105 S.P. to B. St. Michel

Pepys, Samuel; Heath, Helen Truesdell

doi:10.1093/oseo/instance.00005935

Cited by 5 publications

(8 citation statements)

References 0 publications

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“…Throughout the purification procedure the skin-reactivity was paralleled by anti-complementary activity [5], suggesting that there might be a causal relationship between complement-activation and antigenicity or allergenicity. Such a relationship is compatible with a proposed role of complement in the induction of IgM-, IgG-and IgE-responses [17][18][19]. The involvement of complement in these responses might be an indirect one, e.g.…”

supporting

confidence: 83%

House dust extracts contain potent immunological adjuvants

Beukelman

Dijk²,

Aerts

et al. 1987

Immunology Letters

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supporting

confidence: 83%

House dust extracts contain potent immunological adjuvants

Beukelman

Dijk²,

Aerts

et al. 1987

Immunology Letters

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“…C3b and its proteolytic fragments iC3b, C3dg and C3d are thus likely to remain attached to an acceptor site, while they exhibit a second binding site that is able to interact with receptors such as CR1, CR2, CR3 and CR4 through non-covalent bonds (Ross & Medof, 1985). Thus a bridging role can be assumed by C3b, iC3b, C3dg and C3d. Previous results have shown that C3d polymers activate directly B cells Melchers et al, 1986) and that depletion of complement system with cobra-venom factor suppresses the antibody response in mouse (Pepys, 1974). Using C3-deficient guinea pigs, Bottger et al (1986) showed that the secondary antibody response is impaired in the absence of C3: these animals were unable to react to low doses of injected antigen, and they had no amplification of the antibody titre as well as no switch from IgM to IgG, but when the concentration of the antigen was increased the immune response returned to normal.…”

Section: Introductionmentioning

confidence: 93%

Secretion, cleavage and binding of complement component C3 by the human monocytic cell line U937

Maison

Villiers

Colomb

1989

Biochemical Journal

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Secretion of complement component C3 by U937 cells was studied. Preliminary evidence for a cell-associated proteolytic activity specific for C3 is given, as well as for a covalent-like binding of C3 fragments to the cell membranes. Secretion of C3, in the presence of 10 ng of phorbol 12-myristate 13-acetate/ml, is 120-140 ng/10(6) cells per 24 h on the third day after addition of the activator. As shown by SDS/polyacrylamide-gel electrophoresis, the intracellular pro-C3 (200 kDa) and the extracellular secreted C3 (alpha-chain 110 kDa and beta-chain 75 kDa) are identical with the forms of C3 previously characterized from human serum. Incubation of U937 cells in the presence of exogenous radiolabelled C3 shows that membrane-bound proteinase(s), not related to the classical-pathway or the alternative-pathway C3 convertases, is (are) able to cleave C3; this cleavage leads to the binding of the resulting C3 fragments to the cell membrane through reaction of membrane acceptors with the carbonyl group of C3 revealed after disruption of the intramolecular thioester bond. The proteolysis appears to be fairly specific to C3, as C4, which also possesses an intramolecular thioester bond, is not cleaved and does not bind to the cells. p-Nitrophenyl p'-guanidinobenzoate (1 mM) and di-isopropyl phosphorofluoridate (2 mM) are potent inhibitors of the proteolysis, whereas soya-bean trypsin inhibitor (1 mM), leupeptin (0.1 mg/ml) and 1,10-phenanthroline (1 mM) were ineffective. Immunological characterization of the cell-bound C3 fragments with monoclonal antibodies shows an evolution of the proteolysis of the fragments from iC3b to C3dg epitopes. Extraction of membrane-bound fragments by detergent, followed by SDS/polyacrylamide-gel electrophoresis, shows two fragments, of 43 kDa and 46 kDa, with C3dg-like characteristics.

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“…As a result, autoantibodies to these antigens may be more easily triggered by sudden display on dying cells (151) or exposure to immunogenic foreign antigens that happen to crossreact (144,152 (94,95). Consistent with an important proimmunity role, antibody responses are diminished when complement is depleted (88,89), deficient (90), cannot be fixed (91), or when C3d binding to CD21 is blocked (92,93 (184,185).…”

Section: Examples Of Tolerance By Clone Retuningmentioning

confidence: 99%

“…Centrocyte survival vs. apoptosis might result from different intracellular signals elicited by antigen linked to complement C3d components on the surface of follicular dendritic cells compared with antigen-receptor crosslinking by free antigen. Support for this hypothesis comes from the following: (i) the failure of germinal center/memory responses when complement is depleted (88,89), deficient (90), cannot be fixed (91), or when C3d binding to CD21 is blocked (92,93); (ii) the costimulatory effect of coclustering CD21, the C3d receptor on B cells, with antigen receptors (94,95); and (iii) the failure of germinal center development in the absence of CD19 (96), which mediates synergistic signaling between CD21 and antigen receptors (97).…”

mentioning

confidence: 99%

Balancing immunity and tolerance: deleting and tuning lymphocyte repertoires.

Goodnow

1996

Proc. Natl. Acad. Sci. U.S.A.

415

267

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Immunological self-tolerance is ensured by eliminating or inhibiting self-reactive lymphocyte clones, creating physical or functional holes in the B- and T-lymphocyte antigen receptor repertoires. The nature and size of these gaps in our immune defenses must be balanced against the necessity of mounting rapid immune responses to an everchanging array of foreign pathogens. To achieve this balance, only a fraction of particularly hazardous self-reactive clones appears to be physically eliminated from the repertoire in a manner that fully prevents their recruitment into an antimicrobial immune response. Many self-reactive cells are retained with a variety of conditional and potentially flexible restraints: (i) their ability to be triggered by antigen is diminished by mechanisms that tune down signaling by their antigen receptors, (ii) their ability to carry out inflammatory effector functions can be inhibited, and (iii) their capacity to migrate and persist is constrained. This balance between tolerance and immunity can be shifted, altering susceptibility to autoimmune disease and to infection by genetic or environmental differences either in the way antigens are presented, in the tuning molecules that adjust triggering set points for lymphocyte responses to antigen, or in the effector molecules that eliminate, retain, or expand particular clones.

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105 S.P. to B. St. Michel

Cited by 5 publications

References 0 publications

House dust extracts contain potent immunological adjuvants

House dust extracts contain potent immunological adjuvants

Secretion, cleavage and binding of complement component C3 by the human monocytic cell line U937

Balancing immunity and tolerance: deleting and tuning lymphocyte repertoires.

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