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:3.4.21.4 (trypsin)
42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The relationship between the major histocompatibility complex (MHC) and functional receptors on the surface of human lymphocytes was studied. HLA antisera were tested for their effect on the formation of E-, EA-, and EAC'-rosettes by human peripheral blood lymphocytes (PBL). Antisera to various HLA specificities inhibited the formation of EAC'-rosettes, but had no effect on the formation of E-rosettes. The formation of EA-rosettes was inhibited by HLA antisera only in part among the individuals tested. Anti beta2-microglobulin serum resembled HLA antisera in its effect on the formation of the various rosettes. HLA determinants and complement receptors are different entities on the cell surface since elimination of complement receptors by trypsin treatment does not seem to affect the expression of HLA antigens on the cell surface. It is suggested that EAC' receptors are located close to HLA determinants.
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PMID:Association between HLA determinants and complement receptors on human lymphocytes. 7 Aug 64

To investigate the antigenic relationship between the macrophage and lymphocyte Fc receptors (FcR), a monoclonal antibody capable of blocking mouse macrophage Fc receptors was selected. Hybrids were formed by fusing the P3U1 mouse myeloma and spleen cells from a rat immunized with the mouse macrophage-like cell lines J774 and P388D1. The Fab fragment of the monoclonal IgG secreted by clone 2.4G2, inhibited the trypsin-resistant Fc receptor II (FcRII), which is specific for immune aggregates of mouse IgG1 and IgG2b, but had no inhibitory effect on the trypsin-sensitive Fc receptor I (FcRI), which binds monomeric IgG2a and erythrocytes coated with IgG2a. Thus, the monoclonal 2.4G2 IgG appeared to be specific for macrophage FcRII. Further evidence that the 2.4G2 IgG was directed against FcRII came from binding studies of the monoclonal antibody to J774 cells and a series of independently isolated variants which do not express FcRII. These variants of J774 bound 5% as much of the monoclonal antibody as the parent line, which bound 600,000 molecules of 2.4G2 IgG per cell. The antigenic relatedness of mouse lymphocyte FcR to mouse macrophage FcRII was demonstrated by the binding of 2.4G2 IgG to FcR-bearing lymphoid cell lines and the inhibition of the lymphocyte FcR by the monoclonal antibody. Preincubation of spleen cells and peritioneal cells with 2.3G2 IgG likewise inhibited rosette formation with ox erythrocytes coated with rabbit IgG. The ability of the hybridoma IgG to inhibit mouse FcRII was independent of the major histocompatibility complex. The 2.4G2 IgG antigenic determinant was not present on rat, guinea pig, rabbit, or human FcR-bearing cells.
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PMID:Characterization of a monoclonal antibody directed against mouse macrophage and lymphocyte Fc receptors. 9 Jan 8

A simple technique is presented for the identification of particular cell membrane antigens. The method employs labeled membrane antigens that are isolated immunospecifically and subjected to limited trypsin digestion followed by polyacrylamide gel electrophoresis in detergent. A large "core" peptide is produced by proteolysis of murine thymus-leukemia antigens (TLA) and from antigens of the major histocompatibility complex (MHC). The tryptic cores from H-2K and H-2D are regularly distinguishable from the thymus-leukemia antigens (TLA) by gel electrophoresis in one dimension. This chemical distinction is particularly important in the analysis of antigen mixtures isolated with antisera specific for beta 2 microglobulin. These techniques have been used to identify thymus-restricted beta 2 microglobulin-associated antigens on cell membranes from mouse, man, guinea pig, and monkey. In appropriate inbred mouse strains, these are the TLA and it is proposed that in the three other species examined they may be analogues, although not necessarily homologues, of TLA. The broad species distribution of these thymus-restricted cell membrane antigens suggests that they are involved in the differentiation of thymus-dependent lymphocytes (T cells).
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PMID:Limited trypsin cleavage distinguishes MHC and thymus-leukemia antigens. 22 40

Lymphokine-activated killer (LAK) cells exhibit major histocompatibility complex (MHC) unrestricted cytolysis against a wide variety of fresh and cultured tumor cells. Because previous work from our laboratory suggested that trypsin treatment of unseparated populations of LAK cells had a differential effect on lysis of different tumors, in this report we analyzed the lytic specificity of LAK cell clones against a panel of three different targets: MCA, B16 and YAC-1. We found that 21 out of the 24 analyzed murine spleen and bone marrow clones killed a combination of two, but not all three, of these tumor cells. Determinations of the phenotype of 10 LAK cell clones showed six with rearrangements for the T cell receptor (TCR) beta chain gene, suggesting a T cell origin, and four with germ line configurations for the TCR beta and delta chain genes, a result consistent with a non-T cell lineage. This cloning procedure provided an experimental tool to develop new procedures of adaptive immunotherapy.
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PMID:Differential lysis of tumor target cells displayed by lymphokine activated killer (LAK) cell clones. 161 70

Studies on mechanisms for allograft rejection are focused on recognition of major histocompatibility complex (MHC) antigens. In addition, there is evidence for non-MHC-mediated alloreactivity, possibly evoked by tissue-specific antigens. To measure cellular immune responses toward tissue-specific alloantigens, we isolated endothelial cells and smooth muscle cells from small pieces of human atrium at the time of transplantation. Endothelial cells were scraped off the endocardium after trypsin digestion and cultured in fibronectin-coated dishes. Smooth muscle cells were obtained by outgrowth of small pieces of atrium in a culture flask. Morphologic and immunologic characterization showed only minor differences between endothelial and smooth muscle cells cultured from atrium and cells cultured from umbilical vein (endothelial cells) and artery (smooth muscle cells). Furthermore, we studied the proliferative immune responses with endothelial and smooth muscle cells as stimulator cells, with and without induction of MHC class II antigens on these cells by addition of interferon-gamma to the culture. Peripheral blood mononuclear cells showed a proliferative response to donor human atrium endothelial cells, even without pre-incubation with interferon-gamma. Human atrium smooth muscle cells caused only a weak triggering of the mononuclear cells, irrespective of interferon-gamma pre-incubation. Immunofluorescence studies demonstrated HLA-DR expression on these endothelial and smooth muscle cells. These observations may indicate a role for non-MHC, probably tissue-specific, alloantigens expressed by endothelial cells in human cardiac allograft rejection.
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PMID:Endothelial and smooth muscle cells in the heart allograft response: isolation procedure and immunocytochemical features. 183 Feb 21

Infrared spectra have been obtained for 12 globular proteins in aqueous solution at 20 degrees C. The proteins studied, which vary widely in the relative amounts of different secondary structures present, include myoglobin, hemoglobin, immunoglobulin G, concanavalin A, lysozyme, cytochrome c, alpha-chymotrypsin, trypsin, ribonuclease A, alcohol dehydrogenase, beta 2-microglobulin, and human class I major histocompatibility complex antigen A2. Criteria for evaluating how successfully the spectra due to liquid and gaseous water are subtracted from the observed spectrum in the amide I region were developed. Comparisons of second-derivative amide I spectra with available crystal structure data provide both qualitative and quantitative support for assignments of infrared bands to secondary structures. Band frequency assignments assigned to alpha-helix, beta-sheet, unordered, and turn structures are highly consistent among all proteins and agree closely with predictions from theory. alpha-Helix and unordered structures can each be assigned to only one band whereas multiple bands are associated with beta-sheets and turns. These findings demonstrate a method of analysis of second-derivative amide I spectra whereby the frequencies of bands due to different secondary structures can be obtained. Furthermore, the band intensities obtained provide a useful method for estimating the relative amounts of different structures.
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PMID:Protein secondary structures in water from second-derivative amide I infrared spectra. 215 34

In an attempt to identify predominant cell populations that may mediate liver allograft dysfunction, the phenotypic and functional characteristics of lymphoid cells propagated from needle biopsy specimens of rejecting liver transplants were examined. In one case, a T-cell line of host phenotype propagated from a liver allograft biopsy demonstrated significant in vitro suppressor activity. This T-cell line (designated JB) was maintained for almost one year in culture with medium containing human recombinant interleukin 2 and with weekly stimulation by an Epstein-Barr virus-transformed B-cell line derived from the liver donor. Repeated analyses demonstrated that the JB line was phenotypically stable and predominantly CD3+ (86-93%), CD4+ (88-96%), DR+ (96%), Leu8-, CD45R-, CD16-, with a minor CD8+ cell population (less than 5%). The JB line demonstrated proliferative responsiveness upon coculture with cells expressing disparate donor HLA antigens but no in vitro cytotoxic activity. However, JB cells significantly (greater than 90%) suppressed mixed lymphocyte reaction or phytohemagglutinin stimulation of nonautologous peripheral blood lymphocytes. Supernatants of JB cells that had been cultured alone or with irradiated (6000 rads) Epstein-Barr virus-transformed donor B cells mimicked the suppressive activity of the JB cell line, either upon addition in vitro or by transient (4 hr) pretreatment of responder cells at 20 degrees C. JB cell supernatants were nontoxic and free of tumor necrosis factor activity, and their suppressive activity was dose-dependent, nondialyzable (greater than 100 kDa), not overcome by exogenous interleukin 1 or interleukin 2, and heat-resistant up to 56 degrees C. However, the suppressive activity of JB supernatants could be diminished or abrogated by treatment with high temperature (80-100 degrees C), reducing agents, trypsin, or absorption by peripheral blood lymphocytes at room temperature. The suppressive activity of JB cells and supernatants was not alloantigen-specific or major histocompatibility complex-restricted, did not shift mixed lymphocyte reaction kinetics, and was capable of inhibiting in vitro stimulation of peripheral blood lymphocytes in mixed lymphocyte reaction only when presented early in the culture. These findings provide the first evidence for a primary human allograft-derived T-cell line with suppressor-effective function.
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PMID:Characteristics of a human liver allograft--derived T-cell line that exhibits suppressor activity. 257 93

It is reported here that most cytotoxic T lymphocytes (CTL), which recognize class I major histocompatibility complex (MHC) loci, express the T cell differentiation antigen T8. However, a minority of T8+ CTL clones was found to recognize class II MHC antigens. To test the hypothesis that T8 is involved only in T cell recognition of class I MHC antigens, we studied the role of T8 in the cytotoxic activity of class II MHC-specific CTL. Monoclonal antibodies specific for T8 blocked the activity of most class I MHC-specific CTL clones but did not affect the activity of class II MHC-specific CTL clones. Moreover, a mild trypsin treatment of the clones, which removed and T8 determinant, affected the activity of class I MHC but not that of class II MHC-specific CTL clones. These findings indicate that the class II-specific MHC CTL clones described here did not require T8 for their cytolytic activity. The activity of one T8+ class I MHC-specific (HLA-B27) CTL clone (HG-61) against the B cell line JY, which was used to raise this CTL clone, was not blocked by trypsin treatment of this clone. However, the activity of CTL clone HG-61 against target cells different from JY but carrying the appropriate HLA specificity was blocked by anti-T8 antibodies and trypsin treatment. The implications of these findings for the hypothesis that T8 is involved only in the activity of CTL with a relatively low avidity for class I MHC antigens are discussed.
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PMID:The role of T8 in the cytotoxic activity of cloned cytotoxic T lymphocyte lines specific for class II and class I major histocompatibility complex antigens. 257 37

In oxidation-dependent cytotoxicity (ODCC), cytolytic T lymphocytes (CTL) non-specifically recognize, bind to and lyse oxidized target cells (O-TC) but the precise mechanism whereby CTL react with O-TC is far from clear (Berke, G., Immunol. Rev. 1983. 72:5). Here we present evidence that CTL/O-TC interactions are blocked by aldehyde-reactive reagents such as hydroxylamine, adipic acid dihydrazide and thiocarbohydrazide and that preformed CTL/O-TC conjugates dissociate upon reduction with NaBH4, suggesting that active aldehyde groups of O-TC rather than intercellular Schiff bases are involved in the recognition and lysis of O-TC by CTL in ODCC. The aldehydes are bound to trypsin-sensitive, non-H-2 glycoproteins that appear to be different and unique in the three different target cell lines so far examined (EL4, L1210, R1.1). In view of these and previous findings we would like to suggest that in ODCC, active aldehydes react with adjacent major histocompatibility complex and perhaps other cell-surface molecules to create a multitude of modified conformations, responsible for the "polyclonal" (nonspecific) MHC recognition and lysis of O-TC by CTL, as well as for an altered pattern of H-2 antibody binding to O-TC.
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PMID:Interaction of periodate-oxidized target cells and cytolytic T lymphocytes: a model system of "polyclonal MHC recognition". 301 6

It has been shown that HLA-B27 lymphocytes from healthy individuals (B27+ ankylosing spondylitis [AS]-), which are not lysed by an antiserum against Klebsiella K43, can be rendered susceptible to lysis after incubation in the culture filtrate of Klebsiella K43. This finding is compatible with a specific modification by a Klebsiella K43-derived soluble factor of a B27-associated lymphoid cell component. Preliminary characterization of the factor has indicated that it is nondialyzable, but it is heat labile at 56 degrees C for 30 min and has a 35,000-50,000 mol wt. The modifying factor activity of the filtrate is destroyed by neuraminidase but not by trypsin and alpha-chymotrypsin. Furthermore, the ability of the factor to convert B27+AS- lymphocytes can be specifically absorbed by B27+AS- lymphocytes, but not by B27+AS+, B27-AS+, or by B27-AS- lymphocytes, which suggests that B27+AS- cells carry a hypothetical receptor which can specifically bind a Klebsiella K43 antigenic determinant. These results imply that the modification by environmental agents of specific major histocompatibility complex-associated gene products may be an important element in the pathogenesis of the HLA-B27-linked seronegative arthropathies.
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PMID:Characterization of a factor(s) present in Klebsiella culture filtrates that specifically modifies an HLA-B27-associated cell-surface component. 615 68


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