Rotavirus 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.
Rotavirus infectionisamajorcauseoflife-threateninginfantilegastroenteritis.Theinnateimmunesys-
TEM providesanimmediatemechanismofsuppressingviralreplicationandisnecessaryforaneffective
ปรับตัว immuneresponse.Innateimmunityinvolveshostrecognitionofviralinfectionandestab-
lishment ofapowerfulantiviralstatethroughtheexpressionofpro-inflammatorycytokinessuchas
ชนิดที่ 1 interferon (IFN) .Macrophages, thefront-linecellsofinnateimmunity, produceIFNandother
cytokines inresponsetoviralinfection.However, theroleofmacrophagesduringrotavirusinfectionis
ไม่ welldefined.WedemonstrateherethatRRVrotavirustriggerstheproductionofproinflammatory
cytokines frommousebonemarrow-derivedmacrophages.IFNandantiviralcytokineproductionwas
ยกเลิก inrotavirus-infectedMAVS (- / -) macrophages.Thisindicatesthatrotavirustriggersinnate
ภูมิคุ้มกัน inmacrophagesthroughRIG-Iand / orMDA5viralrecognition, andMAVSsignalingisessen-
TIAL forcytokineresponsesinmacrophages.RotavirusinducedIFNexpressioninbothwildtypeand
MDA5 (- / -) ขนาดใหญ่, showingthatMDA5isnotessentialforIFNsecretionfollowinginfection และ
RIG-I andMDA5mayactredundantlyinpromotingrotavirusrecognition.Interestingly, rotavirusnei-
บิดา stimulatedmitogen-activatedproteinkinasesp38andJNKnoractivatedtheNLRP3inflammasome,
แสดงให้เห็นถึง thatthesecomponentsmightnotbeinvolvedininnateresponsestorotavirusinfectionin
ใหญ่ Ourresultsindicatethatrotaviruselicitsintracellularsignalinginmacrophages
ผลในtheinductionofIFNandantiviralcytokines, andadvanceourunderstandingoftheinvolvementof
cellsininnateresponsesagainstrotavirus เหล่านี้
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โรตา infectionisamajorcauseoflife threateninginfantilegastroenteritis . theinnateimmunesys -
แบบเต็มๆ providesanimmediatemechanismofsuppressingviralreplicationandisnecessaryforaneffective immuneresponse . innateimmunityinvolveshostrecognitionofviralinfectionandestab -
lishment ofapowerfulantiviralstatethroughtheexpressionofpro inflammatorycytokinessuchas
1 รอน ( IFN ) macrophages ,linecellsofinnateimmunity หน้าจอ , การป้องกัน produceifnandother
inresponsetoviralinfection อย่างไรก็ตาม theroleofmacrophagesduringrotavirusinfectionis
ไม่ welldefined . wedemonstrateherethatrrvrotavirustriggerstheproductionofproinflammatory cytokines frommousebonemarrow derivedmacrophages . ifnandantiviralcytokineproductionwas
ยกเลิก inrotavirus infectedmavs ( − / − ) แมคโครฟาจ .thisindicatesthatrotavirustriggersinnate
ภูมิคุ้มกัน inmacrophagesthroughrig แผ่นดิน / ormda5viralrecognition andmavssignalingisessen , -
tial forcytokineresponsesinmacrophages . rotavirusinducedifnexpressioninbothwildtypeand
mda5 ( − / − ) showingthatmda5isnotessentialforifnsecretionfollowinginfection macrophages และ rig-i , ,
-
rotavirusnei andmda5mayactredundantlyinpromotingrotavirusrecognition น่าสนใจมี stimulatedmitogen-activatedproteinkinasesp38andjnknoractivatedthenlrp3inflammasome
, แสดง thatthesecomponentsmightnotbeinvolvedininnateresponsestorotavirusinfectionin macrophages . ourresultsindicatethatrotaviruselicitsintracellularsignalinginmacrophages ที่เกิดใน theinductionofifnandantiviralcytokines andadvanceourunderstandingoftheinvolvementof
,เหล่านี้ cellsininnateresponsesagainstrotavirus .
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