| Id |
Subject |
Object |
Predicate |
Lexical cue |
| T1 |
0-125 |
Sentence |
denotes |
Microglial phagocytosis induced by fibrillar beta-amyloid and IgGs are differentially regulated by proinflammatory cytokines. |
| T1 |
0-125 |
Sentence |
denotes |
Microglial phagocytosis induced by fibrillar beta-amyloid and IgGs are differentially regulated by proinflammatory cytokines. |
| T2 |
126-335 |
Sentence |
denotes |
Microglia undergo a phenotypic activation in response to fibrillar beta-amyloid (fAbeta) deposition in the brains of Alzheimer's disease (AD) patients, resulting in their elaboration of inflammatory molecules. |
| T2 |
126-335 |
Sentence |
denotes |
Microglia undergo a phenotypic activation in response to fibrillar beta-amyloid (fAbeta) deposition in the brains of Alzheimer's disease (AD) patients, resulting in their elaboration of inflammatory molecules. |
| T3 |
336-515 |
Sentence |
denotes |
Despite the presence of abundant plaque-associated microglia in the brains of AD patients and in animal models of the disease, microglia fail to efficiently clear fAbeta deposits. |
| T3 |
336-515 |
Sentence |
denotes |
Despite the presence of abundant plaque-associated microglia in the brains of AD patients and in animal models of the disease, microglia fail to efficiently clear fAbeta deposits. |
| T4 |
516-704 |
Sentence |
denotes |
However, they can be induced to do so during Abeta vaccination therapy attributable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abeta plaques. |
| T4 |
516-704 |
Sentence |
denotes |
However, they can be induced to do so during Abeta vaccination therapy attributable to anti-Abeta antibody stimulation of IgG receptor (FcR)-mediated phagocytic clearance of Abeta plaques. |
| T5 |
705-935 |
Sentence |
denotes |
We report that proinflammatory cytokines attenuate microglial phagocytosis stimulated by fAbeta or complement receptor 3 and argue that this may, in part, underlie the accumulation of fAbeta-containing plaques within the AD brain. |
| T5 |
705-935 |
Sentence |
denotes |
We report that proinflammatory cytokines attenuate microglial phagocytosis stimulated by fAbeta or complement receptor 3 and argue that this may, in part, underlie the accumulation of fAbeta-containing plaques within the AD brain. |
| T6 |
936-1049 |
Sentence |
denotes |
The proinflammatory suppression of fAbeta-elicited phagocytosis is dependent on nuclear factor kappaB activation. |
| T6 |
936-1049 |
Sentence |
denotes |
The proinflammatory suppression of fAbeta-elicited phagocytosis is dependent on nuclear factor kappaB activation. |
| T7 |
1050-1246 |
Sentence |
denotes |
Significantly, the proinflammatory cytokines do not inhibit phagocytosis elicited by antibody-mediated activation of FcR, which may contribute to the efficiency of Abeta vaccination-based therapy. |
| T7 |
1050-1246 |
Sentence |
denotes |
Significantly, the proinflammatory cytokines do not inhibit phagocytosis elicited by antibody-mediated activation of FcR, which may contribute to the efficiency of Abeta vaccination-based therapy. |
| T8 |
1247-1619 |
Sentence |
denotes |
Importantly, the proinflammatory suppression of fAbeta phagocytosis can be relieved by the coincubation with anti-inflammatory cytokines, cyclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinflammatory cytokines induce the production of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis. |
| T8 |
1247-1619 |
Sentence |
denotes |
Importantly, the proinflammatory suppression of fAbeta phagocytosis can be relieved by the coincubation with anti-inflammatory cytokines, cyclooxygenase inhibitors, ibuprofen, or an E prostanoid receptor antagonist, suggesting that proinflammatory cytokines induce the production of prostaglandins, leading to an E prostanoid receptor-dependent inhibition of phagocytosis. |
| T9 |
1620-1695 |
Sentence |
denotes |
These findings support anti-inflammatory therapies for the treatment of AD. |
| T9 |
1620-1695 |
Sentence |
denotes |
These findings support anti-inflammatory therapies for the treatment of AD. |