with mPEG-HEL conjugate were cultured with these antigens, then we measured the proliferation and IL-2 production. mPEG-modification lowered the T cell activating capacity of HEL, both in vitro and in vivo. Neither toxicity, nor antigen non-specific immunosuppressive capacity was observed with mPEG-HEL and unconjugated mPEG. Suppressor cells were unlikely to be generated in the mPEG-HEL-primed LNCs. We next examined the behavior of mPEG-HEL during antigen processing. The capacity of HEL and mPEG-HEL to be incorporated by live cells was much the same. However, the susceptibility to various proteases, including endosomal/lysosomal enzymes, was significantly decreased by mPEG modification. The increased resistance of mPEG-HEL to proteolytic degradation implied that the conjugate was poorly presented to T cells. This may be an important factor related to the low immunogenicity of mPEG modified proteins.
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PMID:Reduced immunogenicity of monomethoxypolyethylene glycol-modified lysozyme for activation of T cells. 896 16

The possibility of inducing antigen-presenting capacity in cells normally lacking such capacity, currently represents a major goal in vaccine research. To address this issue we attempted to generate 'artificial' APC able to stimulate CD4+ T cell responses when tumor cells were infected with a single, recombinant, vaccinia virus (rVV) containing the two genes encoding murine MHC class II I-Ak and a third gene encoding the murine B7-1 (mB7-1) costimulatory molecule. To minimize the cytopathic effect and to improve safety, in view of possible in vivo applications, we made this rVV replication incompetent by Psoralen and long wave UV treatment. Tumor cells infected with rVV encoding I-Ak alone, pulsed with hen egg white lysozyme peptide (HEL46-61), induced IL-2 secretion by an antigen-specific T hybridoma. Tumor cells infected with the rVV encoding mB7-1 provided costimulation for activating resting CD4+ T cells in the presence of ConA. Tumor cells infected with the rVV encoding I-Ak and mB7-1, and pulsed with chicken ovotransferrin peptide (conalbumin133-145), induced a significantly higher response in a specific Th2 cell clone (D10.G4.1) as compared to cells infected with rVV encoding I-Ak molecules only. Thus, this replication incompetent rVV represents a safe, multiple gene, vector system able to confer in one single infection step effective APC capacity to non-professional APCs.
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PMID:Induction of antigen-presenting capacity in tumor cells upon infection with non-replicating recombinant vaccinia virus encoding murine MHC class II and costimulatory molecules. 900 58

We have characterized the earliest antigen-specific Th cells in murine mesenteric lymph nodes (MLN), following oral immunization with the hen egg lysozyme (HEL) as antigen and cholera toxin (CT) as adjuvant. We did this by analyzing in vitro proliferation and cytokine production in response to HEL by the MLN T cells. MLN cells taken 5 days after a single oral immunization with HEL and CT provided the earliest source of proliferating HEL-specific T cells. This proliferation was completely inhibited by anti-IL-2, but not inhibited by anti-IL-4 antibody. IL-2 protein was detected in culture supernatants but not IL-4 using ELISA or bioassays. IL-4 mRNA was not found in responding cells using RT-PCR. Some of the day 5 MLN cultures produced IFN-gamma in response to HEL, but isolated T cells from the same MLN did not. Exogenous IL-4 alone did not stimulate day 5 MLN T cells, but IL-4 did synergize with HEL to induce a large proliferative response. The data indicate that the HEL-specific CD4 T cell pool in MLN 5 days after oral immunization is composed of undifferentiated precursor Th cells. These cells have the potential for IL-2 production and IL-4R expression upon re-stimulation in vitro.
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PMID:Detection of precursor Th cells in mesenteric lymph nodes after oral immunization with protein antigen and cholera toxin. 935 61

Stress has been implicated as a factor in the pathogenesis of autoimmune disorders. In order to determine the effect of adrenergic stress on immune responses in vivo, C57BL/6 (B6; H-2b) mice, which respond weakly to hen-egg lysozyme (HEL), were immunized on day 0 with HEL (50-200 microg s.q.) and subsequently injected with epinephrine (EPI; 0.1-0.5 mg/kg s.q.) daily for up to 10 days. Controls included A/J mice (H-2k) which respond strongly to HEL. In some experiments, B6 mice were depleted of CD4+ or CD8+ lymphocytes by monoclonal antibody treatment in vivo, prior to immunization with HEL, and injection with EPI. On day 10, single cell suspensions of draining lymph nodes (LN) and spleen were examined for immune phenotype, proliferative responses to HEL, and lymphokine production. Minimal specific proliferative responses were detected in B6 mice compared to A/J mice. However, lymphocyte proliferation increased in HEL-immunized EPI-treated B6 mice but not in the A/J mice. IL-2-mediated proliferation and IL-2 secretion were both increased in the HEL-immunized EPI-treated B6 mice. The depletion of CD8+ but not CD4+ lymphocytes in vivo abrogated the effects of EPI, whereas adoptive transfer of naive CD8+ splenocytes to the CD8-depleted mice restored specific responses in the HEL-immunized EPI-treated animals. We conclude that EPI augments antigen-specific T-cell responses to HEL in B6 mice by a CD8+ T-cell-dependent mechanism.
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PMID:Epinephrine augments specific T-cell responses to antigen in C57BL/6 (H-2b) weak-responder mice by a CD8+ lymphocyte-dependent mechanism. 964 32


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