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Mechanisms for the depression of mac...

Raley, Michael James.

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Mechanisms for the depression of macrophage function caused by EIgG phagocytic challenge: Depression of cPLA(2) activity and depletion of Fc(gamma) receptors.

紀錄類型:	書目-電子資源 : Monograph/item
正題名/作者:	Mechanisms for the depression of macrophage function caused by EIgG phagocytic challenge: Depression of cPLA(2) activity and depletion of Fc(gamma) receptors./
作者:	Raley, Michael James.
面頁冊數:	149 p.
附註:	Source: Dissertation Abstracts International, Volume: 59-06, Section: B, page: 2534.
Contained By:	Dissertation Abstracts International59-06B.
標題:	Cellular biology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9838572
ISBN:	9780591922455

Mechanisms for the depression of macrophage function caused by EIgG phagocytic challenge: Depression of cPLA(2) activity and depletion of Fc(gamma) receptors.
Raley, Michael James.

Mechanisms for the depression of macrophage function caused by EIgG phagocytic challenge: Depression of cPLA(2) activity and depletion of Fc(gamma) receptors. - 149 p.

Source: Dissertation Abstracts International, Volume: 59-06, Section: B, page: 2534.

Thesis (Ph.D.)--Albany Medical College of Union University, 1998.

Previous studies have shown that the phagocytosis of IgG-coated erythrocytes (EIgG) depresses macrophage functions that are important for normal host defense. The present studies were carried out to determine the mechanism by which phagocytosis of EIgG causes macrophage dysfunction.

ISBN: 9780591922455Subjects--Topical Terms:

3172791
Cellular biology.

Mechanisms for the depression of macrophage function caused by EIgG phagocytic challenge: Depression of cPLA(2) activity and depletion of Fc(gamma) receptors.
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245 1 0 $a Mechanisms for the depression of macrophage function caused by EIgG phagocytic challenge: Depression of cPLA(2) activity and depletion of Fc(gamma) receptors.
300 $a 149 p.
500 $a Source: Dissertation Abstracts International, Volume: 59-06, Section: B, page: 2534.
502 $a Thesis (Ph.D.)--Albany Medical College of Union University, 1998.
520 $a Previous studies have shown that the phagocytosis of IgG-coated erythrocytes (EIgG) depresses macrophage functions that are important for normal host defense. The present studies were carried out to determine the mechanism by which phagocytosis of EIgG causes macrophage dysfunction.
520 $a This study was approached by testing two hypotheses. The first hypothesis was that an oxidative stress is responsible for the depression of respiratory burst capacity and Fc$\gamma$ receptor-mediated phagocytic function following a phagocytic challenge with EIgG and that the oxidative stress resulted from the generation of highly reactive species due to interaction of hemoglobin-derived iron and the products of the F$\gamma$ receptor-stimulated respiratory burst. The results obtained do not provide support for a role for an oxidative stress in the depression of macrophage function following a phagocytic challenge with EIgG. Lipid peroxidation was associated with macrophage dysfunction caused by a challenge with EIgG, and lysosomotropic agents were able to ameliorate the depression of respiratory burst capacity. However, failure of EIgG to deplete GSH or inactivate GA-3-PD suggests that only a mild oxidative stress was induced. In addition, antioxidants and iron chelators were unable to prevent the macrophage dysfunction caused by EIgG phagocytic challenge. A phagocytic challenge with BIgG resulted in an increase in TBARS but no change in $\rm H\sb2O\sb2$ production. Also, inhibition of the respiratory burst during the phagocytic challenge did not alter the changes caused by challenge with EIgG or BIgG. It was observed that erythrocyte contents are required for the depression of respiratory burst capacity, and the ability of lysosomotropic agents to prevent the depression of this function may be related to their ability to limit the digestion of erythrocytes.
520 $a The second hypothesis was that the respiratory burst and phagocytic dysfunction are due to impairment of signaling necessary for these functions. Impairment of PLA$\sb2$ activity could cause a depression of these functions. It was found that a phagocytic challenge with EIgG depressed AA release and that this was associated with impaired PMA-stimulated $\rm H\sb2O\sb2$ production. In addition, exogenous AA prevented the depression of $\rm H\sb2O\sb2$ production. It was also found the cPLA$\sb2$ activity was decreased following a challenge with EIgG. Adding AA had no effect on phagocytic function following a challenge with either EIgG or BIgG. This finding led to the evaluation of Fc$\gamma$ receptor depletion as a possible mechanism for the depression of phagocytic function. It was found that the depression of phagocytic function was correlated with a depression of Fc$\gamma$ receptor binding and a decrease in Fc$\gamma$ receptor expression. (Abstract shortened by UMI.).
590 $a School code: 0362.
650 4 $a Cellular biology. $3 3172791
650 4 $a Immunology. $3 611031
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710 2 $a Albany Medical College of Union University. $3 1262873
773 0 $t Dissertation Abstracts International $g 59-06B.
790 $a 0362
791 $a Ph.D.
792 $a 1998
793 $a English
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=9838572