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白細胞介素-10

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維基百科，自由的百科全書
白細胞介素-10
已知的結構
PDB直系同源搜索: PDBe RCSB
識別號
別名IL10；, CSIF, GVHDS, IL-10, IL10A, TGIF, interleukin 10
外部IDOMIM：124092 MGI：96537 HomoloGene：478 GeneCards：IL10
相關疾病
貝賽特氏症、​潰瘍性結腸炎[1]
基因位置（人類）
1號染色體
染色體1號染色體[2]
1號染色體
白細胞介素-10的基因位置
白細胞介素-10的基因位置
基因座1q32.1起始206,767,602 bp[2]
終止206,774,541 bp[2]
RNA表達模式
查閱更多表達數據
直系同源
物種人類小鼠
Entrez

3586

16153

Ensembl

ENSG00000136634

ENSMUSG00000016529

UniProt

P22301

P18893

mRNA​序列

NM_000572

NM_010548

蛋白序列

NP_000563

NP_034678

基因位置​（UCSC）Chr 1: 206.77 – 206.77 MbChr 1: 130.95 – 130.95 Mb
PubMed​查找[4][5]
維基數據
檢視/編輯人類檢視/編輯小鼠

白細胞介素-10（亦稱為介白素-10，英文：Interleukin 10，簡稱IL-10），也稱為細胞激素合成抑制因子（cytokine synthesis inhibitory factor，CSIF），是一種抗炎症細胞因子。在人類中，IL-10由「IL10」基因編碼。[6]IL-10的訊號需要藉由細胞膜上的介白素-10受體（IL-10受體）傳遞到細胞內。IL-10受體在作用時構型為含四個次單元的蛋白質複合體，其中包含兩個IL-10受體1（IL-10R1）單元以及兩個IL-10受體2（IL-10R2）單元。在接收到IL-10訊號時，IL-10R1會先直接與IL-10結合，之後呼叫（recruit）IL-10R2形成完整複合體，以進行後續的訊號傳遞，IL-10R2並不直接與IL-10結合。[7]IL-10通過JAK1和Tyk2分別磷酸化IL-10受體1、IL-10受體2的胞質尾端，來誘導STAT3信號傳遞。

基因和蛋白質結構

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IL-10蛋白是同型二聚體，每個亞基的長度均為178個氨基酸。[8]

IL-10被歸為2類細胞因子——包括IL-19、IL-20、IL-22、IL-24(Mda-7)、IL-26和I型干擾素（IFN-α,-β,-ε,-κ,-ω），II型（IFN-γ），III型（IFN-λ，[9]也稱為IL-28A，IL-28B，和IL-29）。[10]

表達與合成

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在人類中，IL-10由「IL10」基因編碼，該基因位於1號染色體上，包含5個外顯子[6]，主要由單核細胞產生，並在較小程度上由淋巴細胞產生，即II型T輔助細胞（TH2），肥大細胞，CD4+CD25+Foxp3+調節性T細胞，以及活化的T細胞和B細胞的某些子集。在這些細胞中觸發PD-1後，單核細胞可以產生IL-10[11]。IL-10上調也由GPCR介導，例如β-2腎上腺素[12]和2型大麻素[13]受體。IL-10的表達在未經刺激的組織中極少，似乎需要由共生或病原菌觸發。[14]IL-10表達在轉錄和轉錄後水平受到嚴格調節。刺激TLR或Fc受體途徑後，在單核細胞中觀察到廣泛的IL-10基因座重塑[15]。IL-10誘導涉及ERK1/2，p38和NF-κB信號傳導，以及通過轉錄因子NF-κB和AP-1的啟動子結合而引起的轉錄激活。IL-10可能通過負反饋迴路自動調節其表達，該迴路涉及IL-10受體的自分泌刺激和p38信號通路的抑制[16]。此外，IL-10的表達在轉錄後水平受到廣泛調控，這可能涉及通過富含AU的元件[17]和諸如let-7[18]或miR-106的microRNA控制mRNA的穩定性[19]。

功能

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IL-10是一種在免疫調節和炎症中具有多效性的細胞因子。它下調了巨噬細胞上Th1細胞因子、MHC-II類抗原、共刺激分子的表達。它還增強了B細胞的生存、增殖和產生抗體的能力。IL-10可以阻斷NF-kB活動，並參與JAK-STAT信號轉導通路的調節。

IL-10發現與1991年[20]，最初報道其抑制細胞分泌、抗原呈遞和CD4+細胞活化。[21][22][23][24]進一步的研究表明，IL-10主要抑制脂多糖(LPS)和細菌產物介導的促炎性細胞因子TNFα[25]、IL-1β[25]、IL-12[26]、IFNγ[27]的分泌，這些細胞因子由Toll樣受體（TLR）觸發的骨髓細胞譜系分泌。

對腫瘤的影響

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隨着時間的流逝，IL-10功能的細微差別出現了，因為已證明對荷瘤小鼠的治療可抑制腫瘤轉移[28]。多個實驗室的進一步研究已經產生了進一步支持IL-10在免疫神經學背景下的免疫刺激能力的數據。從IL-10轉基因小鼠[29]中轉染的腫瘤細胞系[30][31]中表達IL-10或用IL-10給藥可控制原發性腫瘤生長並降低轉移負擔。[32][33]最近，聚乙二醇化重組鼠IL-10（PEG-rMuIL-10）已顯示出誘導IFNγ和CD8+T細胞依賴性抗腫瘤免疫力[34][35]。更具體地，已顯示PEG化的重組人IL-10（PEG-rHuIL-10）增強細胞毒性分子粒酶B和穿孔素的CD8+T細胞分泌，並增強T細胞受體依賴性IFNγ的分泌[36]。

在疾病中的作用

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對小鼠的研究表明，肥大細胞也產生IL-10，抵消了這些細胞在變態反應部位的炎症作用[37]。

IL-10能夠抑制由巨噬細胞和Th1T細胞等細胞產生的促炎細胞因子如IFN-γ、IL-2、IL-3、TNFα和GM-CSF的合成。它也顯示出抑制抗原呈遞細胞的抗原呈遞能力的強大能力。但是，它也對某些T細胞（Th2）和肥大細胞具有刺激性，並刺激B細胞成熟和抗體產生。

IL-10檢查環氧合酶Cyclo-oxygenase-2（COX-2）的可誘導形式。缺乏IL-10已被證明可導致COX激活並導致血栓烷受體激活，從而引起小鼠血管內皮和心臟功能障礙。白介素10基因敲除脆弱的小鼠會隨着年齡的增長而出現心臟和血管功能障礙[38]。

IL-10與肌動蛋白有關，因為運動會引起IL-1ra，IL-10和sTNF-R的循環水平增加，這表明體育鍛煉可促進抗炎細胞因子的形成。[39][40]

與健康個體相比，在診斷為多發性硬化症的個體中觀察到較低水平的IL-10[41]。由於IL-10水平的降低，TNFα水平不能得到有效調節，因為IL-10可以調節TNF-α轉化酶[42]。結果，TNFα水平升高並導致炎症。[43]TNFα本身通過TNF受體1誘導少突膠質細胞脫髓鞘，而慢性炎症與神經元脫髓鞘有關。

在黑素瘤細胞系中，IL-10調節NKG2D配體的表面表達。[44]

臨床使用或試驗

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在小鼠中進行的基因敲除研究表明，這種細胞因子在腸道中是必需的免疫調節劑。[45]的確，克羅恩氏病患者對用重組白介素10產生細菌的治療反應良好，證明了IL-10對抵消人體過度活躍的免疫反應的重要性。[46]

根據數據，在臨床試驗中，數千名患有各種自身免疫性疾病的患者接受了重組人IL-10（rHuIL-10）的治療。與預期相反，rHuIL-10治療並未對克羅恩病患者的疾病產生重大影響。[47][48][49]或類風濕關節炎。[50]rHuIL-10治療最初在牛皮癬中顯示出有希望的臨床數據。[51]但在一項隨機，雙盲，安慰劑對照的II期臨床試驗中未能達到臨床意義。[52]對rHuIL-10在人類中作用的進一步研究表明，rHuIL-10除了抑制炎症外，還能夠發揮促炎作用。[53][54]

聚乙二醇化形式

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除這些數據外，目前正在進行一項I期免疫科學臨床試驗，以評估PEG化重組人IL-10（PEG-rHuIL-10，AM0010）的治療能力。[55]與臨床前免疫免疫學數據一致，研究者報告了實質性的抗腫瘤功效。相反於所報告的在體外和體內產生的IL-10的免疫抑制作用，[22][23][24][56][57]治療癌症患者的PEG-重組人白介-10引發的劑量滴定感應的免疫刺激細胞因子IFNγ，IL-18，IL-7，GM-CSF和IL-4的表達。此外，接受治療的患者的外周CD8+T細胞表達活化標記，例如程序性死亡配體1（PD-L1）+，淋巴細胞活化基因3（LAG3）+和Fas配體（FasL）升高，血清TGFβ降低，其摺疊倍數增加。這些發現與使用PEG-rMuIL-10的已發表的臨床前免疫科學報告[34][35]以及以前用rHuIL-10治療人類的發現一致。[53][54]這些數據表明，儘管IL-10可以在細菌產物刺激的髓樣細胞中發揮免疫抑制作用，但對人的rHuIL-10/PEG-rHuIL-10治療主要是免疫刺激。截至2018年 (2018-Missing required parameter 1=month!)AM0010（又名pegilodecakin）正在進行3期臨床試驗。[58]

互動

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已經證明IL-10與白介素10受體α亞基相互作用。[59][60][61][62][63]

IL-10受體複合物也需要IL10R2鏈來啟動信號傳導。這種配體-受體的組合存在於鳥類和青蛙中，也可能存在於骨魚類中。 

參考資料

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