About: A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior

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About: A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior
Creator	Zhou, Yusen Wang, Yong Jia, Leili Song, Hongbin Zhang, Chuanfu Huang, Liuyu Sun, Yansong Tomlinson, Stephen Liu, Xuelin Qiao, Fei Xu, Yuanyong Yang, Yutao
Source	Medline; PMC
abstract	BACKGROUND: Influenza is a respiratory disease that seriously threatens human health. In fact, influenza virus itself does not make critical contribution to mortality induced by influenza, but %22cytokine storm%22 produced by the excessive immune response triggered by the virus can result in inflammatory reaction of lung tissues and fatal lung tissue injury, and thus increase influenza mortality. Therefore, besides antiviral drugs, immunosuppression drugs should also be included in infection treatment. PRESENTATION OF THE HYPOTHESIS: Complement is the center of inflammatory reaction. If complement system is over activated, the body will have strong inflammatory reaction or tissue injury, resulting in pathological process. Many studies have proved that, inflammatory injury of lung tissues caused by influenza virus is closely related to complement activation. Therefore, inhibiting complement activation can significantly reduce inflammatory injury in lung tissues. As complement is both a physiological defense and pathological damage medium, systematic inhibition may result in side effects including infection. Therefore, we design targeting complement inhibitors for complement activation sites, i.e. with CR2 as targeting vector, complement inhibitors like CD59 and Crry are targeted to inflammatory sites to specially inhibit the complement activation in local injury, thus local inflammatory reaction is inhibited. TESTING THE HYPOTHESIS: CR2-CD59 and CR2-Crry targeting complement inhibitors are fusion-expressed, and their biological activity is examined via in vivo and in vitro tests. CR2 targeting complement inhibitors are used to treat mouse influenza viral pneumonia model, with PBS treatment group as the control. The survival and lung tissue injury of the mice is observed and the effect of CR2 targeting complement inhibitors on pneumonia induced by influenza virus is evaluated. IMPLICATIONS OF THE HYPOTHESIS: CR2 targeting complement inhibitors are expected to be ideal drugs for viral pneumonia.
has issue date	2010-02-09(xsd:dateTime)
bibo:doi	10.1186/1743-422x-7-30
bibo:pmid	20144216
has license	cc-by
sha1sum (hex)	c92099607cfae94a24e03a111d12994535cc2eae
schema:url	https://doi.org/10.1186/1743-422x-7-30
resource representing a document's title	A new therapeutic strategy for lung tissue injury induced by influenza with CR2 targeting complement inhibitior
has PubMed Central identifier	PMC2829536
has PubMed identifier	20144216
schema:publication	Virol J
resource representing a document's body	covid:c92099607cfae94a24e03a111d12994535cc2eae#body_text
is schema:about of	named entity 'Therefore' named entity 'process' named entity 'CR2' named entity 'INJURY OF LUNG' named entity 'TISSUE INJURY' named entity 'RESULTING IN' named entity 'MEDIUM' named entity 'HYPOTHESIS' named entity 'TARGETED' named entity 'COMPLEMENT' named entity 'FACT' named entity 'TARGETING' named entity 'ACTIVATED' named entity 'BUT' named entity 'SITES' named entity 'PATHOLOGICAL' named entity 'DRUGS' named entity 'HAVE' named entity 'RESULT' named entity 'DESIGN' named entity 'INCREASE' named entity 'IMMUNOSUPPRESSION' named entity 'RESPIRATORY DISEASE' named entity 'INCLUDED' named entity 'INHIBITED' named entity 'INDUCED' named entity 'TREATMENT' named entity 'LUNG TISSUE' named entity 'CAUSED BY' named entity 'REDUCE' named entity 'IS A' named entity 'MAKE' named entity 'STUDIES' named entity 'RELATED' named entity 'COMPLEMENT SYSTEM' named entity 'INFLUENZA' named entity 'PRESENTATION' named entity 'INHIBITING' named entity 'STORM' named entity 'INFLAMMATORY' named entity 'COMPLEMENT ACTIVATION' named entity 'CD59' named entity 'HUMAN HEALTH' named entity 'SIDE EFFECTS' named entity 'LOCAL' named entity 'DOES NOT' named entity 'INCLUDING' named entity 'PHYSIOLOGICAL' named entity 'INHIBITION' named entity 'LIKE' named entity 'INFLAMMATORY REACTION' named entity 'CRITICAL' named entity 'THERAPEUTIC' named entity 'CR2' named entity 'TISSUE INJURY' named entity 'PATHOLOGICAL PROCESS' named entity 'INDUCED' named entity 'INFLUENZA' named entity 'STRATEGY' named entity 'COMPLEMENT' named entity 'CONTRIBUTION' named entity 'DEFENSE' named entity 'INJURY' named entity 'ANTIVIRAL DRUGS' named entity 'FATAL' named entity 'INFLUENZA VIRUS' named entity 'CRRY' named entity 'LUNG TISSUES' named entity 'CENTER' named entity 'EXCESSIVE'

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