背景[1-6]
人外周血源單個(gè)核細(xì)胞(Peripheral blood mononuclear cell,PBMC)是外周血中具有單個(gè)核的細(xì)胞,包括淋巴細(xì)胞和單核細(xì)胞。PBMC(peripheral blood mononuclear cell),外周血單個(gè)核細(xì)胞,顧名思義,其主要細(xì)胞類型為血液里邊具有單個(gè)核的細(xì)胞,主要包括淋巴細(xì)胞(T\B),單核細(xì)胞,吞噬細(xì)胞,樹突狀細(xì)胞和其他少量細(xì)胞類型。其中淋巴細(xì)胞占很大一部分。
分離PBMC的主要目的是為了將多核細(xì)胞和紅細(xì)胞去除,從而能夠很方便地模擬體外的血液免疫環(huán)境。單核細(xì)胞(monocytes)是血液中的血細(xì)胞,也是體積的白細(xì)胞,是機(jī)體防御系統(tǒng)的一個(gè)重要組成部分。單核細(xì)胞來源于骨髓中的造血干細(xì)胞,并在骨髓中發(fā)育,當(dāng)它們從骨髓進(jìn)入血液時(shí)仍然是尚未成熟的細(xì)胞。目前認(rèn)為它是巨噬細(xì)胞和樹突狀細(xì)胞的前身,具有明顯的變形運(yùn)動(dòng),能吞噬、清除受傷、衰老的細(xì)胞及其碎片。
單核細(xì)胞還參與免疫反應(yīng),在吞噬抗原后將所攜帶的抗原決定簇轉(zhuǎn)交給淋巴細(xì)胞,誘導(dǎo)淋巴細(xì)胞的特異性免疫性反應(yīng)。單核細(xì)胞也是對付細(xì)胞內(nèi)致病細(xì)菌和寄生蟲的主要細(xì)胞防衛(wèi)系統(tǒng),還具有識別和殺傷腫瘤細(xì)胞的能力。與其他血細(xì)胞比較,單核細(xì)胞內(nèi)含有更多的非特異性脂酶,并且具有更強(qiáng)的吞噬作用。當(dāng)機(jī)體發(fā)生炎癥或其他疾病都可引起單核細(xì)胞總數(shù)百分比發(fā)生變化,因此檢查單核細(xì)胞計(jì)數(shù)成為輔助診斷的一種重要方法。
應(yīng)用[7][8]
可用于人外周血單個(gè)核細(xì)胞的尿酸鹽轉(zhuǎn)運(yùn)蛋白基因表達(dá)譜及其在原發(fā)性痛風(fēng)患者表達(dá)量變化的意義:
從20種尿酸鹽轉(zhuǎn)運(yùn)蛋白基因(ABCG2、LGALS9、ABCC4、PDZK1、GCKR、LRRC16A、SLC2A9、SLC5A8、SLC5A12、SLC13A2、SLC13A3、SLC17A1、SLC17A3、SLC16A9、SLC22A6、SLC22A7、SLC22A8、SLC22A11、SLC22A12、SLC22A13)中篩選出在外周血單個(gè)核細(xì)胞(peripheral blood mononuclear cells,PBMCs)中可明確表達(dá)的尿酸鹽轉(zhuǎn)運(yùn)蛋白基因,檢測原發(fā)性痛風(fēng)性關(guān)節(jié)炎(gouty arthritis,GA)患者PBMCs中可表達(dá)的尿酸鹽轉(zhuǎn)運(yùn)蛋白基因mRNA表達(dá)量變化,分析其與GA患者臨床實(shí)驗(yàn)指標(biāo)的關(guān)系,初步探討PBMCs可表達(dá)的尿酸鹽轉(zhuǎn)運(yùn)蛋白在GA患者發(fā)病中可能的作用。
參考文獻(xiàn)
[1]Twenty-eight loci that influence serum urate levels:analysis of association with gout[J].Phipps-Green A J,Merriman M E,Topless R,Altaf S,Montgomery G W,Franklin C,Jones G T,van Rij A M,White D,Stamp L K,Dalbeth N,Merriman T R.Annals of the Rheumatic Diseases.2016(1)
[2]NPT1/SLC17A1 Is a Renal Urate Exporter in Humans and Its Common Gain‐of‐Function Variant Decreases the Risk of Renal Underexcretion Gout[J].Toshinori Chiba,Hirotaka Matsuo,Yusuke Kawamura,Shushi Nagamori,Takashi Nishiyama,Ling Wei,Akiyoshi Nakayama,Takahiro Nakamura,Masayuki Sakiyama,Tappei Takada,Yutaka Taketani,Shino Suma,Mariko Naito,Takashi Oda,Hiroo Kumagai,Yoshinori Moriyama,Kimiyoshi Ichida,Toru Shimizu,Yoshikatsu Kanai,Nariyoshi Shinomiya.Arthritis&Rheumatology.2015(1)
[3]Renal Transport of Uric Acid:Evolving Concepts and Uncertainties[J].Ion Alexandru Bobulescu,Orson W.Moe.Advances in Chronic Kidney Disease.2012(6)
[4]ABCG2 is a High-Capacity Urate Transporter and its Genetic Impairment Increases Serum Uric Acid Levels in Humans[J].Akiyoshi Nakayama,Hirotaka Matsuo,Tappei Takada,Kimiyoshi Ichida,Takahiro Nakamura,Yuki Ikebuchi,Kousei Ito,Tatsuo Hosoya,Yoshikatsu Kanai,Hiroshi Suzuki,Nariyoshi Shinomiya.Nucleosides,Nucleotides and Nucleic Acids.2011(12)
[5]Gout[J].Pascal Richette,Thomas Bardin.The Lancet.2010(9711)
[6]High‐resolution melting analysis for the rapid detection of an intronic single nucleotide polymorphism in SLC22A12 in male patients with primary gout in China[J].M.Guan,J.Zhang,Y.Chen,W.Liu,N.Kong,H.Zou.Scandinavian Journal of Rheumatology.2009(4)
[7]Regulation of the human PDZK1 expression by peroxisome proliferator-activated receptor alpha[J].Keisuke Tachibana,Naohiko Anzai,Chihiro Ueda,Tatsuya Katayama,Daisuke Yamasaki,Takayoshi Kirino,Rika Takahashi,Kenji Ishimoto,Hidenori Komori,Toshiya Tanaka,Takao Hamakubo,Yukihiko Ueda,Hiroyuki Arai,Juro Sakai,Tatsuhiko Kodama,Takefumi Doi.FEBS Letters.2008(28)
[8]王勝嵐.人外周血單個(gè)核細(xì)胞的尿酸鹽轉(zhuǎn)運(yùn)蛋白基因表達(dá)譜及其在原發(fā)性痛風(fēng)患者表達(dá)量變化的意義[D].川北醫(yī)學(xué)院,2016.