Ati

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Langsung menyang: pandhu arah, pados
Ati
Leber Schaf.jpg
Ati wedhus: (1) lobus tengen, (2) lobus kiwa, (3) lobus mawa buntut, (4) lobus kuadratus, (5) arteri ati lan vena portal, (6) kelenjar getah bening ati, (7) kanthong empedu.
Surface projections of the organs of the trunk.png
Proyeksi lumahing organ torso, nuduhaké ati ing tengah
Latin jecur, iecer
Gray's subject #250 1188
Vena vena hepatika, portal vena hepatika
Saraf celiac ganglia, vagus[1]
Precursor foregut
MeSH Ati
Ati iku organ paling gedhé ing badané menungsa.

Ati (basa Yunani: ἡπαρ, hēpar) arupa kelenjar paling gedhé ing njero awak, manggon ana njero rongga weteng sisih tengen, peneré ing sangisoré diafragma. Ati iku sawijining organ ing vertebrata, klebu menungsa. Organ iki duwé peran wigati ing métabolisme lan duwé sapérangan fungsi ing awak/badan klebu panyimpenan glikogen, sintesis protein plasma, lan netralaké obat. Ati uga mrodhuksi bile, kang wigati kanggo pancernan.

Adhedhasar fungsiné, ati uga klebu minangka alat èkskrèsi. Iki amarga ati mbiyantu fungsi ginjal kanthi cara mecah sapérangan senyawa sing asifat racun lan ngasilaké amonia, urea, lan asam urat kanthi mupangataké nitrogen saka asam amino. Prosès pamecahan senyawa racun déning ati diarani prosès detoksifikasi.

Lobus ati kawangun saka sèl parenkimal lan sèl non-parenkimal.[2] Sèl parenkimal ing ati diarani hepatosit, manggoni watara 80% volume ati lan nglakokaké manéka fungsi utama ati. 40% sèl ati ana ing lobus sinusoidal. Hepatosit arupa sèl endodermal sing kastimulasi déning jaringan mesenkimal sacara terus-terusan wiwit embrio nganti ngrembaka dadi sèl parenkimal.[3] Sakwéné wektu mau, dumadi paningkatan transkripsi mRNA albumin minangka stimulan proliferasi lan diferensiasi sèl endodermal dadi hepatosit.[4]

Lumen lobus kawangun saka SEC lan dipanggoni déning 3 jinis sèl liya, kayata sèl Kupffer, sèl Ito, limfosit intrahepatik kayata sèl pit. Sèl non-parenkimal manggoni watara 6,5% volume ati lan mrodhuksi manéka substansi sing ngendhalèkaké akèh fungsi hepatosit.

Filtrasi arupa salah siji fungsi lumen lobus sinusoidal sing misahaké lumahing hepatosit saka getih, SEC duwé kapasitas endositosis sing gedhé banget kanthi manéka ligan kayata glikoprotein, komplèks imun, transferin lan seruloplasmin. SEC uga duwé fungsi minangka sèl presenter antigen sing nyedhiakaké èksprèsi MHC I lan MHC II kanggo sèl T. Sèkrèsi sing dumadi ngliputi manéka sitokina, eikosanoid kayata prostanoid lan leukotriena, endotelin-1, nitrogen monoksida lan sapérangan komponèn ECM.

Sèl Ito ana ing jaringan perisinusoidal, arupa sèl kanthi akèh vesikel lemak ing njero sitoplasma sing ngiket SEC kuwat banget nganti mènèhaké lapisan gandha ing lumen lobus sinusoidal. Nalika ati ana ing kahanan normal, sèl Ito nyimpen vitamin A guna ngendhalèkaké kalenturan matriks èkstraselular sing diwangun mawa SEC, sing uga arupa kalenturan saka lumen sinusoid.

Sèl Kupffer ana ing jaringan intrasinusoidal, arupa makrofaga kanthi kamampuan endositik lan fagositik sing ngéramaké. Sèl Kupffer sadina-dina interaksi karo matérial sing asalé saka saluran pancernan sing ngandhut larutan bakterial, lan nyegah aktivasi èfèk toksin senyawa mau menyang njero ati. Paparan larutan bakterial sing dhuwur, utamané paparan LPS, gawé sèl Kupffer nglakokaké sèkrèsi manéka sitokina sing micu prosès paradhangan lan bisa ngakibataké tatu ing ati. Sèkrèsi antara liya ngliputi spesi oksigen reaktif, eikosanoid, nitrogen monoksida, karbon monoksida, TNF-α, IL-10, minangka rèspon kakebalan turunan jroning fasa infèksi primèr.

Sèl pit arupa limfosit kanthi granula gedhé, kaya sèl NK sing manggon ing ati. Sèl pit bisa ngindhuksi pepati sanalika ing sèl tumor tanpa gumantung ing ekspresi antigen ing komplèks histokompatibilitas utama. Aktivitas sèl pit bisa ditingkataké kanthi stimulasi interferon-γ.

Saliyané iku, ing ati isih ana sel T-γδ, sèl T-αβ lan sèl NKT.

Sebutan medhis kang ana gandhéngané karo ati biasané diwiwiti nganggo hepat- utawa hepatik saka tembung Yunani kanggo ati, yaiku hepar.

Sèl punca[sunting | sunting sumber]

Saliyané hepatosit lan sèl non-parenkimal, ing ati isih ana jinis sèl liya yaiku sèl intra-hepatik sing asring diarani sèl oval,[5] dan hepatosit duktular.[6] Régénerasi ati sawisé hepatektomi parsial, umumé ora nglibataké sèl progenitor intra-hepatik lan sèl punca èkstra-hepatik (hemopoietik), lan gumantung mung marang proliferasi hepatosit. Nanging jroning kahanan nalika proliferasi hepatosit kacandhet utawa katundha, sèl oval sing ana ing aréa periportal bakal ngalami proliferasi lan diferènsiasi dadi hepatosit diwasa.[5][7] Sèl oval arupa wangun diferènsiasi saka sèl progenitor sing ana ing aréa portal lan periportal, utawa kanal Hering,[8] lan mung ditemokaké nalika ati ngalami cidra.[9] Proliferasi sing dumadi ing sèl oval bakal mbentuk saluran èkskrèsi sing ngubungaké aréa parenkima papan dumadiné karusakan ati karo saluran empedu. Epimorfin, sawijining morfogen sing akèh ditemokaké duwé peran ing akèh organ epitelial, katoné uga duwé peran ing pambentukan saluran empedu déning sèl punca hepatik.[10] Sawisé iku sèl oval bakal kadiferensiasi dadi hepatosit duktular. Hepatosit duktular dianggep arupa sèl transisi sing magepokan antarané karo:[11]

gumantung ing jinis gangguan sing nyerang ati.

Ing modhèl tikus kanthi 70% hepatektomi, lan indhuksi regenerasi hepatik kanthi asetilaminofluorena-2, ditemokaké yèn sèl punca sing asalé saka sumsum balung mburi bisa kadiferensiasi dadi hepatosit,[12][13] kanthi médhiasi hormon G-CSF minangka kemokina lan mitogen.[14] Regenerasi juga dapat dipicu dengan D-galaktosamina.[15]

Sèl imunologis[sunting | sunting sumber]

Ati uga duwé peran jroning sistem kakebalan kanthi akèhé sèl imunologis ing sistem retikuendotelial sing duwé fungsi minangka tapis antigen sing kagawa menyang ati liwat sistem portal ati. Papindhahan fasa infèksi saka fasa primèr dadi fasa akut, ditengeri déning ati kanthi ngedhunaké sekresi albumin lan ngunggahaké sekresi fibrinogen. Fasa akut sing terus-terusan bakal ngakibataké simtoma hipoalbuminemia lan hiperfibrinogenemia.[16]

Nalika ati cidra, sèl getih putih bakal distimulasi kanggo migrasi nuju ati lan bebarengan karo sèl Kupffer nyekresi sitokina sing gawé modulasi prilaku sèl Ito.[17] Sèl TH1 mrodhuksi sitokina sing ningkataké rèspon kakebalan selular kayata IFN-gamma, TNF, lan IL-2. Sèl TH2 suwaliké bakal mrodhuksi sitokina sing ningkataké rèspon kakebalan humoral kayata IL-4, IL-5, IL-6, IL-13 lan ningkataké rèspon fibrosis. Sitokina sing disekresi déning sèl TH1 bakal nyandhet diferensiasi sèl T dadi sèl TH2, suwaliké sitokina sekresi TH2 bakal nyandhet proliferasi sèl TH1. Mula rèspon kakebalan asring ditélakaké kapolarisasi menyang rèspon kakebalan selular utawa humoral, nanging durung tau kaloroné.

Fungsi ati[sunting | sunting sumber]

Manéka jinis tugas sing dilakokaké déning ati, dilakokaké déning hepatosit. Nganti saiki durung ditemokaké organ liya utawa organ gawéyan utawa piranti sing bisa nggantèkaké kabèh fungsi ati. Sapérangan fungsi ati bisa digantèkaké kanthi prosès dialisis ati, nanging tèknologi iki isih terus dikembangaké kanggo perawatan panandhang gagal ati.

Minangka kelenjar, ati ngasilaké:

Saliyané nglakokaké prosès glikolisis lan siklus asam sitrat kaya sèl ing umumé, ati uga duwé peran jroning metabolisme karbohidrat liyané:

lan ing lintasan katabolisme:

Ati uga nyadhangaké sapérangan substansi, saliyané glikogen:

Régénerasi sèl ati[sunting | sunting sumber]

Kamampuan ati kanggo nglakokaké régénerasi arupa sawijining prosès sing wigati banget supaya ati bisa pulih saka karusakan sing ditimbulaké saka prosès detoksifikasi lan imunologis. Régénerasi kagayuh kanthi interaksi sing komplèks banget antara sèl sing ana jroning ati, ing antarané hepatosit, sèl Kupffer, sèl endotelial sinusoidal, sèl Ito lan sèl punca; karo organ ekstra-hepatik, kayata kelenjar tiroid, kelenjar adrenal, pankreas, duodenum, hipotalamus.[21]

Hépatosit, iku sèl sing unik banget. Potènsi hépatosit kanggo nglakokaké proliferasi, muncul nalika dumadi kélangan massa sèl,[22] sing diarani fasa prima utawa fasa kompetènsi réplikatif[23] sing umumé dipicu déning sèl Kupffer liwat sekresi sitokina IL-6 lan TNF-α. Ing fasa iki, hepatosit ngleboni siklus sèl saka fasa G0 menyang fasa G1.

TNF-α bisa mènèhaké èfèk proliferatif utawa apoptotik, gumantung ing spesi oksigen réaktif lan glutathion, minimal 4 faktor transkripsi diaktivasi sadurungé hepatosit mlebu menyang njero fasa proliferasi, yaiku NF-κB, STAT-3, AP-1 lan C/EBP-beta.[24]

Proliferasi hépatosit diindhuksi déning stimulasi sitokina HGF lan TGF-α, lan EGF[24] kanthi rong lintasan. HGF, TGF-α, lan EGF arupa faktor patuwuhan sing asalé saka substrat serina lan protein logam[25] sing ngindhuksi sintesis DNA.[23] Lintasan pisanan yaiku lintasan IL-6/STAT-3 sing duwé peran jroning siklus sèl liwat siklin D1/p21 lan pangreksan sèl kanthi paningkatan rasio FLIP, Bcl-2, Bcl-xL, Ref1, lan MnSOD. Lintasan kaloro yaiku lintasan PI3-K/PDK-1/Akt sing ngendhalèkaké ukuran sèl liwat molekul mTOR, saliyané minangka dat anti-apoptosis lan antioksidan.

Hormon tri-iodotironina, saliyané ngedhunaké kadhar kolesterol ing ati,[26] uga duwé kapasitas jroning proliferasi hépatosit minangka mitogen sing duwé peran ing siklin D1,[27] nambah cepet konsumsi O2 déning mitokondria kanthi ngaktivasi transkripsi ing gen ambegan nganti ningkataké prodhuksi spesi oksigen réaktif.[28] Sekresi ROS menyang njero sitoplasma hépatosit bakal ngaktivasi faktor transkripsi NF-κB.[29] Ing sèl Kupffer, ROS jroning sitoplasma, bakal ngaktivasi sekresi sitokina TNF-α, IL-6 lan IL-1 kanggo disekresi. Ikatan sing dumadi antarané katelu sitokina iki karo hépatosit bakal ngindhuksi ekspresi pancerep enzim antioksidan, kayata mangan superoksida dismutase, i-nitrogen monoksida sintase, protein anti-apoptosis Bcl-2, haptoglobin lan fibrinogen-β sing diperlokaké hépatosit jroning proliferasi.[30] Stres oksidatif sing bisa ditimbulaké déning ROS uga karusakan sing bisa ditimbulaké déning manéka sitokina, bisa diilangaké kanthi asupan tosoferol (100 mg/kg) utawa senyawa panyandhet gadolinium klorida (10 mg/kg) kaya sing diduwèni déning sèl Kupffer, sadurungé stimulasi hormon tri-iodotironina,[31] éwadéné laju proliferasi hépatosit dikendhalèkaké déning kadhar etanolamina minangka faktor hepatotrofik humoral.[32]

Kamampuan ati kanggo ngèlakokaké régenerasi wis dikawruhi wiwit jaman Yunani kuna saka crita mitos ngenani sawijining titan sing jenengé Prometheus.[33] Kamampuan iki bisa sirna, nganti hépatosit ora bisa mlebu menyang njero siklus sèl, senajan kèlangan sebagéyan massané, yèn dumadi fibrosis ati. Lintasan fibrosis sing ora énggal éntuk parawatan, saya suwé bakal ngrembaka dadi sirosis ati[34] lan ngudokaké panandhangé kanggo nglakoni transplantasi ati utawa hépatèktomi kanggo tetep urip.

Régenerasi ati sawisé hépatèktomi parsial arupa prosès sing rumit banget ing sangisoré pangaruh owah-owahan hémodinamika, modulasi sitokina, hormon faktor patuwuhan lan aktivasi faktor transkripsi, sing ngarah ing prosès mitosis. Hormon PRL sing disekresi déning kelenjar hipofisis ngindhuksi respon hépatotrofik minangka mitogen sing duwé peran jroning prosès proliferasi lan diferensiasi.[35] PRL mènèhi pangaruh marang paningkatan aktivitas faktor transkripsi sing duwé peran jroning proliferasi sèl, kayata AP-1, c-Jun lan STAT-3; lan diferensiasi lan kareksané metabolisme, kayata C/EBP-alfa, HNF-1, HNF-4 lan HNF-3. c-Jun arupa salah siji protein panyusun AP-1.[36] Indhuksi NF-κB ing fasa iki diperlokaké kanggo nyegah apoptosis lan micu derap siklus sèl sing wajar.[37] Ing wektu iki, peran retinil asetat dadi vital banget, amarga fungsiné sing nambah massa DNA lan protein sing dikandhut.[38]

Panyakit ing ati[sunting | sunting sumber]

Ati arupa organ sing nopang kalangsungan urip mèh kabèh organ liya ing njero awak. Amarga papan sing strategis banget lan fungsi multi-dimensional, ati dadi rentan banget marang tekané manéka penyakit. Ati bakal ngrèspon manéka panyakit mau kanthi ngradhang, sing diarani hepatitis

Asring uga hepatitis diwiwiti karo réaksi radhang patobiokimiawi sing diarani fibrosis hati,[39] kanthi simtoma paraklinis arupa paningkatan rasio plasma laminin, sawijining glikoprotein sing disekresi sèl Ito, asam hialuronat lan sajenis aminopeptida yaiku prokolagen tipe III,[40] dan CEA.[41] Fibrosis ati bisa disebabaké déning asoré rasio plasma HGF,[42][43] utawa amarga infèksi viral, kayata hepatitis B, patogen sing disebabaké déning infèksi akut sajenis virus DNA sing duwé fokus infèksi arupa cithakan transkripsi sing diarani cccDNA sing kametilasi,[44] utawa hepatitis C, patogen sarupa hepatitis B sing disebabaké déning infèksi virus RNA kanthi fokus infèksi arupa metilasi DNA, utamané liwat mékanisme ekspresi genetik berkas GADD45B, saéngga ngakibataké siklus sèl hépatosit dadi kacandhet-candhet.[45][46]

Fibrosis ati merlokaké pananganan seawal mungkin, kaya ing modhèl tikus, stimulasi proliferasi hépatosit bakal ngluruhaké fokus infèksi virus hepatitis B,[47] sadurungé ngrembaka dadi sirosis ati utawa karsinoma hepatoselular. Sawisé dumadi kanker ati, senyawa siklosporina sing duwé potènsi kanggo micu proliferasi hépatosit, malah bakal nyepetaké ngrembakané sèl kanker,[48] amarga sèl kanker ngalami hiperplasia hépatik, yaiku proliferasi sing ora dibarengi aktivasi faktor transkripsi genetik. Iki bisa diindhuksi mawa stimulasi timbal nitrat (LN, 100 mikromol/kg), siproteron asetat (CPA, 60 mg/kg), lan nafenopin (NAF, 200 mg/kg).[49]

Hépatitis uga bisa diwiwiti kanthi defisiensi mitokondria ing njero hepatosit, sing diarani steatohepatitis. Disfungsi mitokondria bakal duwé dampak tumrap homeostasis senyawa lipid lan paningkatan rasio spesi oksigen reaktif sing ngindhuksi TNF-α.[50] Iki bakal terus ing pangendhepan lemak, stres oksidatif lan peroksidasi lipid,[51] sarta marakaké mitokondria dadi rentan marang pepati déning nekrosis akibat asoré rasio ATP jroning matrik mitokondria, utawa déning apoptosis liwat pambentukan apoptosom lan paningkatan permeabilitas membran mitokondria kanthi mekanisme Fas/TNF-α. Panyuwunan energi sing dhuwur ing kahanan iki nyebabaké mitokondria ora bisa mulihaké cadhangan ATP nganti bisa micu sirosis ati,[51] éwadéné peroksidasi lipid bakal nyebabaké karusakan ing DNA mitokondria lan membran mitokondria sisih njero sing diarani sardiolipin, kanthi paningkatan laju oksidasi-beta asam lemak, bakal dumadi akumulasi elektron ing respiratory chain komplèks I lan III sing ngedhunaké kadhar antioksidan.[50]

Sèl hépatosit apoptotik bakal dicerna déning sèl Ito dadi fibrinogen kanthi réaksi fibrogenesis sawisé diaktivasi déning prodhuk saka peroksidasi lipid lan rasio leptin sing dhuwur. Apoptosis kronis banjur dikompènsasi kanthi paningkatan laju proliferasi hépatosit, dikanthèni DNA sing rusak déning disfungsi mitokondria, lan nyebabaké mutasi genetik lan kanker.

Ing modhèl tikus, melatonin arupa senyawa sing ngedhunaké fibrosis ati,[52] sauntara ing modhèl klinci, kurkumin arupa senyawa organik sing ngedhunaké paraklinis steatohepatitis,[53] sauntara hormon serotonin[54] lan kurangé asupan metionina lan kolina[55] mènèhi èfèk suwaliké kanthi resistansi adiponektin.[56]

Disfungsi mitokondria uga ditemokaké ing kabèh patogenesis ati, saka kasus radhang nganti kanker lan transplantasi.[57] Ing kolestasis kronik, asam ursodeoksikolat bebarengan karo GSH silih sinergis minangka antioksidan sing ngreksa sardiolipin lan fosfatidil serina nganti nyegah dumadiné sirosis ati.[58]

Pangaruh alkohol[sunting | sunting sumber]

Alkohol ditepungi duwé fungsi immunosupresif marang sistem kakebalan awak, kalebu ngredhem ekspresi kluster diferensiasi CD4+ lan CD8+ sing diperlokaké jroning njaga tahaning ati marang infèksi viral, utamané HCV.[59] Alkohol uga ngredhem rasio kemokina IFN ing lintasan transduksi sinyal selular, saliyané ningkataké résiko dumadiné fibrosis.[60]

Akèh lintasan metabolisme mènèhi kontribusi marang alkohol kanggo ngindhuksi stres oksidatif.[61] Salah siji lintasan métabolisme sing asring diaktivasi déning etanol yaiku indhuksi enzim sitokrom P450 2E1. Enzim iki nimbulaké spesi oksigen réaktif kaya radikal anion superoksida lan hidrogen peroksida, sarta ngaktivasi subtrat toksik klebu etanol dadi prodhuk sing luwih réaktif lan toksik. Sèl dendritik katoné arupa sèl sing paling kapengaruh déning kandhutan etanol ing njero alkohol. Ing pacobèn migunakaké modhèl tikus, etanol ningkataké rasio plasma IL-1β, IL-6, IL-8, TNF-α, AST, ALT, ADH, γ-GT, TG, MDA lan ngredham rasio IL-10, GSH,[62] faktor transkripsi NF-κB lan AP-1.[63]

Pangaruh alkaloid[sunting | sunting sumber]

Kopi, salah siji komplèks senyawa alkaloid saka golongan purina xantina karo asam klorogenat lan lignan,[64] ing studi epidemiologis, disimpulaké minangka salah siji faktor pamudhun risiko dumadiné diabetes mellitus tipe 2,[65][66] penyakit Parkinson, sirosis ati lan karsinoma hepatoselular,[67] lan saya apiké toleransi glukosa.[64] Konsumsi kopi sacara kronis kabukti ora nyebabaké tekanan getih dhuwur nanging sacara akut ngakibataké paningkatan tekanan getih sauntara jroning selang wektu cendhak,[68] lan plasma homosisteina[67] saéngga bisa dadi ancaman kanggo panandhang gangguan kardiovaskular.[65]

Konsumsi kopi sacara teratur bisa ngedhunaké rasio enzim ALT sarta aktifitas enzimatik ing lintasan métabolisme ati,[69] sing asring disebabaké déning[70] infèksi viral, indhuksi obat-obatan, karacunan, kahanan iskemik, steatosis (akibat alkohol, diabetes, obesitas), panyakit otoimun,[71] lan resistansi insulin, sindrom metabolisme,[72] lan kakèhen dat wesi.[73] Saliyané ALT, kopi uga ngedhunaké enzim ati liyané, yaiku gamma-GT lan alkalina fosfatase.[74] lan mènèhi èfèk antioksidan lan detoksifikasi fasa II amarga senyawa diterpena, kafestol lan kahweol,[75] saéngga nyegah dumadiné prosès karsinogenesis.[76][77] Proses tersebut disertai dengan gamma-GT sebagai indikator utama.[78]

Transplantasi ati[sunting | sunting sumber]

Tèknologi transplantasi ati arupa asil sing dikembangaké saka panlitèn ing sapérangan bidhang studi kadhokteran. Ing taun 1953, Billingham, Brent, lan Medawar nemokaké yèn toléransi kimerisme[79] bisa diindhuksi déning infus sèl hematolimfopoietik donor ing modhèl tikus.[80]

Nalika taun 1958 studi canine ngembangaké sawijining téori ngenani molekul hépatotrofik ing portal pambuluh walik ing ati lan nemokaké hormon insulin minangka faktor hépatotrofik utama saka sapérangan faktor liya sing ana.[81] Ing wektu sing mèh bebarengan téori ngenani transplantasi multiviseral lan ati uga ngrembaka saka studi imunosupresi sing nyinaoni algoritma empiris saka pangenalan pola lan rèspon térapis. Nalika awal 1960, dibuktèkaké yèn canine lan allograft manungsa nduwé toléransi kimersime sing bisa kaindhuksi otomatis kanthi bantuan imunosupresi, nganti akir 1962 disimpulaké kanthi klèru, yèn transplantasi nglibataké loro sistem kakebalan sing béda. Konsekwènsi kasimpulan kasebut dadi dogma yèn tolerogenisitas ati, dhasaré béda, ora mung karo sumsum balung mburi, nanging karo kabèh organ awak liyané.[80] Keklèron iki ora kakorèksi kanthi becik tekan taun 1990.[79]

Transplantasi ati sing pisanan dilakokaké ing Denver nalika taun 1963,[82] pisanan kasil kacathet nalika taun 1967 kanthi azatioprina, prednison lan globulin anti-limfoid, déning Thomas E. Starzl saka Amérika Sarékat, disusul déning kasilé transplantasi sumsum balung mburi manungsa nalika taun 1968.[79] Rentang wektu antara taun 1967 tekan 1979 nyathet kaping 84 transplantasi ati ing bocah kanthi 30% daya tahan urip tekan 2 taun.[82]

Nrembakané studi imunosupresi banjur mènèhaké kabecikan lan pangarep-arep urip luwih dawa kanggo pasien, antarané kanthi panggantian azatioprina mawa siklosporina nalika taun 1979, banjur kagantèkaké mawa takrolimus nalika taun 1989.[81]

Nalika taun 1992, dikembangaké téori mikrokimerisme leukosit donor[83] kanthi cakupan donor saka silsilah sing béda, sing mènèhaké pangarep-arep urip sing dawa banget kanggo panampa donor organ, sawisé dikawruhi gegandhèngan antarané aspèk imunologis saka transplantasi, infèksi, toléransi déning sumsum balung mburi, neoplasma lan kelainan otoimun, sing diarani minangka mekanisme seminal. Rèspon kakebalan lan toléransi kakebalan antarané organ donor lan awak ditemokaké arupa fungsi saka migrasi lan lokalisasi leukosit.[80] Salah siji temuané yaiku aktivasi sistem kakebalan turunan déning sel NK lan interferon-γ langsung sawisé transplantasi rampung dilakokaké.[84] Ing modhèl tikus, sèl hépatosit donor ditemokaké asifat antigenik banget saéngga njalari rèspon panulakan, sing bisa dilakokaké sacara mandhiri utawa bebarengan antarané sèl T CD4 lan sèl T CD8.[85]

Kanggo iku diperlokaké terapi imunosupresif sing intensif sadurungé transplantasi dilakokaké, sing diarani preparative regimen utawa conditioning kanggo nyegah panulakan organ donor déning sistem kakebalan inang.[86] Terapi imunosupresif mau ditujokaké kanggo nekan sèl T lan sèl NK inang guna mènèhaké ruwang ing njero sumsum balung mburi kanggo transplantasi sèl punca hematopoietik saka organ donor liwat terapi mielosupresif, kanggo kaseimbangan répopulasi sèl donor karo sèl asil diferensiasi saka sèl punca inang.

Diwasa iki, transplantasi ati dilakokaké mung nalika ati wis mlebu jenjang akir sawijining panyakit, utawa wis dadi disfungsi akut sing diarani fulminant hepatic failure. Kasus transplantasi ati ing manungsa umumé disebabaké déning sirosis ati akibat saka hépatitis C kronis, katergantungan alkohol, hepatitis otoimun lsp.

Tèknik umum sing dipigunakaké yaiku transplantasi ortotopik, yaiku panempatan organ donor ing posisi anatomik sing padha karo posisi awal organ sadurungé. Transplantasi ati duwé potènsi bisa ditrepaké, mung yèn panampa organ donor ora duwé kahanan liya sing ngeboti, kayata kanker metastatis ing njaba organ ati, katergantungan marang obat-obatan utawa alkohol. Sapérangan ahli duwé pedoman ing kriteria Milan kanggo selèksi pasien transplantasi ati.

Organ donor, diarani allograft, biasané asalé saka manungsa liya sing nembé nilar donya akibat tatu utek traumatik (kadaverik). Tèknik transplantasi liya migunakaké organ manungsa sing isih urip, oprasi hepatektomi ngangkat 20% ati ing sègmèn Coinaud 2 lan 3 saka wong diwasa kanggo didonoraké marang sawijining bocah, nalika taun 1989.

Wacan terusan[sunting | sunting sumber]

Rujukan[sunting | sunting sumber]

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Pranala njaba[sunting | sunting sumber]

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Sistem pancernan - sunting

Tutuk | Faring | Kerongkongan | Lambung | Pankreas | Kantung empedu | Ati | Usus alus (usus rolas driji, usus kosong, usus penyerepan) | Usus gedhé | Usus buntu | Umbai cacing | Rektum | Anus

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