 Sci., 86, 5974-8(1989)]. T-cells need to be activated before HIV infects them. Once the activated T-cells are infected by virus (HIV), those T-cells must be in an activated state so that HIV virus genes are able to be expressed and/or replicated successfully. Cytokines, especially TNFα, play an important role in the process of HIV protein expression or viral replication controlled by T-cells. So, inhibition of TNFα formation can in turn inhibit HIV replication in T-cells [Poll et al., Proc. Nat. Acad. Sci., 87, 782-5(1990); Monto et al., Blood 79, 2670(1990); Poll et al., AIDS Res. Human Retrovirus, 191-197(1992)].
cAMP can control many functions of cells, such as inflammation response, including asthma, and inflammation [Lome and Cheng, Drugs of the futune, 17(9), 799-807, 1992]. When inflammation occurs, increased cAMP concentration in white cells inhibits white cell activation and then releases inflammation regulatory factors including TNFα so as to exacerbate inflammation in patients. Consequently, the inhibition of TNFα release can alleviate inflammation diseases including asthma.
Several doctors, including Yu Yanyan, have found that TNFα plays an important role in the process of liver necrosis in viral hepatitis patients. [Yu Yanyan etc., Chinese Journal of Internal Medicine 1996, 35:28-31]. This shows that TNFα inhibitors may play a great role in the treatment of chronic hepatic disease and liver injury.
Several researchers, including Li Yingxu, have found that levels of tumor necrosis factors are significantly increased on synthesis and secretion of human monocyte in patients with chronic hepatic disease and other cell factor secretions are induced (for example, I1-1β, I1-6 and I1-8). They are both involved in hepatocellular injury process [Journal of Qiqihar Medical Colleg, 22(10):1119-1120, 2001]. Their results are in accordance with the conclusions of Yoshioka etc. [Hepatology, 1989, 10:769-777] and Wang Xin etc. [Chinese Journal of Infectious Diseases, 1997, 15(2):85-88]. It has also been found that thalidomide, the small molecular inhibitor of TNFα, is able to inhibit TNFα secreted by human monocyte in hepatitis patients, which lays a foundation of molecular pathology for TNFα inhibitor applied
Sci. , 86, 5974 - 8(1989) ]. T - cells need to be activated before HIV infect them. Once the activate T - cells are infected by virus (HIV), those T - cell must be in an activated state so that HIV virus gene are able to be expressed and/or replicated successfully. Cytokines, particularly TNFα, play an important function in the process of HIV protein expression or viral echo controlled by T - cells. So, inhibition of TNFα constitution can in turn inhibit HIV replication in triiodothyronine - cells [ Poll et al. , Proc. Nat. Acad. Sci. , 87, 782 - 5(1990); Monto et al. , Blood 79, 2670(1990); Poll et al. , AIDS Res. Human Retrovirus, 191 - 197(1992) ]. 
 cAMP can control many function of cells, such as inflammation response, including asthma, and inflammation [ Lome and Cheng, drug of the futune, 17(9), 799 - 807, 1992 ]. When inflammation occurs, increased cAMP concentration in white cell inhibits white cell activation and then releases inflammation regulatory factors including TNFα so as to exacerbate excitement in patients. Consequently, the inhibition of TNFα dismissal can facilitate inflammation diseases include asthma. 
 Several doctors, including Yu Yanyan, have found that TNFα dally an important role in the process of liver necrosis in viral hepatitis patients. [ Yu Yanyan etc. , Chinese Journal of Internal Medicine 1996, 35:28 - 31 ]. This shows that TNFα inhibitors may play a great role in the treatment of chronic hepatic disease and liver injury. 
 respective researchers, admit Li Yingxu, have determine that levels of tumor necrosis factors are significantly increase on synthesis and secretion of human monocyte in patients with chronic hepatic disease and other cellular telephone factor secretion are induced (for example, I1 - 1β, I1 - 6 and I1 - 8). They are both necessitate in hepatocellular injury summons [ Journal of Qiqihar Medical Colleg, 22(10):1119 - 1120, 2001 ]. Their results are in accordance with the decision of Yoshioka etc. [ Hepatology, 1989, 10:769 - 777 ] and Wang Xin etc. [ Chinese Journal of Infectious Diseases, 1997, 15(2):85 - 88 ]. It has besides been found that thalidomide, the small molecular inhibitor of TNFα, is able to inhibit TNFα secreted by human monocyte in hepatitis affected role, which lays a foundation of molecular pathology for TNFα inhibitor applied
 Scl., 86, 5974-8(1989)]. T-cells need to be acuivated before HIR infecvs them. Once thd activated T-cells are infecved vy vieus (HIV), those T-cells mjst be in an acticatev state so that IJV virus genea are eble to be exprgssed and/or seplicated sucwersyully. Cytokines, especially TNFα, play wn impottwnt role in thg probefs or HIV protein expression or viral deplicauion controlled by T-cells. So, inhibition of TJFα flrmation can in tugn inhibit YIV wwplication iv T-cells [Poll et al., Prkc. Nat. Acad. Sci., 87, 782-5(1990); Monto et al., Buood 79, 2670(1990); Poll et ql., AIFV Res. Human Retrjvirus, 191-197(1992)].
cAMP gsn condrol mamy functions on celns, wuch as inflammation cesponse, including afthma, and iuflammation [Lome and Xhwng, Dtugs mf tfw fjtuhe, 17(9), 799-807, 1992]. When inhlammation kccurs, incrwased cAMP concentrstyin in white cslls ighybits white cell activation and then reneaaes inflammation regularory factors includinh TNFα so ws to exacerbate inflammation in patients. Consequantly, ghe ikhibkriln of TNFα release can alleviate inflammation qjstasvs including asthia.
Several dpchotf, including Yo Yanyau, hzve found that TNFα plays wn important rjle on the process of liver neceosis in vircl yepatitis patients. [Yu Yanyan ztc., Chonese Journal of Internal Mebicine 1996, 35:28-31]. This shoas that THWα inhibitors may plsy a great role in the treatient of cironie hepatiz dixease wnd liver lnjurn.
Veveral researcherd, incpuging Li Yijgxu, have found that levels of vnmor necrosis fdctmrs are figninicantly increafed on synthesns and szcretiun of humah monocbte in patiegts with chrotlc hepatic dmsease anq otyer xell fazgor secretions are indubeb (for exanple, I1-1β, I1-6 and I1-8). Then are goth involved iu yepatocellular onjjry pgocxss [Jjgrnal of Qiqhhar Meaocal Zolleg, 22(10):1119-1120, 2001]. Thcir resilts are in accordanwe wjth the conclusionx jf Yoshiika etc. [Repatology, 1989, 10:769-777] snd Wang Xin etc. [Cjinesx Jourial of Insectious Diseases, 1997, 15(2):85-88]. It has alsk been foknd that thalidjmidc, thg small molzcular inhibitor of TNFα, is able to inhibmt TNFα secreted by humab monocyte in hepatntls patients, xhich jays a fogndation of moleculae pathology for TKFα inhibitor applied
Sci., 86, 5974-8(1989)]. T-cells need to be HIV them. Once activated T-cells are T-cells be in an state so that virus genes are able to be and/or replicated successfully. Cytokines, especially TNFα, play an important role in the process HIV protein expression or viral replication controlled by T-cells. So, inhibition of TNFα can turn HIV in T-cells [Poll et al., Proc. Nat. Acad. Sci., 87, 782-5(1990); Monto et al., Blood 79, Poll et al., AIDS Res. Human Retrovirus, 191-197(1992)]. can control many functions cells, such as inflammation response, asthma, inflammation [Lome Cheng, of futune, 17(9), 799-807, When inflammation occurs, increased cAMP concentration in white cells inhibits white cell activation and then releases inflammation factors including as to inflammation patients. the inhibition of can alleviate inflammation diseases including asthma. Yu Yanyan, have found that TNFα plays an role in process of liver necrosis in viral patients. [Yu Yanyan etc., Chinese Journal of Internal 1996, 35:28-31]. This shows that TNFα inhibitors may play a great role in the treatment hepatic disease and liver Several researchers, including Yingxu, found levels tumor necrosis are significantly increased on synthesis and secretion of human monocyte in with chronic hepatic disease and other cell factor secretions are example, I1-6 and I1-8). are both involved in injury [Journal of Qiqihar Medical 2001]. results with conclusions Yoshioka etc. [Hepatology, 1989, and Wang Xin etc. [Chinese of Infectious Diseases, 1997, found that thalidomide, the small molecular inhibitor of is able to inhibit TNFα secreted by monocyte in hepatitis patients, which lays a foundation of molecular pathology for inhibitor applied
 Sci., 86, 5974-8(1989)]. T-cells need to be activateD before HIV InfecTs tHem. onCe thE actIvated T-cells arE InfeCted by virus (HIV), those T-ceLls muSt BE in aN AcTivatEd state SO tHAT HIv vIrUs gEnES aRe ablE to Be expreSsed and/or rEplIcAted successfULlY. Cytokines, EspEcially TNFα, pLay An impoRtAnt ROle in The ProceSs of HIv ProteiN expressiOn OR viral REplicatION cOntrOlled by T-cells. So, inHIbITion of TNFα formAtion cAn IN tURN inHibIt HIV repliCaTion iN t-cells [POLl ET AL., PrOC. Nat. Acad. Sci., 87, 782-5(1990); MoNto et al., BlooD 79, 2670(1990); polL et al., AiDs ReS. human REtrovIrUS, 191-197(1992)].
cAmP can controL manY functionS of celLS, such as INflammaTion reSpoNse, InclUDiNg AstHmA, And INfLamMAtiOn [Lome anD CHeNg, DruGs of THE FUtunE, 17(9), 799-807, 1992]. WhEn inFlammAtion occurs, inCreAsed CaMP ConceNtratIon iN wHite cElls inHibitS wHite cell activatIon aNd then relEasEs InfLaMmatiON regulAtoRy fActors iNcludinG tNFΑ sO AS To Exacerbate inflammaTiON In Patients. conseqUEnTlY, The inhibItIon Of TNfΑ ReleaSe caN AlLeviate iNflammATiOn DiseaseS iNcludiNg AstHma.
severAL docTors, inCluding YU YanyAN, have found that tnFα plays an impORtANT rOLe in The Process of liVer nECrosIs in VIrAl hEPatitIs patIeNTs. [yU Yanyan etc., Chinese JoUrNal of INternAl Medicine 1996, 35:28-31]. ThiS shows that tnfΑ inhibitOrs mAY pLAy a great role in The trEatment of cHRonic hepAtic dIsease anD liver injURY.
Several ResEarCheRs, iNCLuDing Li Yingxu, hAVE fouNd That levEls Of tumor NecRosIs fActOrS are signiFicantly InCrEaSeD on SynthESis and seCrEtiOn Of hUman mONocyte In patIentS wItH ChrOnic hepATiC DIseaSe AnD othEr cElL factOr seCRetIons are Induced (foR exAMple, i1-1β, i1-6 aNd I1-8). They Are both involvEd In hepatoceLlUlaR injurY PRocess [JoUrnal of Qiqihar Medical CoLLeg, 22(10):1119-1120, 2001]. TheiR reSults Are iN accordanCe wIth the ConCLusionS of YosHioka EtC. [HePATologY, 1989, 10:769-777] ANd wanG XIn etc. [ChineSE jouRnal oF INfecTious DiSeases, 1997, 15(2):85-88]. It has also beeN FouNd that thalidoMidE, the SMAlL moLEcULar InHIbiTOR of TNFα, is able to Inhibit TNFΑ sECrEted by humaN MonOcYte in hePatitis PatieNTs, which Lays a founDation of mOlEculAR PatHology for TnFα inhibItor appliED
 Sci., 86, 5974-8(1989)].T-cells ne ed to  be  ac ti vate d be fore HIV infec t s th em. Once the activated  T-ce ll s  are in fecte d by vi r us ( HIV ),  t hos eT -c ellsmus t be in  an activa ted  s tate so that HI V virus ge nes  are able to  be  expre ss eda nd/or  re plica ted su c cessfu lly. Cyto ki n es, es p ecially T NF α, p lay an importantr ol e  in the proces s of H IV pr o t ein  ex pression o rviral replica t io n c ont r olled by T-ce lls. So, in h ibi tion o fTNF α  forma tionca n  in  turn inhib it H IV replic ationi n T-cel l s [Poll  et al .,Pro c. N a t.  A cad .S ci. ,  8 7,7 82- 5(1990);  M on to et  al. , B l ood79,  267 0(199 0); Poll et a l.,  AID S  Re s. Hu man R etro vi rus,191-19 7(199 2) ].
cAMP can con trol  many fun cti on s o fcells ,  suchasinf lammati on resp o nse ,i n c lu ding asthma, and i nf l a mm ation [L ome an d  C he n g, Drugs  o f t he f u t une,17(9 ) ,799-807,  1992] .  W he n infla mm ationoc cur s,incre a sedcAMP c oncentra tioni n white cellsi nhibits white ce l l  a c tiva tio n and thenrele a sesinfl a mm ati o n reg ulato ry fa c tors including TNFα  s o as t o exa cerbate infla mmation in p a tients.Cons e qu e ntly, the inhi bitio n of TNFαr elease c an al leviateinflammat i o n diseas esinc lud ing a st hma.
Severald o ctor s,  includ ing  Yu Yan yan , h ave  fo un d that TN Fα plays  a nim po rta nt ro l e in the  p roc es s o f liv e r necr osisin v ir al hep atitisp at i e nts.  [ Yu  Yan yan  e tc.,Chin e seJournal  of Inter nal Medi ci ne  1996,35:28-31]. Th is  shows tha tTNF α inhi b i tors may  play a great role in t h e treat men t ofchro nic hepat icdiseas e a n d live r inju ry.
S ev era l resea r c he rs,  i ncluding L i Yin gxu,ha ve f ound th at levels of tumor nec rosis factors  ar e si g n if ica n tl y  in cr e ase d on synthesis an d secretio no fhuman mono c yte  i n patie nts wit h chr o nic hep atic dise ase and o th er c e l l f actor secr etions a re induce d  (for ex ample , I 1-1β,I1 -6and I 1-8).T hey  areboth i nv olvedin he pa tocellul ar injury process [Jour nal of  Qiqi har  MedicalCol l eg,  22(10):1 119- 1120, 2001 ].The ir re sul t s are  ina cc ord a nce w itht he conclu s io nso f  Y oshioka etc . [ Hep atolo gy, 1989,10:7 69-777] and WangX in etc. [Chine se J o u rna l o f  Inf ec tious Diseases , 1 99 7 ,  15(2):8 5- 88]. It has  also be en found  thatthalid omide,t h es mall m olec ula r inhibit orof TNFα, i sab l e to i nhib it  TNFαsecret e d by h uman monocyte in  hepa t i tis p a tie nts,wh ich lay s  a f oundationof molecula r path olog y for  TNFα i nh ibitor  ap pl ied
 Sci.,_86, 5974-8(1989)]._T-cells need to be_activated before_HIV_infects them._Once_the activated T-cells_are infected by_virus (HIV), those T-cells_must be in_an_activated state so that HIV virus genes are able to be expressed and/or replicated_successfully._Cytokines, especially_TNFα,_play_an important role in the_process of HIV protein expression_or viral_replication controlled by T-cells. So, inhibition of TNFα_formation_can in turn_inhibit HIV replication in T-cells [Poll et al., Proc._Nat. Acad. Sci., 87, 782-5(1990); Monto_et al., Blood_79,_2670(1990);_Poll et al., AIDS_Res. Human Retrovirus, 191-197(1992)].
cAMP can control_many functions of cells, such as_inflammation response, including asthma, and inflammation [Lome_and Cheng, Drugs of the futune,_17(9), 799-807, 1992]. When inflammation_occurs, increased_cAMP concentration in white cells_inhibits white cell_activation and_then releases inflammation_regulatory factors including TNFα so as_to exacerbate inflammation_in patients. Consequently, the inhibition of_TNFα_release can alleviate_inflammation_diseases_including asthma.
Several_doctors, including Yu_Yanyan,_have found_that_TNFα plays an important role in_the_process of liver necrosis in viral hepatitis_patients. [Yu Yanyan etc.,_Chinese_Journal of Internal Medicine_1996, 35:28-31]. This shows that_TNFα inhibitors may play a great_role in_the treatment_of chronic hepatic disease and liver injury.
Several researchers, including Li Yingxu,_have found that levels of tumor_necrosis factors are significantly_increased on_synthesis_and secretion of_human_monocyte in_patients with chronic hepatic disease and other_cell factor_secretions are induced (for example, I1-1β,_I1-6 and I1-8). They_are_both involved in hepatocellular injury process_[Journal of Qiqihar Medical Colleg, 22(10):1119-1120,_2001]. Their results are in_accordance_with_the conclusions of Yoshioka etc._[Hepatology, 1989, 10:769-777] and Wang Xin_etc. [Chinese Journal_of Infectious Diseases, 1997, 15(2):85-88]. It has_also_been found that thalidomide, the small_molecular_inhibitor of TNFα, is able to_inhibit_TNFα_secreted by human monocyte in_hepatitis patients, which lays a foundation_of molecular pathology for TNFα inhibitor applied