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)

Hen egg lysozyme 52-61-specific CD4+ T cells responded by interleukin 2 (IL-2) secretion to any peptide containing this epitope regardless of length of NH2- and COOH-terminal composition. However, CD4- variants could only respond to peptides containing the two COOH-terminal tryptophans at positions 62 and 63. Substitutions at these positions defined patterns of reactivity that were specific for individual T cells inferring a T cell receptor (TCR)-based phenomenon. Thus, the fine specificity of major histocompatibility complex (MHC)-peptide recognition by the TCR was dramatically affected by CD4 and the COOH-terminal peptide composition. Peptides that failed to induce IL-2 secretion in the CD4- variants nevertheless induced strong tyrosine phosphorylation of CD3 zeta. Thus, whereas the TCR still recognized and bound to the MHC class II-peptide complex resulting in protein phosphorylation, this interaction failed to induce effective signal transduction manifested by IL-2 secretion. This provides a clear example of differential signaling mediated by peptides known to be naturally processed. In addition, the external domains of CD4, rather than its cytoplasmic tail, were critical in aiding TCR recognition of all peptides derived from a single epitope. These data suggest that the nested flanking residues, which are present on MHC class II but not class I bound peptides, are functionally relevant.
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PMID:Amino acid residues that flank core peptide epitopes and the extracellular domains of CD4 modulate differential signaling through the T cell receptor. 751 3

Although several attempts at the immunohistochemical characterization of histiocytosis have recently been made there is only one paper which reports a case of cerebral Langerhans cell histiocytosis (LCH) diagnosed by biopsy. This paper presents a bioptically diagnosed case of juvenile histiocytosis. The panel of antibodies used was as follows: anti-S-100, 2 different antibodies to anti-interleukin 2, anti-lysozyme, anti-LEU M1, anti-MAC 387, anti-major histocompatibility complex II and anti-GFAP. Microglia markers--Griffonia simplicifolia and RCA 1 lectins were also utilized. The proliferating cells produced a positive response to S-100, lysozyme and a partially positive response to HLA DR, but responded negatively to MAC 387, LEU M1, lectins, IL2R and GFAP. Our results were compared and analyzed in the light of those obtained by other authors.
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PMID:Immunohistological study of a case of cerebral Langerhans cell histiocytosis in brain biopsy. 772 76

The role of sympathetic neurotransmission in regulation of T-cell function was examined in mice. After in vivo priming with a model protein antigen, hen egg white lysozyme (HEL), the specific proliferative recall response of lymph node cells (LNCs) was examined. The release of endogenous catecholamines by amphetamine (5 mg/kg, 45 min prior to sacrifice) markedly inhibited the proliferative response of LNCs. Combined alpha- and beta-adrenergic blockade (phentolamine, 1.0 mg/kg+propranolol, 2.5 mg/kg) prevented this effect of amphetamine on proliferation. In vitro, the alpha-adrenergic agonist phenylephrine, but not the beta-agonist isoproterenol, inhibited proliferation in a dose-dependent manner, up to 80%. The effect of phenylephrine was blocked by the alpha-adrenoceptor antagonist phentolamine. The effects of catecholamines appear to be mediated at the level of antigen processing/presentation: Amphetamine given prior to sacrifice inhibited interleukin 2 production when irradiated spleen cells were used to present HEL and HEL-related peptides to HEL-specific T-cell hybridomas. In summary, the sympathetic nervous system seems to inhibit antigen processing/presentation and, indirectly, T-helper responses.
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PMID:Sympathetic regulation of T-helper cell function. 839 64

This study aimed to evaluate some aspects of the immune response in 10 cardiopathic patients during the execution of percutaneous transluminal coronary angioplasty (PTCA) by obtaining blood samples from coronary sinus. In particular we considered some PMN functions as well as lysosomal release and oxidative metabolism evaluated as chemiluminescence and superoxide anion (O2) production. We also studied serum levels of complement C3 and C4, lymphocyte populations (CD3, CD4, CD8, CD19, CD16) and plasmatic determinations of interleukin 2 (IL2). After PTCA, we found a decrease of total count of blood lymphocytes, whereas the number of neutrophils remained unchanged. The decrease involved to a similar extent the lymphocyte subsets CD3, CD4 and CD8, whereas CD19 and CD16 were unchanged. The plasmatic levels of IL2 did not show any significant modification. Concerning PMN, their chemiluminescence was significantly increased after PTCA as compared to basal values: this response was promptly detectable in isolated PMN, both without and with stimulation with fMLP. Similarly superoxide anion production, both spontaneous and stimulated, was increased in PMN suspensions after PTCA, even if this increase did not reach statistical significance. As regards circulating levels of lysosomal enzymes, we found a significant increase of plasmatic levels of elastase, whereas the serum determinations of lysozyme and betaglucuronidase did not change. Concerning the complement system, we found a significant decrease of complement fractions C3 and C4. In conclusion, our results showed certain changes in some humoral and cellular systems; in particular the neutrophil activation through the release of proteolytic enzymes and the generation of oxygen radicals could increase the damage to vessel walls and activate other systems having a negative effect in the ischaemia-associated consequences.
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PMID:Changes of some immune functions after percutaneous transluminal coronary angioplasty (PTCA). 887 Dec 63

In the defense against Mycobacterium leprae, macrophages play an essential part in the mechanism of bacterial lysis but require the presence of cytokines such as interleukin 2 and gamma interferon from lymphocytes in order to effectively kill the organisms in any number. While there have been many studies of the lymphocytes in lesions of leprosy, less attention has been given to the immunohistochemical characterization of the macrophage populations. In this study, the cutaneous lesions of 69 patients with leprosy (42 lepromatous, 5 mid-borderline, and 22 tuberculoid) were evaluated by immunohistochemistry for the expression of S100 protein, CD1a, CD68, muramidase, HLA-DR, and Factor 13a. The macrophages from lesions of polar, subpolar, and borderline lepromatous leprosy patients expressed S100 protein intensely and constantly. In contrast, the lesions of polar and subpolar tuberculoid leprosy had very few cells that were immunoreactive for S100 protein ('S100+') in the granulomas in the dermis. The macrophages in all lesions were reactive for CD68 and muramidase. In paraffin sections, macrophages of lepromatous lesions failed to stain for HLA-DR, whereas in tuberculoid lesions, they were strongly positive for HLA-DR. Three patients with histoid leprosy (relapse lesions) had lesions that were strongly positive for Factor 13a and were negative for S100 protein ('S100-'). Given the possible chemotactic and migration inhibition effects of the calcium-binding proteins of the S100 family, these data suggest a possibly important role for S100 protein in the accumulation of macrophages in lepromatous leprosy, and also reveal infection of Factor 13a + dermal dendritic cells in histoid leprosy.
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PMID:Multibacillary leprosy: lesions with macrophages positive for S100 protein and dendritic cells positive for Factor 13a. 987 Jun 71


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