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Receptor complement

CDS Defines MHC class I-restricted T cell subset present on NK cells CDIO Known to be common acute leukaemia antigen CDlla Known to be zn a chain of LFA-1 (leucocyte function antigen-1) present on several types of leucocyte and which mediates adhesion CDllc Known to be z complement receptor 4 a chain. [Pg.280]

Con A Concanavalin A COPD Chronic obstructive pulmonary disease COS Fibroblast-like kidney cell line established from simian cells CoVF Cobra venom CP Creatine phosphate Cp Caeruloplasmin c.p.m. Counts per minute CPJ Cartilage/pannus junction Cr The chemical symbol fir chromium CR Complement receptor CRl, CR2 CR4 Complement receptor types 1, 2 and 4 CR3-a Complement receptor type 3-[Pg.281]

Mac- Macrophagp-l antigen a member of the /3-2 integrin family of cell adhesion molecules (also abbreviated to M41), ako known as monocyte antigen-1 (M-1), complement receptor-3 (CR3), CDllb/CD18... [Pg.284]

SC ID Severe combined immunodeficiency syndrome sCRl Soluble type-1 complement receptors... [Pg.286]

Luan NM, Teramura Y, Iwata H (2011) Immobilization of soluble complement receptor 1 on islets. Biomaterials 32 4539 1545... [Pg.199]

Figure 1.4. Recognition of bacteria by neutrophils. Invading bacteria are opsonised by serum proteins, such as complement fragments (e.g. C3b) and immunoglobulins. The plasma membranes of neutrophils possess receptors for these opsonins (e.g. Fc receptors and complement receptors). Thus, occupancy of these opsonin receptors triggers phagocytosis and activates events such as the respiratory burst and degranulation. Note that the receptors and opsonins are not drawn to scale. Figure 1.4. Recognition of bacteria by neutrophils. Invading bacteria are opsonised by serum proteins, such as complement fragments (e.g. C3b) and immunoglobulins. The plasma membranes of neutrophils possess receptors for these opsonins (e.g. Fc receptors and complement receptors). Thus, occupancy of these opsonin receptors triggers phagocytosis and activates events such as the respiratory burst and degranulation. Note that the receptors and opsonins are not drawn to scale.
Figure 1.15. Complement activation via the alternative pathway. Always present in serum are trace amounts of C3b, which may attach to recognition sites on, for example, yeast cell walls. C3b may combine with serum factor B to form C3bB, and this complex is acted upon by factor D to form C3bBb. This latter complex is a C3 convertase and may act upon C3 to form more C3b to amplify the process. The C3bBb-coated particles may activate other complement components (C4-C9) or be recognised by complement receptors on neutrophils. Figure 1.15. Complement activation via the alternative pathway. Always present in serum are trace amounts of C3b, which may attach to recognition sites on, for example, yeast cell walls. C3b may combine with serum factor B to form C3bB, and this complex is acted upon by factor D to form C3bBb. This latter complex is a C3 convertase and may act upon C3 to form more C3b to amplify the process. The C3bBb-coated particles may activate other complement components (C4-C9) or be recognised by complement receptors on neutrophils.
Kurzinger, K., Springer, T. A. (1982). Purification and structural characterization of LFA-1, a lymphocyte function-associated antigen, and Mac-1, a related macrophage differentiation antigen associated with the type three complement receptor. J. Biol. Chem. 257,12412-18. [Pg.125]

Primary alcohols inhibit the up-regulation of CR3 (complement receptor) molecules on the plasma membrane during neutrophil activation, indicating that PLD products are required for the translocation of specific granules,... [Pg.226]

Fibronectin is an extracellular matrix protein that mediates a variety of cellular effects. It is important in cell-cell and cell-substratum interactions ( 3.9), mediates reticuloendothelial cell activity and binds both to Clq (the first component of complement) and to bacteria. It also increases the tu-mouricidal activity of macrophages and activates complement receptors, by regulating the binding of C3b-coated particles to neutrophils. It may mediate attachment of Staphylococcus aureus to neutrophils and may also play a role as an adhesion factor, promoting the adhesion of neutrophils to surfaces. Fibronectin mRNA (8.7-8.8 kb) is detected only at low levels in... [Pg.257]

Hinglais, N., Kazatchkine, M., Mandet, C., Appay, M., and Bariety, J. (1989) Human liver Kupffer cells express CRT, CR3, and CR4 complement receptor antigens. Lab Invest. 61, 509-513. [Pg.190]

Brown, E. J. (1991) Complement receptors and phagocytosis. Curr. Opin. Immunol. 3, 76-82. [Pg.289]

CD 11c 150 Monocytes, granulocytes a chain of pl50, 95 (complement receptor/adhesion molecule)... [Pg.10]

Bacteria bind to complement components and the bacterium-complement complexes bind complement receptors on the surface of macrophages. Phagocytosis may also be mediated by specific antibodies that function as opsonins, which bind to particles, rendering them susceptible to phagocytosis. The bacterium-antibody complex then binds the macrophages via the Fc receptor and phagocytosis begins. [Pg.656]

Hughes DA, Gordon S. Expression and function of the type 3 complement receptor in tissues of the developing mouse. Journal of Immunology 1998, 160, 4543 1552. [Pg.52]

In addition, ADCC is enhanced by binding of iC3b to complement receptor 3 on the surface of immune cells. [Pg.60]

There are several relatively new therapeutic modalities for the treatment of SLE. Trying to eliminate pathogenic anti-dsDNAs, Ferguson etal. developed an antigen-based heteropolymer (AHP) (F3). AHP is a bispecific dsDNA x monoclonal antibody (mAb) complex (dsDNA x anti-CRl mAb) that enables the use of the unique immune complex-binding and clearing capacity of the complement receptor (CR1) on primate erythrocytes. In vitro studies of AHP show a substantial reduction (>90%) of anti-dsDNA titer (F20). In vivo studies in two rhesus monkeys indicate that the erythrocyte-bound antibodies are rapidly cleared from the circulation (F3). [Pg.154]

Once deposited, there are multiple mechanisms by which an immune complex initiates an inflammatory reaction (Fig. 2). Foremost among these is activation of the complement system. Immune complexes can activate the classical complement pathway as well as, indirectly or directly, the alternative complement pathway. The biologic activities of complement activation which are relevant to tissue inflammation include the generation of anaphylatoxins C5a and C3a (H29) and chemotactic peptide C5a (H29, T6), direct and indirect membrane lysis by the terminal complement components C56789 (T17), leukocytosis by C3e (G8), macrophage activation by Bb (G12), immune complex solubilization by C3b (C21), and immune adherence, the binding and activation of cells bearing complement receptors. [Pg.6]


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