ฉันรักการแปลRotavirus infectionisam

ฉันรักการแปลRotavirus infectionisamajorcauseoflife-threateninginfantilegastroenteritis.Theinnateimmunesys-
tem providesanimmediatemechanismofsuppressingviralreplicationandisnecessaryforaneffective
adaptive immuneresponse.Innateimmunityinvolveshostrecognitionofviralinfectionandestab-
lishment ofapowerfulantiviralstatethroughtheexpressionofpro-inflammatorycytokinessuchas
type-1 interferon(IFN).Macrophages,thefront-linecellsofinnateimmunity,produceIFNandother
cytokines inresponsetoviralinfection.However,theroleofmacrophagesduringrotavirusinfectionis
not welldefined.WedemonstrateherethatRRVrotavirustriggerstheproductionofproinflammatory
cytokines frommousebonemarrow-derivedmacrophages.IFNandantiviralcytokineproductionwas
abolished inrotavirus-infectedMAVS(−/−) macrophages.Thisindicatesthatrotavirustriggersinnate
immunity inmacrophagesthroughRIG-Iand/orMDA5viralrecognition,andMAVSsignalingisessen-
tial forcytokineresponsesinmacrophages.RotavirusinducedIFNexpressioninbothwildtypeand
MDA5 (−/−) macrophages,showingthatMDA5isnotessentialforIFNsecretionfollowinginfection,and
RIG-I andMDA5mayactredundantlyinpromotingrotavirusrecognition.Interestingly,rotavirusnei-
ther stimulatedmitogen-activatedproteinkinasesp38andJNKnoractivatedtheNLRP3inflammasome,
demonstrating thatthesecomponentsmightnotbeinvolvedininnateresponsestorotavirusinfectionin
macrophages. Ourresultsindicatethatrotaviruselicitsintracellularsignalinginmacrophages,resulting
in theinductionofIFNandantiviralcytokines,andadvanceourunderstandingoftheinvolvementof
these cellsininnateresponsesagainstrotavirus.
©

ผลลัพธ์ (อังกฤษ) 1:

I love infectionisamajorcauseoflife-threateninginfantilegastroenteritis.Theinnateimmunesys-Rotavirus translationtem providesanimmediatemechanismofsuppressingviralreplicationandisnecessaryforaneffectiveadaptive immuneresponse.Innateimmunityinvolveshostrecognitionofviralinfectionandestab-lishment ofapowerfulantiviralstatethroughtheexpressionofpro-inflammatorycytokinessuchastype-1 interferon(IFN).Macrophages,thefront-linecellsofinnateimmunity,produceIFNandothercytokines inresponsetoviralinfection.However,theroleofmacrophagesduringrotavirusinfectionisnot welldefined.WedemonstrateherethatRRVrotavirustriggerstheproductionofproinflammatorycytokines frommousebonemarrow-derivedmacrophages.IFNandantiviralcytokineproductionwasabolished inrotavirus-infectedMAVS(−/−) macrophages.Thisindicatesthatrotavirustriggersinnateimmunity inmacrophagesthroughRIG-Iand/orMDA5viralrecognition,andMAVSsignalingisessen-tial forcytokineresponsesinmacrophages.RotavirusinducedIFNexpressioninbothwildtypeandMDA5 (−/−) macrophages,showingthatMDA5isnotessentialforIFNsecretionfollowinginfection,andRIG-I andMDA5mayactredundantlyinpromotingrotavirusrecognition.Interestingly,rotavirusnei-ther stimulatedmitogen-activatedproteinkinasesp38andJNKnoractivatedtheNLRP3inflammasome,demonstrating thatthesecomponentsmightnotbeinvolvedininnateresponsestorotavirusinfectioninmacrophages. Ourresultsindicatethatrotaviruselicitsintracellularsignalinginmacrophages,resultingin theinductionofIFNandantiviralcytokines,andadvanceourunderstandingoftheinvolvementofthese cellsininnateresponsesagainstrotavirus.©

ผลลัพธ์ (อังกฤษ) 2:

I love to translate Rotavirus Infectionisamajorcauseoflife-Threateninginfantilegastroenteritis.Theinnateimmunesys-
TEM Providesanimmediatemechanismofsuppressingviralreplicationandisnecessaryforaneffective
Adaptive Immuneresponse.Innateimmunityinvolveshostrecognitionofviralinfectionandestab-
Lishment Ofapowerfulantiviralstatethroughtheexpressionofpro-Inflammatorycytokinessuchas
Type-1 interferon (IFN) .Macrophages, Thefront-Linecellsofinnateimmunity, ProduceIFNandother
Inresponsetoviralinfection.However cytokines, Theroleofmacrophagesduringrotavirusinfectionis
not Welldefined.WedemonstrateherethatRRVrotavirustriggerstheproductionofproinflammatory
cytokines Frommousebonemarrow-Derivedmacrophages.IFNandantiviralcytokineproductionwas
Inrotavirus abolished. -infectedMAVS (- / -) Macrophages.Thisindicatesthatrotavirustriggersinnate
Immunity InmacrophagesthroughRIG-Iand / OrMDA5viralrecognition, AndMAVSsignalingisessen-
tial Forcytokineresponsesinmacrophages.RotavirusinducedIFNexpressioninbothwildtypeand
MDA5 (- / -) macrophages, ShowingthatMDA5isnotessentialforIFNsecretionfollowinginfection, and
RIG-I AndMDA5mayactredundantlyinpromotingrotavirusrecognition.Interestingly, Rotavirusnei-
Ther Stimulatedmitogen-Activatedproteinkinasesp38andJNKnoractivatedtheNLRP3inflammasome,
Demonstrating Thatthesecomponentsmightnotbeinvolvedininnateresponsestorotavirusinfectionin.
macrophages. Ourresultsindicatethatrotaviruselicitsintracellularsignalinginmacrophages, resulting
in TheinductionofIFNandantiviralcytokines, Andadvanceourunderstandingoftheinvolvementof
these Cellsininnateresponsesagainstrotavirus.
©.

ผลลัพธ์ (อังกฤษ) 3:

I love Rotavirus translation. Infectionisamajorcauseoflife-threateninginfantilegastroenteritis.Theinnateimmunesys -
TEM. Providesanimmediatemechanismofsuppressingviralreplicationandisnecessaryforaneffective
adaptive. Immuneresponse.Innateimmunityinvolveshostrecognitionofviralinfectionandestab -
lishment. Ofapowerfulantiviralstatethroughtheexpressionofpro-inflammatorycytokinessuchas
.Type-1 interferon (IFN). Macrophages thefront-linecellsofinnateimmunity produceIFNandother
cytokines,,, Inresponsetoviralinfection.However theroleofmacrophagesduringrotavirusinfectionis
not,, Welldefined.WedemonstrateherethatRRVrotavirustriggerstheproductionofproinflammatory
cytokines. Frommousebonemarrow-derivedmacrophages.IFNandantiviralcytokineproductionwas
.Abolished inrotavirus-infectedMAVS (signed / signed). Macrophages.Thisindicatesthatrotavirustriggersinnate
immunity. InmacrophagesthroughRIG-Iand / orMDA5viralrecognition andMAVSsignalingisessen -
TiAl,, Forcytokineresponsesinmacrophages.RotavirusinducedIFNexpressioninbothwildtypeand
MDA5 (signed / signed),, macrophages showingthatMDA5isnotessentialforIFNsecretionfollowinginfection and
.RIG-I, andMDA5mayactredundantlyinpromotingrotavirusrecognition.Interestingly rotavirusnei -
ther. Stimulatedmitogen-activatedproteinkinasesp38andJNKnoractivatedtheNLRP3inflammasome
demonstrating,, Thatthesecomponentsmightnotbeinvolvedininnateresponsestorotavirusinfectionin
macrophages.? Ourresultsindicatethatrotaviruselicitsintracellularsignalinginmacrophages, the resulting
.In, theinductionofIFNandantiviralcytokines andadvanceourunderstandingoftheinvolvementof
these. Cellsininnateresponsesagainstrotavirus.
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