Disease relevance of Antigen-Antibody Reactions

• Monoclonal antibodies to adhesion molecules (P-selectin, L-selectin, CD11, CD18), complement fragments and receptors attenuate neutrophil-mediated injury (vascular injury, infarction), but clinical application may encounter limitations due to antigen-antibody reactions with the peptides [1].
• The two epitopes of HTLV-I proteins exhibiting the most specific antigen-antibody reaction reside within amino acids 100-130 of p19, a core protein encoded by gag, and amino acids 175-199 of gp46, an envelope glycoprotein encoded by env [2].
• Specific aggregation of latex particles due to antigen-antibody reaction occurred only when antigen was latex bound, as found in a study using Escherichia coli 0111:B4 extract [3].
• A solid-phase radioimmunoassay technique was used to quantitate antigen-antibody reactions between various human cell lines and lung cancer patients' sera [4].
• Results with purified mumps virus proteins demonstrated that the antigen-antibody reactions that partake in the C.A.-ELISA are mainly associated with the nucleoprotein antigen [5].

High impact information on Antigen-Antibody Reactions

• This antigen-antibody reaction was specifically blocked by the monosaccharide rhamnose, a component of the polysaccharide surface coat of many bacteria, including C. bovis [6].
• The prostaglandin analogue failed to prevent serum complement consumption in response to the antibody injection or affect the CH50 level at the preinjury stage, indicating that neither complement inactivation nor interference with the antigen-antibody reaction was involved in the hepatic protection [7].
• After reaction between goat anti-rabbit IgG conjugated to alkaline phosphatase and rabbit IgG bound to the solid phase, this specific antigen-antibody reaction was enzymatically amplified by alkaline phosphatase conversion of [3H]adenosine 5'-monophosphate to [3H]adenosine [8].
• Atebrin and the hydroxy precursors of several heterocyclic nitrogen mustards caused more than a 50% inhibition of the antigen-antibody reactions [9].
• Thus liposome binding was judged to represent an antigen-antibody reaction not binding to Fc receptors expressed by cells infected with HSV [10].

Biological context of Antigen-Antibody Reactions

• Its ability to cause contraction of isolated airways and in vivo bronchoconstriction in the guinea-pig is due to the release of histamine and arachidonate metabolites, mediator systems similar to those evoked by antigen-antibody reactions in the guinea-pig lung [11].

Anatomical context of Antigen-Antibody Reactions

• The data suggest that alprogen purified from aloe inhibits multiple signals as well as blocking Ca(2+) influx caused by mast cells activated with specific antigen-antibody reactions and that then the inhibition of histamine and leukotriene release follows [12].
• Omitting osmium allowed ample antigen-antibody reactions but could not prevent the release of glycosylphosphatidylinositol-anchored CA IV from the membranes, which led to apparent background staining [13].
• However, ultraviolet (UV)-irradiation (8400 erg/mm2) of SV did not impair the inducibility of CAA and 51Cr-labelled HeLa cells infected with UV-irradiated SV (UV-SV) became readily cytolysed by C4-deficient guinea-pig complement without antigen-antibody reaction [14].
• The antigen-antibody reaction product was expressed in the extracellular matrix, as well as on the cell membrane of certain cells [15].
• Jujubosides A1 and C and acetyljujuboside B were found to inhibit the histamine release from rat peritoneal exudate cells induced by antigen-antibody-reaction [16].

Associations of Antigen-Antibody Reactions with chemical compounds

• A parallelism was observed between the total amount of glycogen in the sensitized lung and the total amount of histamine released from the lung by antigen-antibody reactions [17].
• The interaction with leucoagglutinin is highly specific, and the shape of the precipitin curve is that of an antigen-antibody reaction; precipitation is specifically inhibited by N-acetyl-D-galactosamine [18].
• Antibody interaction with the glutamine (Q) residue was determined to be of major importance in the antigen-antibody reaction [19].
• The antigen-antibody reaction of human choriogenadotropin has been potentiometrically investigated by use of a cyanogen bromide-treated electrode coated with the corresponding anti-serum [20].
• In radioimmunoassay of digoxin by the dextran-coated charcoal method, duration of the incubation period for the antigen-antibody reaction and time allowed for dextran-coated charcoal to absorb the free antigen are critical factors [21].

Gene context of Antigen-Antibody Reactions

• CONCLUSION: Our results indicated that HDM-provoked asthma is associated with overproduction of LT with an antigen-antibody reaction, while AIA is associated with overproduction of LT with a shift to the 5-lipoxygenase series of the arachidonate cascade [22].
• This is to be compared with a factor of less than 10 for charged and neutral substrates of acetylcholinesterase, and with a similar factor in antigen-antibody reactions [23].
• The inhibitory effect of neurotensin was not seen when histamine release was induced by an antigen-antibody effect of neurotensin was not seen when histamine release was induced by an antigen-antibody reaction or by the ionophore, A 23187 [24].
• They found that due to the different specificities of monoclonal antibodies, 2 antigen-antibody reactions, AFP with immobilized antibody and AFP with labeled antibody, could be accomplished in a single step [25].
• Due to their different specificities the antibody attached to the solid phase and the one conjugated to the enzyme did not compete for binding to AFP making it possible to complete the two antigen-antibody reactions required in a single, short incubation [26].

Analytical, diagnostic and therapeutic context of Antigen-Antibody Reactions

• On the basis of analysis by gel filtration and recent findings of immunopathological studies, a postulate was made that a complement derived chemotactic factor, possibly a C5 cleavage product, developed as a result of antigen-antibody reaction in the stratum corneum of psoriatic lesions [27].
• The latex agglutination immunoassay technique uses polymer colloids as carriers of adsorbed proteins to enhance the antigen-antibody reaction [28].
• The antigen-antibody reaction increased rapidly at low concentrations and reached a plateau at 10 micrograms PS/ml as measured by nephelometry of the group 9 PS against 9V MAb binding [29].

References