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THE C3-ACTIVATOR SYSTEM: AN ALTERNATE PATHWAY OF COMPLEMENT ACTIVATION

Götze, Otto; Müller-Eberhard, Hans J.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/09/1971 EN
Relevância na Pesquisa
65.59%
Evidence has accumulated indicating the existence of a second complement activation mechanism which is functionally analogous to C1, C2, and C4. The noncomplement protein C3PA, previously recognized through its ability to form a complex enzyme with a protein from cobra venom, appears to be the precursor of the C4,2 analogue. It is a thermolabile β-globulin with a molecular weight of 80,000. When serum is treated with naturally occurring plant or bacterial polysaccharides, the C3PA is cleaved into at least two fragments, one having the electrophoretic mobility of a γ-globulin and a molecular weight of 60,000, and the other being an acidic peptide with a molecular weight of 20,000. The larger fragment has the ability to cleave C3 into C3a and C3b and is therefore called C3 activator. It arises from the action of an as yet unidentified serum enzyme upon the C3PA, which is tentatively called C3PA convertase. In addition to endotoxins, yeast cell walls, inulin, and agar, aggregates of immunoglobulins were found to be activating substances, including human IgA, guinea pig γ1, and duck antibody. Serum depleted of C3PA had reduced E. coli bactericidal and increased hemolytic activity. The relationship of the C3-activator system to experimental and clinical observations has been discussed.

MECHANISMS OF LYSOSOMAL ENZYME RELEASE FROM LEUKOCYTES EXPOSED TO IMMUNE COMPLEXES AND OTHER PARTICLES

Weissmann, Gerald; Zurier, Robert B.; Spieler, Paul J.; Goldstein, Ira M.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/09/1971 EN
Relevância na Pesquisa
65.59%
Human PMN release lysosomal enzymes (β-glucuronidase, acid phosphatase) when exposed to immune complexes, but do not release cytoplasmic LDH. The cells remain viable, and failure of LDH to appear in supernatants is not due to selective absorption or inactivation. Release of enzymes is not due to platelet contamination and is only partially enhanced by fresh serum. The selective release of lysosomal enzymes after uptake of complexes resembles that induced by inert particles of zymosan, and can be distinguished from the concurrent release of all enzymes after cell death induced by membrane-lytic crystals of MSU. Uptake of complexes, zymosan, or MSU particles is accompanied by concomitant increases in C-1 oxidation of glucose. Although MSU-induced damage can be retarded by the presence of Tris buffer, immune complexes and zymosan selectively release lysosomal hydrolases in the presence or absence of Tris buffer. Agents which elevate the level, within cells, of cAMP (PGE1, theophylline, 2-CA) and cAMP itself inhibit the selective extrusion of acid hydrolases from leukocytes without affecting the viability of cells. Leukocytes may respond to immune particles by regurgitating a portion of their lysosomal hydrolases during phagocytosis.

COMPLEMENT-DERIVED LEUKOTACTIC FACTORS IN PATHOLOGICAL FLUIDS

Ward, Peter A.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/09/1971 EN
Relevância na Pesquisa
55.6%
Leukotactic factors derived from the complement sequence consist of C5-related products, including the small cleavage product and the higher molecular weight complex (C567). A leukotactically active cleavage product (of low molecular weight) has also been described. The C5-related factors have been found in two conditions: soluble tissue extracts of immunologic vasculitis and in synovial fluids from patients with rheumatoid arthritis. The C3-related product has been found in synovial fluids from patients with inflammatory, nonrheumatoid arthritis and in extracts of experimentally infarcted myocardium. The presence of these factors may be causally related to the acute inflammatory nature of the cellular exudates.

INTERACTION OF CELLS WITH IMMUNE COMPLEXES: ADHERENCE, RELEASE OF CONSTITUENTS, AND TISSUE INJURY

Henson, Peter M.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/09/1971 EN
Relevância na Pesquisa
65.69%
Neutrophils are essential mediators of tissue damage in many forms of immune complex-induced injury. In vitro, they have been shown to release some of their content of injurious constituents upon reaction with immune complexes (Fig. 10). If the complexes are distributed along a nonphagocytosable surface, degranulation to the exterior of the cell is observed. When the complexes were phagocytized, however, degranulation into the phagocytic vacuole, and some loss of enzymes into the surrounding medium, occurred. This may have resulted from a momentary opening of the vacuole to allow ingestion of additional particles, as was demonstrated with the electron microscope. This phenomenon was particularly noticeable when the particles were relatively large. Far more immune complex is required to induce release when in a phagocytosable form than when on a nonphagocytosable membrane. Neutrophils may be attracted to sites of immune complex deposition in many parts of the body (arteries, heart, skin, brain, kidney, joints) by complement-mediated processes. In some situations, e.g. in the joint fluid, they would encounter free immune complexes, phagocytose them, and release enzymes. In many others, in which immune complexes may be distributed along surfaces...

MECHANISMS INVOLVED IN THE DEPOSITION OF IMMUNE COMPLEXES IN TISSUES

Cochrane, Charles G.
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/09/1971 EN
Relevância na Pesquisa
65.65%
The mechanisms reponsible for the deposition of circulating immune complexes have been analyzed. An active process appears to be responsible in both a laboratory model in guinea pigs and in acute immune complex disease (serum sickness) in rabbits. In rabbits, after the injection of antigen to induce serum sickness, immune complexes appear in the circulation. In addition, homocytotropic (IgE) antibody is formed which binds to the surface of basophils. Leukocyte suspensions containing these basophils, when combined with specific antigen, release a soluble factor that causes clumping of platelets and release of their vasoactive amines. An excellent correlation was found between the presence of this mechanism of release of vasoactive amine and the deposition of immune complexes in serum sickness of rabbits. Antagonists of vasoactive amines or depletion of platelets, the major circulating reservoir of these amines, suppressed the deposition of circulating immune complexes and inhibited glomerulitis and arteritis. Upon entering the walls of vessels, the complexes became lodged immune complexes, greater than 19S in size, were deposited along the membranes. The data suggest that at a time when immune complexes appear in the circulation of an immunized rabbit...

IMMUNOLOGICAL RELEASE OF HISTAMINE AND SLOW-REACTING SUBSTANCE OF ANAPHYLAXIS FROM HUMAN LUNG : I. MODULATION BY AGENTS INFLUENCING CELLULAR LEVELS OF CYCLIC 3',5'-ADENOSINE MONOPHOSPHATE

Orange, Robert P.; Austen, W. Gerald; Austen, K. Frank
Fonte: The Rockefeller University Press Publicador: The Rockefeller University Press
Tipo: Artigo de Revista Científica
Publicado em 01/09/1971 EN
Relevância na Pesquisa
65.67%
The sensitization of human lung with atopic serum is both time and temperature dependent. Highly purified IgE myeloma protein is capable of blocking sensitization of human lung with atopic serum whereas myeloma proteins of the IgG subgroups are inactive. Drugs capable of increasing cellular levels of CAMP such as β-adrenergic agents and methylxanthines inhibit the antigen-induced release of both histamine and SRS-A from human lung and these agents demonstrate synergism when used together. The β-adrenergic blocking agent, propranolol, prevents epinephrine-induced inhibition of the immunologic release of the mediators. Diethylcarbamazine also inhibits the antigen-induced release of histamine and SRS-A from human lung and a synergism between this drug and epinephrine is observed. Predominantly α-adrenergic stimulation achieved by combining propranolol with epinephrine or norepinephrine not only prevented the inhibitory activity of the sympathomimetic amines but also resulted in an enhanced release of histamine and SRS-A. These observations suggest that whereas increases in cellular levels of CAMP are inhibitory, decreases in cellular levels of CAMP enhance the antigen-induced release of the mediators.

Early induction of IL-1 receptor antagonist (IL-1Ra) in infants and children undergoing surgery.

O Nualláin, E M; Puri, P; Reen, D J
Fonte: PubMed Publicador: PubMed
Tipo: Artigo de Revista Científica
Publicado em /08/1993 EN
Relevância na Pesquisa
35.59%
The cytokine response to injury or trauma is of interest in terms of both its mediation of the acute phase response and its possible relation to the immunological depression observed after major surgery. In this study, the production of cytokines IL-1 beta, tumour necrosis factor-alpha (TNF-alpha), IL-6 and the naturally occurring inhibitor of IL-1, IL-1Ra, have been investigated in infants and children undergoing Swenson's pull-through operation for Hirschsprung's disease. Samples of peripheral blood were taken before, during and after surgery for the measurement of cytokines. IL-1Ra levels increased significantly (P < 0.01) at 2 h after commencement of surgery, with maximal levels for individual patients being attained between 3 h and 5 h (range 7.6-67.9 ng/ml). The mean level of IL-1Ra was maximal (26.2 ng/ml) at 5 h and returned to baseline levels between 24 h and 72 h. There were no changes observed in the circulating levels of IL-1 beta in nine out of 11 patients following commencement of surgery. TNF-alpha levels did not increase in any of the patients studied. IL-6 levels increased significantly (P < 0.02) 3 h after commencement of surgery, reaching maximum concentrations at 24 h (range 20-670 pg/ml), with levels falling between 48 h and 72 h. This study demonstrates...