M1和M2型巨噬细胞表型的比较分析.pdf

1、 l : 2008-02-15 “:D STe: B( 1983-) , 3, V,1V Y % fZ bYT: (E-mail: sdxiongfd 126. com) ; # YTM1M2 %V1 s李 康, 郭 强, 王翠妮, 陈 敏, 徐 薇# , 熊思东(v f 3 ,v ZD f“ Z200032)K1:YVM1M2 %VM1S1 s, Nk % VS# ilb?ZEIFN-C#LPS| %M1 %,IL-4M2 %bsYRT-PCR ZE_ M1 Vr;ELISA_IL-12IL-10s ;FACS_ % s0VrbTA U: M1 %B ( inducible nitric o

2、xide synthase, iNOS)Vr OF A6, IL-12 3A9F, CD16/ 32Vr ;7M2 %I ( arginase 1, Arg-1)Vr O %A4, IL-10s 9F,i OVr CD206DECTIN-1bV1 sTV , iN-OSVraIL-12s CD16/ 32 VkM1 %,7Arg-1aCD206DECT IN-1 kM2 % XVSb1oM: M1 %; M2 %;Vsms |: R392. 12DS M : AcI|: 1001-2478( 2008) 03-0177-07%TB V ?%8,8 =Y/,VC A ?s 1, 2b “ - ?

3、 ?, %1 VsM 1 %( classically activated macrophage) ,M 29 %( alternatively activatedmacrophage) 3, 4b8 !Hq/,YVIFN-C#( lipopolysaccharides, LPS) 3M 1 %YVT h2%y0( IL-4aIL-13) 3M 2 %, 8 = %M V ?,X %s1 m b8 3 %h /, %VC ,YVVsk % X % ?“1ZEbXD1V o 5, 6a%y0s 7, 8V s0Vr 9, 10Z usM 1M2%b 7, “ -,1M1M2%V+dBb NVS#

4、 il, v ZE8 M 1M2 %,M1M 2VM1S_,7M 1 VS, 8 =k % HVS44 LG b1 ZE1.1 1. 1. 1 实验动物 C57BL/ 6l ( H-2ba4 6-,I) ,816 20 g,1 Z X LK b b) !v L Sb1. 1. 2 主要试剂 % !RPMI 1640( GibcoBRL ) ,l d b( Gibco BRL ) , L-!( L-Glutamine) (U k4 ) ,F(N )a ; ) ( Z 0) ,O ( 3 ) ;l FIFN-C( Pep-rotech ) , LPS( Sigma ) ,l FIL-4( Pepr

5、otech ) ; T aq DNA adNT PPCR k4( Biostar ) , T RIzol(S 3) , DEPC( Genetimes ) , M-M uLV ReverseT ranscriptase( M BI ) ; A-sbl IL-10 ELISA_ k4#177#5C f62008 M28 3 ( eBioscience ) ,l IL-12 ELISA_ k4( eBioscience ) ; FITCS:v Fl F4/ 80 F8( CALTA G Laboratories ) , PES: f Fv IgG ( H + L) F8( eBioscience)

6、 , PES: Fl CD16/ 32( FcCIII / FcCII s8, 2. 4G2) F8( BD Pharmingen ) ,S:v Fl CD206 F8( Serotec ) ,S:v Fl M GL F8 ErasmusDP-ieter Leenen q 0. 05) ; IL-4 P %sM 2 IL-10s A9F( P 0. 05) (m4BC) ;IL-4OsM 2, CD16/ 32 q (; 0. 05) (m4C) ,7CD206DECTIN-1Vr q M0A9( P 0. 01) (m4B) , DECT IN-1 (; A 6( P 0. 01) , (m

7、4C) ; M GL q (; (n AMbm2 M1M2 % 1o VrsA.yVr ; B. ( 1.OF; 2. IFN-C+ LPS; 3.IL-4) ( * P 0. 01a* * P 0. 05)m3 M1M2 %y0s M1.OF; 2.IFN-C+ LPS; 3.IL-4(* P 0.05; * * P 0.01)2.5 M1M2 %V1 s M 1M2 %VS 1 s, NtVS# ilbT V2 U, M1 Vr ? z usM 1M2 %; IL-12snM1 %,7IL-10s %s A; CD16/ 32M 1 %Vr1AM2, M2M1 %M1, CD206DECT

8、IN-1Vr A bT4 U: IL-12s aiNOSVr# CD16/ 32Vr VkM1 %; A rg-1VraCD206#DECT IN-1Vr, VkM 2 %b#180# 5C f62008 M28 3 m4 M1M2 % s0Vr1.OF; 2. IFN-C+ LPS; 3. IL-4( * P 0. 05a* * P 0. 01)3 ) % B s% 8,8=,VC+V? 1, 3, 12bMantovani 12 %iB“ ? ,7M 1M 2 % B bM1 %YVs %y0 ty0,i4 F,_ fs,? fS j ?; M 2 % F4 ? ,iYVs %y0IL-1

9、0/T GF-B/ fs,f?1T 13bYVVk % , % 3 h Hq/ ? ? 1il 14b 7, VS k us %, M 1M 2 %V+ byN, 8v?ZE M1M 2 %,sYXVS _,M 1 s?C: M 1 %iNOSVr OM2 % ( A 6, IL-12 3A9F, CD16/ 32A U Vr; M 2 %Arg-1Vr OM 1 %A4, IL-10s 9F,i OVr CD206DECTIN-1,7M GLVr AMb1 sTV : IL-12s aiNOSVr# CD16/ 32Vr VkM 1 %;7Arg-1VraCD206#DECT IN-1Vr,

10、 kM 2 % XVSb f /, iNOSArg-1Vr% s e, % ?1TbRauh 5?CSHIP( Src homology 2- containing inosito-l 5.-phosphatase) Jl %Arg-1VrA9F,i O L Arg-1M2 % Vl ? 3k LM8#, k , H %NO3 s ,V7 ?r ? 3b7H er-bert 6 %/ %+sIL-4 s8 Jl ( LysM CreIL-4RA- / flox ) LM 2 %YV/Th1Q f #181#M1M2 %V1 s T,yLysM Cre IL-4RA- f/ loxl 8 = %

11、E sT h2%y0( IL-4IL-13)O|, PM 2 % 3p,VCiNOSVrArg-1,# fh bAnthony 15L 9 L:kT h2% VM 2 %? b“h8T, f:kQ1r%,7 rArg-11byN, iNOSArg-1 VkM1M2 %, H9 1 ?VbIL-10VrIL-12 3h $ lM 2 % VS,NVM 2 % f ?1bWeber 16?Cglatirameracetate V%s IL-10,7IL-12 3h , L M 2V% VYVT%h EAE?h, Denning 17?C* % %y0IL-10Vr A ,9 VT% f1b LTA

12、 UIL-4O %IL-10s 9F,i OM1 %As, V ?%hM2y 1, IL-10Th2%y0M 2 i ilVSb k %V S,XDX, Stratis 18CD16/ 32V L d M 1%i, V ? 1; Luo 19Anthony 15|CD206Tl M2 %VS,KT iemessen 20?CCD4+ CD25+ Foxp3+T% V P %CD206V s0 Vr; Odegaard 10Vats 11DECT IN-1TM 2 %s0V,?C V 898 s8-C( PPAR-C, peroxisome proliferator-activated rece

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23、 T cell responses. Nat Im-m unol, 2007, 8: 1086-1094. 18 Stratis A, Pasparakis M, Rupec RA, et al. Pathogenic rolefor skin macrophages in a mouse model of keratinocyte-in-duced psoriasis-like skin inflamm ation J . J Clin Invest,2006, 116: 2094-2104. 19 Luo Y, Zhou H , Krueger J et al. Targeting tum

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