淋巴球功能性抗原1

淋巴球功能性抗原1（英文：Lymphocyte function-associated antigen 1, LFA-1）是淋巴球上的細胞黏附分子，屬於黏附分子中整合素（integrin）超家族。[1] LFA-1對淋巴球的遷移很重要，能幫助淋巴球離開血流並進入組織。LFA-1亦能幫忙減緩中性球的流速好讓表皮細胞能抓住他們。[2] 此外，LFA-1也參與细胞毒性T细胞的胞殺過程、粒细胞與单核细胞的抗體調節胞殺作用。[3]自2007年起，已經發現了LFA-1的6個配體：ICAM-1（英语：ICAM-1）、ICAM-2（英语：ICAM-2）、ICAM-3、ICAM-4、ICAM-5和JAM-A [2]。最近顯示LFA-1與ICAM-1的互動能刺激T細胞分化的傳訊途徑。[4][1]

結構

LFA-1的結構是兩個非共價鍵結合的次單體組成的異二聚體醣蛋白[3]。LFA-1的兩個次單體分別是α次單體與β次單體[2]，α次單體一開始被命名為aL（在1983年時）[2]，又名CD11a，β次單體則另稱B2[2]或CD18，B2存在於所有整合黏附素中。所以LFA-1又稱CD11aCD18。ICAM的結合位在α次單體上的I-蛋白質域[5]。因為I-蛋白質域上有雙價陽離子，所以這個特定結合位通常被稱作金屬離子依賴型黏附區（metal-ion dependent adhesion site, MIDAS）[5]。

活化

在非活化狀態下，LFA-1呈現彎曲狀構型，對ICAM的結合活性也很低[5]，因為彎曲狀構型埋藏了MIDAS。 趨化因子會刺激LFA-1的活化過程[5]。LFA-1的活化過程起自胞內G蛋白Rap1的活化[2]。Rap1協助解除LFA-1的α與β次單體間的束縛，導致半延伸狀態。這個構型改變會刺激蛋白質聚集並組成一活化複合體，這個活化複合體會再鬆動α與β次單體[2]。化學趨化因子也會刺激β次單體上的類I蛋白質域，使β次單體上的MIDAS結合到α次單體上的I蛋白質域的谷氨酸。這個結合過程會使β次單體拉下I蛋白質體的7螺旋，暴露出α次單體上的MIDAS，以利結合。這會使LFA-1經歷構型改變至完整延伸狀態。這種活化LFA-1的過程被稱作｢inside-out｣傳訊，能使LFA-1藉由構型改變切換結合的親和力[5]。

發現

細胞黏附因子的早期發現包含使用單株抗體來抑制細胞黏附的過程，那些會與單株抗體結合的抗原被認為是細胞辨識過程中的重要分子[2]。這些實驗產生了一個名詞：整合黏附素，描述這些蛋白質在細胞黏附過程及細胞外基質（ECM）和細胞骨架的跨模交互作用中的整合角色[2]。LFA-1這種白血球整合黏附素首先由Timothy Springer在1980年代於老鼠中發現[2]。

白血球黏附缺乏症

白血球黏附缺乏症（英语：Leukocyte Adhesion Deficiency）（LAD）是一種體染色體隱性遺傳的自體免疫疾病，起因於表面重要黏附分子（包含LFA-1）的缺失[6] 。這種缺失會影響到白血球[6] ，造成無效的白血球遷移與吞噬作用[3]。LAD的患者通常中性球的功能低落[2]。LAD的其中一種亞型，LAD1，是起因於缺乏有β次單體的整合黏附素，包含LFA-1[3]。LAD1的常見症狀是反覆的細菌感染、傷口癒合失敗、化膿和粒細胞增生（granulocytosis）[7]。CD11和CD18的低表現量也是LAD1的成因，CD11位在第16對染色體上而CD18在第21對上[6]。


参见

參考文獻

  1. ^ 1.0 1.1 M., Lackie, J. A dictionary of biomedicine 1st ed. Oxford: Oxford University Press. 2010. ISBN 9780191727948. OCLC 663104793. 
  2. ^ 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 Adhesion molecules : function and inhibition. Ley, Klaus, 1957-. Basel: Birkhauser. 2007. ISBN 9783764379759. OCLC 261225084. 
  3. ^ 3.0 3.1 3.2 3.3 Oxford dictionary of biochemistry and molecular biology. Cammack, Richard, Ph. D. Rev. ed. Oxford: Oxford University Press. 2006. ISBN 9780191727641. OCLC 743217704. 
  4. ^ Verma NK, Kelleher D. Not Just an Adhesion Molecule: LFA-1 Contact Tunes the T Lymphocyte Program. Journal of Immunology. 2017-08, 199 (4): 1213–1221. PMID 28784685. doi:10.4049/jimmunol.1700495. 
  5. ^ 5.0 5.1 5.2 5.3 5.4 Protein-protein interactions in drug discovery. Dömling, Alexander. Weinheim: Wiley-VCH. 2013. ISBN 9783527648238. OCLC 828743731. 
  6. ^ 6.0 6.1 6.2 Akbari, H.; Zadeh, M. M. Leukocyte adhesion deficiency. Indian Journal of Pediatrics. 2001-01, 68 (1): 77–79 [2018-05-20]. ISSN 0019-5456. PMID 11237241. （原始内容存档于2018-03-08）. 
  7. ^ Anderson, D. C.; Springer, T. A. Leukocyte adhesion deficiency: an inherited defect in the Mac-1, LFA-1, and p150,95 glycoproteins. Annual Review of Medicine. 1987, 38: 175–194 [2018-05-20]. ISSN 0066-4219. PMID 3555290. doi:10.1146/annurev.me.38.020187.001135. （原始内容存档于2018-10-11）. 

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