Mouse models carrying patient-derived mutations in IRF3 and TBK1 enable mechanistic characterization of herpes simplex encephalitis

Author(s):  
Manja Idorn
2018 ◽  
Vol 29 (7-8) ◽  
pp. 425-445 ◽  
Author(s):  
Mathieu Mancini ◽  
Silvia M. Vidal

1996 ◽  
Vol 76 (02) ◽  
pp. 184-186 ◽  
Author(s):  
Kenji lijima ◽  
Fumiyo Murakami ◽  
Yasushi Horie ◽  
Katsumi Nakamura ◽  
Shiro Ikawa ◽  
...  

SummaryA 74-year-old female developed pneumonia following herpes simplex encephalitis. Her white blood cell counts reached 28,400/μl, about 90% of which consisted of granulocytes. The polymorphonuclear (PMN) elastase/α1-arantitrypsin complex levels increased and reached the maximum of 5,019 ng/ml, indicating the release of a large amount of elastase derived from the granulocytes. The mechanism of PMN elastase release was most likely to be granulocyte destruction associated with phagocytosis. The cleavage of fibrinogen and fibrin by PMN elastase, independent of plasmin, was indicated by the presence of the fragments in immunoprecipitated plasma from the patient corresponding to elastase-induced FDP D and DD fragments and the absence of fragments corresponding to plasmin-induced FDP D and DD fragments on SDS-PAGE. These findings suggested that the large amount of PMN elastase released from the excessive numbers of granulocytes in this patient with herpes simplex encephalitis and pneumonia, induced the cleavage of fibrinogen and fibrin without the participation of plasmin.


1983 ◽  
Vol 1 (2) ◽  
pp. 79-81 ◽  
Author(s):  
Victor J. Ojeda ◽  
Michael Archer ◽  
Terry A. Robertson ◽  
Marion R. Bucens

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