Hycult Biotech/TREM1, Mouse, mAb L5B8, FITC/HM1098F/100 µg

ThemonoclonalantibodyL5-B8recognizes-mousetriggeringreceptorexpressedonmyeloidcells-1(TREM-1).TREM-1isa30kDamonomerictransmembraneactivatingreceptor.TREM-1isamemberoftheimmunoglobulinsuperfamily.TREM-1isexpressedatlowlevelsintheearlydevelopmentofthehematopoieticsysteminthepromonoisticstage,andathighlevelsonthesurfaceofimmunecells,includingneutrophils,monocytesandmacrofages.TREM-1issynthesizedasa234aminoacid(aa)precursorwithasignalpeptide(16aa),anextracellulardomain(184aa),atransmembranedomain(29aa),andashortcytoplasmicdomain(5aa).Theshortintracellulardomainassociateswithasignal-transductionmolecule,DNAX-activationprotein12(DAP12),triggeringthesecretionofinflammatorycytokinesthatamplifythehostresponsetomicrobialagents.TREM-1actsinsynergywithToll-likereceptorsignalingpathwaysinamplifyingtheinflammatoryresponse.PlateletsexpressanaturalligandforTREM-1.
TheexpressionofTREM-1isgreatlyupregulatedonphagocyticcellsinthepresenceofbacteriaandfungi.TREM-1hasaroleinsepsis,inflammatoryboweldisease(IBD)andmultiplesclerosis.Incontrast,TREM-1isnotupregulatedinsamplesfrompatientswithnon-inefctiousinflammatoryconditions.Duringinfections,receptorexpressionismodulatedandsolubleTREM-1(sTREM-1,17kDa)isreleased.TREM-1isshedfromthemembraneofactivatedphagocytesandcanbefoundassTREM-<1in&gt;bodyfluidslikeplasmaandbronchoalveolarlavagefluid(BAL).
ElavatedlevelsofsTREM-1haveaaccuracyandsensitivityindetectingmicrobialinfectionsasunderlyingdisease.FurThermore,sTREM-1hasbeenassociatedwithnon-infectiousinflammatoryconditionslikemajorabdominalsurgery,pepticulcerdiseaseandCOPD.