Hycult Biotech/sTREM1, Human, mAb 15G7/HM2304/100 µg

Monoclonalantibody15G7recognizeshumantriggeringreceptorexpressedonmyeloidcells1(TREM-1).TREM-1ismemberofafamilyofcellsurfacereceptorswhichfunctionasmodulatorsoftheinflammatoryresponseinsepsis.TREM-1iswidelyexpressedoncellsofthemyeloidlineageandactsasaninflammatorytriggerandamplifierafterfungalandbacterialcontact.Expressionispredominantlyseenonneutrophils,monocytes,macrophages,microglia,osteoclastsanddendriticcells.TheTREMfamilyconsistofTREM-1,TREM-2,TREM-3(mouse)andTREM-liketranscript1&2.Theyaremembersofthetransmembraneimmunoglobulinsuperfamily.TREM-1isa30kDmonomericproteinsynthesizedasa234aminoacid(aa)precursorwithasignalpeptide(16aa),anextracellulardomain(184aa),atransmembranedomain(29aa),andashortcytoplasmicdomain(5aa).TheligandofTREM-1isunknown.TheengagementofTREMs,afterassociationwiththeadapterproteinDAP12(DNAactivatingprotein12)whichcontainsanimmunoreceptortyrosine-basedactivationmotif,triggersasignallingpathwaythatleadstointracellularcalciummobilization,actincytoskeletonrearrangement,andactivationofseveraltranscriptionfactors.TREM-1actsinsynergywithToll-likereceptorsignalingpathwaysinamplifyingtheinflammatoryresponse.Duringinfections,receptorexpressionismodulatedandsolubleTREM-1(sTREM-1,17kDa)isreleased.TREM-1isshedfromthemembraneofactivatedphagocytesandcanbefoundassTREM-1intissueandbodyfluidslikeplasmaandbronchoalveolarlavagefluid(BAL).SomestudiessuggestthatsTREM1istranscribedfromanalternativemRNA.sTrem-1isunabletotransmitasignalbutcompetesforbindingwithendogenousligands.Therebydampentheamplificationloopwhichisactivatedwhentheinfectionisstarted.sTREM1levelsarepossiblyaprognosticMarkerforsepsis.However,someotherstudiesshowalsoelevatedlevelsinnon-infectiouscausesofinflammation(e.g.Crohndisease).AtleastsTREM-1inbiologicalfluidsoftencorrelateswithseverityofdisease.