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Antigen Receptors

Autoimmune Disease. Figure 2 Generation of autoreactivity. APC, antigen presenting cell IFN, interferon LPS, lipopolysaccharide MHC, major histocompatibility complex T, T-lymphocyte TCR, Tcell (antigen) receptor TLR, toll like receptors. For details see text. [Pg.240]

The hallmark of T- and B-lymphocytes is that each single lymphocyte expresses antigen receptors of a single specificity that was created randomly during the development of that individual lymphocyte. This is achieved mainly by sequential genetic rearrangement... [Pg.614]

Immune Defense. Figure 3 Drugs involved in suppressing innate and adaptive immune response. Abbreviations mob monoclonal antibody, TCR T-cell antigen receptor, IL-2 interleukin-2, R receptor, CD cluster of differentiation. [Pg.617]

Muronomab-CD3 is a murine monoclonal antibody directed against the CD3 complex of the T-lymphocyte antigen receptor. This drug selectively diminishes the T-lymphocyte pool resulting in a strong lymphopenia. Similar to other nonhuman antibodies the generation of human antimurine antibodies (HAMA) limits its long-term use. [Pg.619]

Cyclosporine A (CsA) is a water-insoluble cyclic peptide from a fungus composed of 11 amino acids. CsA binds to its cytosolic receptor cyclophilin. The CsA/cyclophilin complex reduces the activity of the protein phosphatase calcineurin. Inhibition of this enzyme activity interrupts antigen receptor-induced activation and translocation of the transcription factor NEAT to the nucleus which is essential for the induction of cytokine synthesis in T-lymphocytes. [Pg.620]

The NHR contains also the conserved Calcineurin docking site, PxlxIT, required for the physical interaction of NEAT and Calcineurin. Dephosphorylation of at least 13 serines residues in the NHR induces a conformational change that exposes the nuclear localization sequences (NLS), allowing the nuclear translocation of NEAT. Rephosphorylation of these residues unmasks the nuclear export sequences that direct transport back to the cytoplasm. Engagement of receptors such as the antigen receptors in T and B cells is coupled to phospholipase C activation and subsequent production of inositol triphosphate. Increased levels of inositol triphosphate lead to the initial release of intracellular stores of calcium. This early increase of calcium induces opening of the plasma membrane calcium-released-activated-calcium (CRAC) channels,... [Pg.847]

Mechanism of peripheral immune tolerance characterized by a state of functional unresponsiveness induced in T cells by suboptimal or partial stimulation. Engagement of the antigen receptor in the absence of costimulation signaling induces anergy in T cells, which become unable to respond to new stimulations. [Pg.1177]

T Cell Anergy T Cell Antigen Receptor T Cell Receptors T-cells... [Pg.1503]

Oltz EM Regulation of antigen receptor gene assembly in lymphocytes. Immunol Res 2001 23 121. [Pg.395]

IgM Produced in the primary response to an antigen. Fixes complement. Does not cross the placenta. Antigen receptor on the surface of B cells. [Pg.594]

Serum concentrations lie between 0.5 and 2.5mgml. IgM can fix complement and a single molecule can initiate the complement cascade. IgM (with IgD) is the major immunoglobulin expressed on the surface ofB cells where it acts as an antigen receptor. [Pg.290]

Suppressor T cells. These cells can be specific for the antigen receptors on both B and T cells and thereby can suppress the activity of these two groups of cells. [Pg.296]

Idiotypic network. Idiotypic determinants (idiotypes) are unique antigenic epitopes characteristic of the antigen receptors on the surface of T and B cells. They are associated with the variable regions of these receptors. Antibodies produced by B cells as the result of antigenic stimulation can themselves stimulate the production of auto-anti-idiotypic antibodies which have the ability to combine with the B-cell receptor (Ig) and thus can dampen down the immune response. Idiotypes may likewise stimulate the production of T cells specific for idiotypic determinants. Jerne (1974) postulated his... [Pg.296]

The human caliciviruses, norovirus (NoV) and sapovirus, have also been described as small round structured viruses, for their 27-30 nm capsids. The NoV capsid consists of 180 copies of the VPl major capsid protein packed as an icosahedron (Prasad et ah, 1999) and the VP2 minor capsid protein, which may contribute to stability (Bertolotti-Ciarlet et al., 2002). The S domain of VPl forms the inner shell of the capsid, while the P domain protrudes from the capsid surface and contributes to binding the histoblood group antigen receptor (Cao et ah, 2007) and antigenicity (Donaldson et ah, 2008 Lindesmith et ah, 2010). [Pg.2]

Segerer S, Regele H, Mack M, et al. The duffy antigen receptor for chemokines is up-regulated during acute renal transplant rejection and crescentic glomerulonephritis. Kidney Int 2000 58 1546-1556. [Pg.153]

Mange KC, Prak EL, Kamoun M, et al. Duffy antigen receptor and genetic susceptibility of African Americans to acute rejection and delayed function. Kidney Int 2004 66 1187-1192. [Pg.154]

Middleton J, Americh L, Gayon R, et al. A comparative study of endothelial cell markers expressed in chronically inflamed human tissues MECA-79, Duffy antigen receptor for chemokines, von Willebrand factor, CD31, CD34, CD 105 and CD146. J Pathol 2005 206(3) 260-268. [Pg.196]

Patterson AM, Siddall H, Chamberlain G, Gardner L, Middleton J. Expression of the duffy antigen/receptor for chemokines (DARC) by the inflamed synovial endothelium. J Pathol 2002 197(1) 108-116. [Pg.196]


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See also in sourсe #XX -- [ Pg.296 , Pg.297 ]




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