CD68 on rat macrophages binds tightly to S100A8 and S100A9 and helps to regulate the cells’ immune functions

Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society

关键词: receptor‐;    like protein;    autocrine;    inflammation;    ulcerative colitis;   

DOI  :  10.1189/jlb.2A0415-170RRR

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

S100A8andS100A9(S100proteins)areregulatorsofimmunecellsofmyeloidorigin.WhereasS100proteinsarefoundathighconcentrationsinsuchcells,theirimmunologicrolesremainunclear.Wefocusedonclusterofdifferentiation68(CD68).TheaimofthisstudyistoinvestigatewhetherCD68bindstoextracellularS100A8and/orS100A9andsubsequentlyparticipatesintheregulationofthecells’immunefunctions.ELISAandaffinitychromatographyshowedthatbothrecombinantratS100A8(r‐S100A8)andr‐S100A9boundtor‐CD68,butnottor‐CD14.Flowcytometryclearlyshowedevidencessupportingabovethe2results.Asanalyzedbyflowcytometry,alessamountofr‐S100A8orr‐S100A9boundtothemacrophagestreatedwithsomedeglycosylationenzymes.Inaninvitroassay,theexpressionlevelsofS100A8andS100A9weresignificantlysuppressedafterthemacrophageshadbeentreatedwithananti‐CD68antibody(ED1).Asstimulatedmacrophageswithr‐S100A9,theexpressionofIL‐1βmRNAinmacrophages,whichweretreatedwithanti‐TLR4or‐RAGEantibodies,wassignificantlysuppressed.r‐S100A8up‐regulatedIL‐6andIL‐10mRNAs,whiler‐S100A9didTNF‐αandIL‐6mRNAs,althoughtheseregulationswerenotstatisticallysignificant.SmallinterferingCD68alsosignificantlysuppressedactivationofmacrophagesthroughanautocrinepathwaybyr‐S100A8orr‐S100A9.InmacrophagesstimulatedwithLPS,fluorescentimmunologicstainingshowedthatmostCD68colocalizedwithS100A8orS100A9andthatthelevelsofall3moleculesweremarkedlyincreased.Inconclusion,CD68onmacrophagesbindstoS100A8andS100A9andthereby,playsaroleintheregulationofthecells’immunefunctions...

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