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)

Although an outwardly rectifying K+ conductance (IK,A) is prominently expressed in human alveolar macrophages, the expression of this conductance in human monocyte-derived macrophages (HMDMs) is rare. We have analyzed the induction of the expression of IK,A in voltage-clamped, in vitro differentiated HMDMs by a number of stimuli which produce either priming or activation of macrophages. Cultures were stimulated with lipopolysaccharide (LPS, 2 micrograms/ml), interleukin 2 (IL-2, 100 U/ml), or combinations of LPS and either recombinant interferon-gamma (gamma-IFN, 10 U/ml), phorbol myristate acetate (PMA, 0.01 or 1 microgram/ml) and platelet activating factor (PAF, 20 ng/ml) for periods of up to 24 hr. Treatment of the cells with either LPS or IL-2 greatly enhanced the frequency of current expression. Treatment with either PMA or gamma-IFN alone did not induce current expression; treatment of the cells with a combination of LPS and either PMA, gamma-IFN, or PAF did not enhance current expression over that observed with LPS alone. The expression of the outwardly rectifying K+ current was observed in 36% (n = 321) of the cells for cultures treated with LPS and 33% (n = 55) of the cells for cultures treated with IL-2. The inactivating outward K+ current was absent in cells which were not treated with either LPS or IL-2. The kinetics of current activation and inactivation appeared identical to that previously described for the transient-inactivating outward current of the human alveolar macrophage. Cycloheximide (1 microgram/ml), an inhibitor of protein synthesis, completely suppressed LPS-induced current expression. No correlation was found between peak current amplitude and cell size in LPS-activated cells expressing the outwardly rectifying K+ current, indicating that current density was not held constant from cell to cell. The coupling of ion channel expression and secretion in individual HMDMs was studied using the reverse hemolytic plaque assay. Although an enhancement of K+ current expression was observed following either LPS or IL-2 treatment, a quantitatively similar and uniform increase in the percentage of either IL-1 or lysozyme-secreting cells was not observed. The frequency of current expression in cells identified as secreting tumor necrosis factor-alpha (TNF-alpha), interleukin 1 (IL-1), or lysozyme was the same or decreased over that observed for nonsecreting cells.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Lipopolysaccharide induction of outward potassium current expression in human monocyte-derived macrophages: lack of correlation with secretion. 155 35

Ligation of interleukin 2 (IL2) is known to regulate both protein tyrosine and serine/threonine phosphorylation. A family of leukocyte transmembrane proteins whose cytoplasmic domain exhibits intrinsic protein tyrosine phosphatase activity is collectively called CD45 and is identified by a set of common cell surface epitopes. Although CD45 is known to be a phosphoprotein, it is not known how phosphorylation specifically regulates its function. We therefore identified a cell line, the IL4-dependent line CTLL-2.4, in which CD45 could be phosphorylated in response to addition of IL2. These cells are a variant of an IL2-dependent murine cell line which were selected for long-term growth on IL4 but which retain the ability to proliferate on exposure to IL2. Incubation of CTLL-2.4 in low serum concentrations followed by stimulation with IL2 caused a three- to fivefold increase in the phosphorylation of CD45 in a time- and concentration-dependent manner. CD45 in non-stimulated cells contained one major tryptic phosphopeptide, whereas, after exposure of the cells to IL2, two new phosphopeptides were present in CD45. The pattern of IL2-induced phosphorylation was different from that found following addition of phorbol 12-myristate 13-acetate (PMA) to the cells. Although IL2 induced rapid and potent tyrosine phosphorylation in CTLL-2.4 cells, all of the basal and cytokine-activated phosphorylation of CD45 occurred on serine residues. The IL2-stimulated phosphorylation caused no change in the amount of cell surface CD45 and no alteration of its catalytic activity using an artificial tyrosine phosphorylated substrate-RCM-lysozyme. We speculate that the increase in phosphorylation of CD45 may modify its association with potential substrates. The differences in the phosphorylation patterns induced by IL2 and PMA further suggest that more than one kinase can use CD45 as substrate and that IL2 activates a protein serine/threonine kinase different from protein kinase C.
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PMID:Interleukin 2 stimulates serine phosphorylation of CD45 in CTLL-2.4 cells. 185 Mar 60

Although macrophages are considered the prototype of antigen presenting cells (APC), recent studies have emphasized the potential role of several parenchymal and mesenchymal cells in this process. We have studied the capacity of cultured glomerular visceral epithelial cells (GEC) to act as effective APC and compared this capacity with that demonstrated by peritoneal macrophages. Affinity-purified and in vitro propagated rat GEC were exposed to hen egg lysozyme, keyhole limpet hemocyanin, and cationic ferritin. As effector cells, we used antigen-specific T cell hybridomas; the level of antigen presentation was assessed by determining the level of interleukin 2 (IL-2) present in tissue culture supernatants. Cytokine-treated GEC were capable of processing and presenting all antigens in a dose-dependent manner. Crucial for antigen presentation were intracellular processing of antigen and the presence of Ia on the cell surface. Our findings indicate that GEC can act as effective APC, and further suggest that this capacity may be relevant to cell-mediated immune injury at the level of the glomerular capillaries in vivo.
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PMID:Antigen processing and presentation by glomerular visceral epithelium in vitro. 200 35

Histochemical and immunohistochemical studies have been reported in only a few cases of sinus histiocytosis with massive lymphadenopathy (SHML) to date. These indicate that SHML cells belong to the macrophage/histiocyte family, but their exact origin is still unknown. We determined the antigenic phenotype of SHML cells in sections from 20 cases of routinely fixed, paraffin-embedded tissue and from two cases of fresh frozen tissue using a broad panel of antibodies to macrophage/histocyte, B-, and T-cell antigens. SHML cells expressed the following: (1) S-100 protein, (2) "pan-macrophage" antigens such as EBM11, HAM 56, and Leu-M3, (3) antigens functionally associated with phagocytosis (Fc receptor for IgG, complement receptor 3), and lysosomal activity (lysozyme, alpha 1-antichymotrypsin, and alpha 1-antitrypsyn), (4) antigens associated with early inflammation (Mac-387, 27E10), (5) antigens commonly found on monocytes, but not tissue macrophages (OKM5, Leu-M1), and (6) "activation" antigens (Ki-1 and receptors for transferrin and interleukin 2). These data suggest that SHML cells are true functionally activated macrophages that may be recently derived from circulating monocytes.
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PMID:Immunophenotypic characterization of sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease). 218 14

In vivo-activated interleukin 2 responsive T cell clones were generated from peripheral blood (PB) and synovial fluid (SF) of rheumatoid arthritis (RA) patients and from normal control PB. The specificity of these clones was assessed by measuring proliferation induced by the connective tissue elements (CTE) collagen types I and II, native and denatured, proteoglycans, and irrelevant control antigens. The cloned T cells from RA patients but not from normal subjects responded in vitro with proliferation to all CTE but not to control antigens purified protein derivative, ovalbumin, or lysozyme. Proliferation occurred in the presence and absence of accessory cells (AC), but the responses were consistently higher in the presence of AC. Antibodies to HLA-DR abrogated the proliferative response to CTE suggesting that DR expression was necessary for the induction of proliferation. These findings demonstrate the existence of clonable T cells responsive to CTE in PB and SF of RA patients. Expression of reactivity to CTE may contribute to the chronicity of the inflammation in RA.
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PMID:Interleukin 2 responsive T cell clones from rheumatoid and normal subjects: proliferative responses to connective tissue elements. 246 52

We report a case of cutaneous T cell lymphoma (CTCL) treated with local injection of recombinant interleukin 2 (rIL-2). The biopsy specimen showed marked infiltration of large convoluted cells admixed with small lymphocytes and histiocytes in the epidermis, dermis and subcutis. After six injections of rIL-2, 4 nodules out of 5 on the left lower leg disappeared and the remaining large nodule was diminished in size. A biopsy specimen from the diminished nodule showed infiltration of small lymphocytes with histiocytes and plasma cells in the dermis. The atypical cells, large hyperconvoluted lymphocytes, had disappeared. A large number (28%) of lysozyme- and alpha 1-anti-chymotrypsin-positive cells were demonstrated by immunohistochemistry. The patient maintained complete remission for a period of 13 months. He then noticed a small red nodule on the back of the left foot, which was histologically confirmed as a recurrence. Chemotherapy cleared the lesion.
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PMID:A case of cutaneous T cell lymphoma treated with recombinant interleukin 2 (rIL-2). 246 89

Synthetic peptides corresponding to sequences 46-62 and 51-62 of mouse lysozyme and 46-61 of hen egg-white lysozyme (HEL) were used as competitors in a variety of T cell responses. The competitors, according to their binding specificity for major histocompatibility complex (MHC) were expected to inhibit T cell responses restricted to I-Ak, but not those restricted to I-Ad, I-Ek molecules. In competition experiments with T cell hybridomas, the poor binder I-Ed molecule required 10- to 15-fold higher competitor concentrations than the good binder I-Ak molecule to achieve 50% inhibition of antigen presentation. Similarly, the nonresponder state of H-2d mice to HEL peptide 46-61 could be overcome by increasing the immunizing dose, and proliferative T cell responses to different antigens in association with a variety of class II MHC molecules could be blocked by the mouse lysozyme and HEL peptides. Thus, the capability of some and failure of other MHC molecules to bind certain peptides appeared quantitative, rather than of an all or none nature, in these experimental systems. The susceptibility of uncloned T cell lines to peptide competitors was found to decrease with time. Lines maintained by repeated restimulation with antigen and APC, but without exogenous interleukin 2, acquired resistance within weeks. In contrast, T cell clones retained their susceptibility to peptide competitors over a long period of time. The latter data raise the possibility that a competition between ubiquitous (self) peptides and foreign antigen may result in the selection of T cells that have high avidity for the activating antigen-MHC complex, and are thus relatively resistant to competition at the level of antigen presentation.
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PMID:Inhibition of T cell response with peptides is influenced by both peptide-binding specificity of major histocompatibility complex molecules and susceptibility of T cells to blocking. 278 51

The immunological reactivity against the N-terminal region of hen egg-white lysozyme (HEL) has been investigated by a synthetic peptide (PHEL) comprising residue 1-18 of HEL and by an analogue peptide (PREL) in which phenylalanine at position 3 is substituted by tyrosine. Both peptides are immunogenic in (C57BL/10 X DBA/2)F1 mice genetically responder to HEL. In C57BL/6 mice, genetically nonresponder to HEL, PREL induces anti-peptide antibodies that also bind to PHEL whereas PHEL is not immunogenic. Thus, a single amino acid substitution in a synthetic peptide converts a nonresponder mouse strain into a responder one. Anti-PHEL antibodies demonstrate a higher binding to HEL than anti-PREL antibodies, indicating that phenylalanine at position 3 is important for induction of anti-peptide antibodies able to recognize native HEL. At the T cell level the two peptides show very high bidirectional cross-reactivity between themselves and with HEL for interleukin 2 production, antigen-specific proliferation and delayed-type hypersensitivity response, whereas conservation of phenylalanine at position 3 is required for induction of suppressor cells cross-reactive with HEL. This indicates that the N-terminal region of HEL contains epitope(s) able to induce the same level of helper T cell activity as the native HEL molecule. However, helper T cells do not discriminate between PHEL and PREL whereas phenylalanine at position 3 is critical for HEL-specific suppressor T cell induction.
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PMID:Analysis of lysozyme-specific immune responses by synthetic peptides. I. Characterization of antibody and T cell-mediated responses to the N-terminal peptide of hen egg-white lysozyme. 293 8

The present study tests whether the specific inhibition of helper T (Th) cell (and T hybridomas) by suppressor T (Ts) cells is a phenotypic trait of Th cells correlating with their acquired specificity for antigen/major histocompatibility complex or a genotypic trait not related to selection of the T cell repertoire for antigen. To do this we took advantage of the fact that H-2d parental strains of mice commonly restrict recognition of chicken egg-white lysozyme to the L3 peptide (a.a. 105-129) and H-2b parental mice to the L2 peptide (a.a. 13-105). F1 hybrids of these strains display two subsets of lysozyme-reactive T cells, one for each parental phenotype. Using (B10 X B10.D2)F1 mice reconstituted with B10.D2 bone marrow, we were able to develop genetic H-2d T cell clones that could express an atypical specificity, that is L2/I-Ab. Clones of this type, like genetic H-2b, are also sensitive to the inhibiting effects of HEL-activated Ts cells. To overcome some of the drawbacks of using heterogeneous populations of T, B and accessory cells in our assays, we constructed T hybridomas from HEL-immune, chimeric lymph node T cell blasts which respond to a unique antigen/major histocompatibility complex with production of the lymphokine interleukin 2. Our results indicate that all HEL/I-Ab-specific T cells (helper and hybridomas) are inhibited by suppression regardless of the T cell's haplotype at the H-2 locus: H-2b (B10), H-2d (D2) or H-2b,d (BDF1). Furthermore, there is a strict correlation between the antigen and I-A specificity: I-Ab-restricted T cells recognize non-L3 determinants even though some are derived from H-2d mice.
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PMID:An adjunct trait of HEL/I-Ab-specific T helper cell is sensitivity to antigen-specific immunosuppression. 296 40

Cyclosporine (CsA) was tested for its ability to inhibit antigen presentation by spleen cells or the B lymphoma line A20 to T cell hybridomas specific for hen egg-white lysozyme (HEL). Antigen-presenting cells (APC) were treated with CsA or nonimmunosuppressive derivatives thereof during or prior to encounter with antigen. The APC were then washed extensively and incubated in CsA-free medium for 6 hr before the T hybridoma cells were added. Under these conditions, CsA had no effect on antigen presentation up to the cytostatic regimen (1 microgram/ml). Omission of the 6-hr interval between CsA treatment of APC and the addition of T hybridoma resulted in inhibition of interleukin 2 production, although the CsA concentrations required were 10-75-fold higher than the ones inhibiting T cells directly (IC50: 100-150 ng/ml vs. 2-10 ng/ml). The responses to both HEL and a synthetic peptide of HEL sequence 105-120 were inhibited, indicating that the step influenced by the drug was not antigen-processing. The nonimmunosuppressive derivatives remained ineffective under these conditions. The results illustrate that the carryover of CsA from APC to T cells can mimic a drug effect on antigen presentation. Therefore, the demonstration of a CsA effect on antigen presentation can only be considered as conclusive when the readout of APC function is not a T cell response.
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PMID:Lack of influence of cyclosporine on antigen presentation to lysozyme-specific T cell hybridomas. 326 67


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